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1
Nurullahoğlu-Atalık, KE, S. Kutlu, H. Solak, and R. Özen Koca. "Cilostazol enhances atorvastatin-induced vasodilation of female rat aorta during aging." Physiology International 104, no. 3 (September 2017): 226–34. http://dx.doi.org/10.1556/2060.104.2017.3.3.
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Statins have cholesterol-independent effects including an increased vascular nitric oxide activity and are commonly used by patients with cardiovascular disease. Such patients frequently have cardiovascular diseases, which may be treated with cilostazol, a platelet aggregation inhibitor. This study was designed to investigate whether combined use of cilostazol would increase the inhibitory effect of statin on vascular smooth muscle and how maturation would affect these responses. Female Wistar rats, aged 3–4 months (young) and 14–15 months (adult), were sacrificed by cervical dislocation and the thoracic aorta was dissected and cut into 3- to 4-mm-long rings. The rings were mounted under a resting tension of 1 g in a 20-ml organ bath filled with Krebs–Henseleit solution. Rings were precontracted with phenylephrine (10−6 M), and the presence of endothelium was confirmed with acetylcholine (10−6 M). Then, the concentration–response curves were obtained for atorvastatin alone (10−10 to 3 × 10−4 M; control) and in the presence of cilostazol (10−6 M) in young and adult rat aortas. This experimental protocol was also carried out in aorta rings, which had been pretreated with NG-nitro-l-arginine methyl ester (l-NAME, 10−4 M). Atorvastatin induced concentration-dependent relaxations in young and adult rat thoracic aorta rings precontracted with phenylephrine. The pIC50 value of atorvastatin was significantly decreased in adult rat aortas. In addition, pretreatment of aortas with cilostazol enhanced the potency of atorvastatin in both young and adult aortas. Incubation with l-NAME did not completely eliminate the relaxations to atorvastatin in the presence of cilostazol. These results suggest that combined application of cilostazol with atorvastatin was significantly more potent than atorvastatin alone. Combined drug therapy may be efficacious in delaying the occurrence of cardiovascular events.
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Pieper, G. M., D. A. Mei, P. Langenstroer, and S. T. O'Rourke. "Bioassay of endothelium-derived relaxing factor in diabetic rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H676—H680. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h676.
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The bioassay technique was utilized to quantitate endothelium-derived relaxing factor (EDRF) released from perfused donor segments of control and diabetic rat aorta. In the presence of indomethacin, perfusates of donor segments with endothelium were allowed to superfuse recipient detector rings of normal rat aorta without endothelium. Under basal conditions, relaxations of the bioassay rings to perfusates of control and diabetic donor segments were similar. Perfusion of donor segments with acetylcholine produced relaxation of bioassay rings, which was decreased from endothelial perfusion of diabetic donor segments. These relaxations were inhibited by addition of methylene blue to the detector ring or by perfusion of donor segments with nitro-L-arginine. Infusion of superoxide dismutase (SOD) at a site proximal to the donor segment normalized relaxations induced by acetylcholine addition to diabetic donors. In contrast, infusion of SOD distal to the donor had no effect on acetylcholine-stimulated relaxations of detector rings from control donors while attenuating, paradoxically, the relaxations of detector rings from diabetic donors. These results suggest that diabetic rat aortas release similar levels of EDRF in response to acetylcholine, but the action of EDRF arising from diabetic donors is attenuated by enhanced release of oxygen-derived free radicals, which limits EDRF-mediated relaxation of vascular smooth muscle.
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Langenstroer, P., and G. M. Pieper. "Regulation of spontaneous EDRF release in diabetic rat aorta by oxygen free radicals." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 1 (July 1, 1992): H257—H265. http://dx.doi.org/10.1152/ajpheart.1992.263.1.h257.
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The interaction of endothelium-derived relaxing factor (EDRF) and oxygen-derived free radicals may potentially play an important role in the pathophysiology of complications associated with diabetes. In the present study, we investigated spontaneous EDRF release in diabetic rat aorta that is unmasked by the addition of superoxide dismutase (SOD). SOD produced a significantly greater relaxation in diabetic aorta compared with control aorta using both aortic ring and bioassay preparations. This relaxation was unaltered by pretreatment with catalase or indomethacin. Removal of the endothelium or pretreatment with either NG-monomethyl-L-arginine or methylene blue eliminated SOD-induced relaxation in both control and diabetic rings. Measurement of antioxidant enzymes revealed an elevation in catalase in diabetic aorta, with no difference in the SOD or glutathione peroxidase activity. The increase in catalase activity suggests increased exposure of diabetic aorta to hydrogen peroxide. Pretreatment of rings with the catalase inhibitor, 3-amino-1,2,4-triazole, attenuated the SOD-induced relaxation in diabetic aortic rings but had no effect in control aortic rings. In summary, our observations suggest that the diabetic rat aorta releases more spontaneous EDRF than control aorta; however, the activity of EDRF on vascular smooth muscle tone is masked by increased destruction by oxygen-derived free radicals.
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Kutchai, Howard, and Lisa M. Geddis. "Lactate Transport in Rat Aorta." Journal of Vascular Research 22, no. 2 (1985): 84–93. http://dx.doi.org/10.1159/000158587.
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1. Ouabain (10 mM) and gramicidin (5 µg/ml) do not inhibit lactate uptake by rat aortic rings. This supports the integretation that a Na<sup>+</sup> gradient is not involved in lactate transport. 2. Dinitrophenol (25 µM) fails to inhibit lactate uptake, suggesting that oxidative metabolism is not required for lactate uptake. 3. DIDS (4,4’-diisothiocyano-2,2’-stilbenedisulfonate), quercetin, and α-cyano-4-hydroxycinnamate – agents that have been reported to inhibit lactate transport in other cell types -were ineffective in inhibiting lactate transport in rat aortic rings.4. Inhibition of lactate uptake by glyceraldehyde is not stereospecific, does not involve inhibition of glucose phosphorylation, and does not appear to involve interaction with membrane sulfhydryls. PCMBS (p-chloromercuribenzenesulfonate) does not markedly inhibit the initial rate of lactate uptake, but diminishes the lactate space at later times.5. Pyruvate, phenylpyruvate, and thiolactate inhibit lactate uptake, but propionate and glycolate are poor inhibitors.
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Bouchard, Jean-François, Éric C. Dumont, and Daniel Lamontagne. "Modification of vasodilator response in streptozotocin-induced diabetic rat." Canadian Journal of Physiology and Pharmacology 77, no. 12 (November 15, 1999): 980–85. http://dx.doi.org/10.1139/y99-106.
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Functional dilatory response in streptozotocin-induced diabetic rats was investigated using thoracic aortas, isolated hearts, and mesenteric beds. Dose-response curves to the PGI2 analogue iloprost on phenylephrine-preconstricted rings of diabetic rats and controls were comparable. In contrast, decreased vasodilation in diabetic rats was observed when dose-response curves to iloprost were performed in hearts and on phenylephrine-preconstricted mesenteric beds. Dose-response curves to forskolin, an adenylyl cyclase activator, performed with hearts and phenylephrine-preconstricted aortic rings and isolated mesenteric beds of diabetic rats and controls were comparable. However, a decreased vasodilation to the ATP-sensitive potassium channel (KATP) activator lemakalim was observed in diabetic hearts, but not in aortic rings and mesenteric beds. In conclusion, under our experimental conditions, diabetes mellitus affects the vasodilation to iloprost in both coronary and mesenteric beds, but not in the aorta. In the heart, this modification of vascular reactivity may be due to a decrease in KATP channel mediated response and not to a decreased activity of adenylyl cyclase. At this time, in the isolated mesenteric bed, the mechanism of this modification in vascular reactivity remains unknown.Key words: diabetes mellitus, iloprost, KATP channels, adenylyl cyclase, aorta, coronary circulation, mesenteric bed.
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Chakraborty, Indrani, Nirmal Chandra Sukul, Rungrapa Mesripong, Nattaya Chaothanaphat, Prasan Dhummaupakorn, and Anirban Sukul. "High dilutions of homeopathic remedies induce relaxation of rat aorta precontracted with Noradrenalin." International Journal of High Dilution Research - ISSN 1982-6206 12, no. 43 (December 2, 2021): 44–51. http://dx.doi.org/10.51910/ijhdr.v12i43.627.
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BACKGROUND
Homeopathic potencies have been reported to produce alteration of contraction in isolated rat ileum in an organ bath. Potentized homeopathic drugs like Lycopus V and Aurum met are used for the treatment of hypertension.
AIM
The purpose of this study is to see whether Lycopus V 30 CH and Aurum met 30 CH could produce relaxation of isolated rat aorta in the organ bath.
METHODS
The aorta of rats were dissected out, placed in Krebs-Henseleit solution, cleared of connective tissue and endothelium and cut into 2-2.5 mm long rings. The rings were fixed in organ baths with the upper end connected by a string to an isometric transducer which was finally attached through a data acquisitation equipment to a computer. Aurum met 30 CH Lycopus V 30 CH, and their medium 90% ethanol were added separately to the bathing fluid containing the aorta rings which were precontracted with noradrenalin (NA).
RESULTS
Both the drugs produced significant relaxation of the aorta (p
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Tsakadze, Nina L., Sanjay Srivastava, Sunday O. Awe, Ayotunde S. O. Adeagbo, Aruni Bhatnagar, and Stanley E. D'Souza. "Acrolein-induced vasomotor responses of rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (August 2003): H727—H734. http://dx.doi.org/10.1152/ajpheart.00269.2003.
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Acrolein is a highly reactive aldehyde pollutant and an endogenous product of lipid peroxidation. Increased generation of, or exposures to, acrolein incites pulmonary and vascular injury. The effects of acrolein on the vasomotor responses of rat aortic rings were studied to understand its mechanism of action. Incubation with acrolein (10–100 μM) alone did not affect the resting tone of aortic vessels; however, a dose-dependent relaxation of phenylephrine-precontracted aortic rings was observed. Acrolein-induced relaxation was slow and time dependent and the extent of relaxation after 100 min of application was 44.7 ± 4.1% (10 μM), 56.0 ± 5.6% (20 μM), 61.0 ± 7.9% (40 μM), and 96.1 ± 2.1 (80 μM), respectively, versus 14.2 ± 3.3% relaxation in the absence of acrolein. Acrolein-induced vasorelaxation was prevented by endothelial denudation and was abolished on pretreatment with the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester, the guanylyl cyclase inhibitor 1 H-[1,2,4]oxidazolo[4,3- a]quinoxaline-1-one, or the cyclooxygenase inhibitor indomethacin. Inhibition of K+ channels (by tetrabutylammonium) or Na+-K+-ATPase (by ouabain) did not significantly prevent acrolein-mediated vasorelaxation. Exposure to acrolein in the presence or absence of other compounds elicited slow wave vasomotor effect in 77% of aortic vessels versus 1.4% in control. Vasomotor responses were also studied on aortic rings prepared from rats fed 2 mg · kg–1 · day–1 acrolein for 3 alternate days by oral gavage. These vessels developed a significantly lower contractile response to phenylephrine compared with controls. Together, these results indicate that acute acrolein exposure evokes delayed vasorelaxation due to a nitric oxide- and prostacyclin-dependent mechanism, whereas in vivo acrolein exposure compromises vessel contractility.
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Omanwar, S., B. Saidullah, K. Ravi, and M. Fahim. "Vasorelaxant effects of mercury on rat thoracic aorta." Human & Experimental Toxicology 33, no. 9 (December 17, 2013): 904–10. http://dx.doi.org/10.1177/0960327113512341.
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Mercury, a heavy metal, is widespread and persistent in the environment and has been elucidated as a possible risk factor in cardiovascular diseases. Mercury has been reported to selectively impair the nitric oxide (NO) pathway in the vascular endothelium as a consequence of oxidative stress. Conversely, mercury per se causes endothelium-dependent vasorelaxation at lower concentration via the NO pathway. Little is known about the effects of mercury per se on other endothelial mediators. To elucidate possible mechanisms involved in this action, isometric tension was measured in aortic rings precontracted with phenylephrine (10 µM) from Wistar rats. Responses to increasing concentrations of inorganic mercuric chloride (10−12–10−5 M) were obtained in the presence and absence of endothelium. Inorganic mercury produced a biphasic response in endothelium-intact aortic rings and produced only vasoconstriction in endothelium-denuded aortic rings. To study the possible underlying mechanisms for the biphasic response of mercury, increasing concentrations of mercuric chloride (10−12–10−5 M) were used before and after NG-nitro-l-arginine methyl ester (L-NAME (10−4 M)), glybenclamide (10−5 M), superoxide dismutase (10 U/ml) + catalase (100 U/ml), and nifedipine (10−4 M) treatment. Results suggest that mercury produces endothelium-dependent relaxation at low concentration mediated by endothelial-generated NO and endothelium-derived hyperpolarizing factor and endothelium-independent contraction resulting from the blockade of l-type Ca2+ channels by generation of free radicals.
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Delp, M. D., T. Holder-Binkley, M. H. Laughlin, and E. M. Hasser. "Vasoconstrictor properties of rat aorta are diminished by hindlimb unweighting." Journal of Applied Physiology 75, no. 6 (December 1, 1993): 2620–28. http://dx.doi.org/10.1152/jappl.1993.75.6.2620.
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Prolonged bed rest and exposure to weightlessness in humans result in cardiovascular alterations that are characterized by orthostatic intolerance and decreased exercise capacity. Modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Rat hindlimb unweighting (HU) was used as an animal model to determine whether prolonged decreases in weight-bearing activity induce changes in vasoreactivity of peripheral arterial vessels. Responses to vasoactive compounds were examined in vitro using isolated abdominal and thoracic aortic rings. Maximal isometric contractile tension evoked by the vasoconstrictors KCl (10–100 mM), norepinephrine (NE; 10(-9)-10(-4) M), phenylephrine (10(-9)-10(-4) M), arginine vasopressin (10(-13)-3 x 10(-5) M), and CaCl2 (10(-6)-10(-2) M) was lower in abdominal aortic rings from HU rats. Sensitivity [agonist concentration that produced 50% of maximal vasoconstrictor response (EC50)] to KCl was enhanced in segments from HU animals but was not different for the other constrictors. Maximal contractile responses of thoracic aortic rings to KCl (10–100 mM) and NE (10(-9)-10(-4) M) were also attenuated by HU. In abdominal aortic rings preconstricted with 10(-4) M NE, maximal vasodilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and 8-bromoguanosine 3',5'-cyclic monophosphate (10(-6)-10(-2) M) were greater in vessel rings from HU rats. However, with 10(-7) M NE preconstriction, maximal dilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and acetylcholine (10(-9)-10(-4) M) were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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Jing, Ming, Saiid Bina, Ajay Verma, Jayne L. Hart, and Sheila M. Muldoon. "Effects of Halothane and Isoflurane on Carbon Monoxide-induced Relaxations in the Rat Aorta." Anesthesiology 85, no. 2 (August 1, 1996): 347–54. http://dx.doi.org/10.1097/00000542-199608000-00017.
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Background Halothane and isoflurane previously were reported to attenuate endothelium-derived relaxing factor/nitric oxide-mediated vasodilation and cyclic guanosine monophosphate (cGMP) formation in isolated rat aortic rings. Carbon monoxide has many chemical and physiologic similarities to nitric oxide. This study was designed to investigate the effects of halothane and isoflurane on carbon monoxide-induced relaxations and cGMP formation in the isolated rat aorta. Methods Isometric tension was recorded continuously from endothelium denuded rat aortic rings suspended in Krebs-filled organ baths. Rings precontracted with submaximal concentrations of norepinephrine were exposed to cumulative concentrations of carbon monoxide (26-176 microM). This procedure was repeated three times, with anesthetics delivered 10 min before the second procedure. Carbon monoxide responses of rings contracted with the same concentration of norepinephrine (10(-6) M and 2 x 10(-6) M) used in the anesthetic-exposed preparations also were examined. The concentrations of cGMP were determined in denuded rings using radioimmunoassay. The rings were treated with carbon monoxide (176 microM, 30 s) alone, or carbon monoxide after a 10-min incubation with halothane (0.34 mM or 0.72 mM). To determine whether the sequence of anesthetic delivery influenced results, vascular rings pretreated with halothane were compared with nonpretreated rings. Results Carbon monoxide (26-176 microM) caused a dose-dependent reduction of norepinephrine-induced tension, with a maximal relaxation of 1.51 +/- 0.07 g (85 +/- 7% of norepinephrine-induced contraction). Halothane (0.34 mM and 0.72 mM) significantly attenuated the carbon monoxide-induced relaxations, but only the highest concentration of isoflurane (0.53 mM) significantly attenuated the carbon monoxide-induced relaxations. Carbon monoxide (176 microM) significantly increased cGMP content (+88.1 +/- 7.1%) and preincubation of the aortic rings with halothane (0.34 mM and 0.72 mM) inhibited this increase (-70.7 +/- 6.8% and -108.1 +/- 10.6%, respectively). When aortic rings and carbon monoxide were added simultaneously to Krebs solution equilibrated with halothane (0.72 mM), no inhibition of cGMP formation occurred. Conclusion Carbon monoxide-induced endothelium-independent relaxations of rat aortic rings were decreased by clinically relevant concentrations of halothane and isoflurane. The carbon monoxide-induced elevations of cGMP were attenuated by halothane only when the anesthetic was incubated with aortic rings before carbon monoxide treatment. The possible clinical significance of the actions of the anesthetics on this endogenous vasodilator is yet to be determined.
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Castillo, Carlos, Juan Asbun, Bruno Escalante, Carlos M. Villalón, Pedro López, and Enrique F. Castillo. "Thiopental inhibits nitric oxide production in rat aorta." Canadian Journal of Physiology and Pharmacology 77, no. 12 (November 15, 1999): 958–66. http://dx.doi.org/10.1139/y99-103.
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We studied whether thiopental affects endothelial nitric oxide dependent vasodilator responses and nitrite production (an indicator of nitric oxide production) elicited by acetylcholine, histamine, and A23187 in rat aorta (artery in which nitric oxide is the main endothelial relaxant factor). In addition, we evaluated the barbiturate effect on nitric oxide synthase (NOS) activity in both rat aorta and kidney homogenates. Thiopental (10-100 µg/mL) reversibly inhibited the endothelium-dependent relaxation elicited by acetylcholine, histamine, and A23187. On the contrary, this anesthetic did not modify the endothelium-independent but cGMP-dependent relaxation elicited by sodium nitroprusside (1 nM - 1 µM) and nitroglycerin (1 nM - 1 µM), thus excluding an effect of thiopental on guanylate cyclase of vascular smooth muscle. Thiopental (100 µg/mL) inhibited both basal (87.8 ± 14.3%) and acetylcholine- or A23187-stimulated (78.6 ± 3.9 and 39.7 ± 5.6%, respectively) production of nitrites in aortic rings. In addition the barbiturate inhibited (100 µg/mL) the NOS (45 ± 4 and 42.8 ± 9%) in aortic and kidney homogenates, respectively (measured as 14C-labeled citrulline production). In conclusion, thiopental inhibition of endothelium-dependent relaxation and nitrite production in aortic rings strongly suggests an inhibitory effect on NOS. Thiopental inhibition of the NOS provides further support to this contention.Key words: thiopental, rat aorta, endothelium-dependent relaxation, nitric oxide synthesis.
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McMahon, E. G., and R. J. Paul. "Effects of forskolin and cyclic nucleotides on isometric force in rat aorta." American Journal of Physiology-Cell Physiology 250, no. 3 (March 1, 1986): C468—C473. http://dx.doi.org/10.1152/ajpcell.1986.250.3.c468.
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The present study was undertaken to determine the extent to which cyclic nucleotide-induced relaxation in the intact rat aorta is mediated at the level of the contractile system. The relaxant effects of the cyclic nucleotide analogues [8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) and dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP)] and forskolin were examined in both the intact vessel and a Triton X-100-skinned preparation of rat thoracic aorta. Relaxation of a norepinephrine-induced contraction was essentially complete 30 min after the addition of 50 microM 8-BrcGMP [% relaxation = 87.2 +/- 4.4% (n = 4)], 100 microM DBcAMP [98.2 +/- 1.2% (n = 4)], and 1 microM forskolin [107.0 +/- 3.3% (n = 5)]. These same doses were ineffective in relaxing precontracted skinned rat aortic rings compared with the relaxation achieved in the intact vessel. The largest relaxation in the skinned aortas was achieved with the addition of 1 microM forskolin [17.4 +/- 1.5% (n = 4)]. The addition of catalytic subunit of cAMP-dependent protein kinase had no effect on isometric tension in the precontracted skinned aorta. Preincubation with the cyclic nucleotide analogues or forskolin in a low-Ca2+ solution (pCa less than 8) was also ineffective in inhibiting subsequent isometric tension development. Our results suggest that only a very small fraction of the relaxation with cyclic nucleotides and forskolin in the intact rat aorta is due to the action of these agents at the level of the contractile system.
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Abebe, Worku, and Mahmood S. Mozaffari. "Taurine depletion alters vascular reactivity in rats." Canadian Journal of Physiology and Pharmacology 81, no. 9 (September 1, 2003): 903–9. http://dx.doi.org/10.1139/y03-088.
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We recently showed that chronic taurine supplementation is associated with attenuation of contractile responses of rat aorta to norepinephrine and potassium chloride. However, the potential involvement of endogenous taurine in modulation of vascular reactivity is not known. Therefore, we examined the effect of β-alanine-induced taurine depletion on the in vitro reactivity of rat aorta to selected vasoactive agents. The data indicate that both norepinephrine- and potassium-chloride-induced maximum contractile responses of endothelium-denuded aortae were enhanced in taurine-depleted rats compared with control animals. However, taurine depletion did not affect tissue sensitivity to either norepinephrine or potassium chloride. By contrast, sensitivity of the endothelium-denuded aortae to sodium nitroprusside was attenuated by taurine depletion. Similarly, taurine deficiency reduced the relaxant responses of endothelium-intact aortic rings elicited by submaximal concentrations of acetylcholine, and this effect was associated with decreased nitric oxide production. Taken together, the data suggest that taurine depletion augments contractility but attenuates relaxation of vascular smooth muscle in a nonspecific manner. Impairment of endothelium-dependent responses, which is at least in part associated with reduced nitric oxide generation, may contribute to the attenuation of the vasorelaxant responses. These vascular alterations could be of potential consequence in pathological conditions associated with taurine deficiency.Key words: rat aorta, β-alanine, taurine depletion, vascular reactivity.
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Pieper, G. M., and G. J. Gross. "Oxygen free radicals abolish endothelium-dependent relaxation in diabetic rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 4 (October 1, 1988): H825—H833. http://dx.doi.org/10.1152/ajpheart.1988.255.4.h825.
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The present experiments were conducted to determine whether endothelium-dependent relaxation is impaired in chronic (10-12 wk), streptozotocin-induced diabetic rat aortas and to determine the specificity and sensitivity of diabetic vasculature to oxygen-derived free radicals. Endothelium-dependent relaxation by acetylcholine and ADP was severely impaired in diabetic rat aorta, whereas endothelium-independent relaxation by nitroglycerin or papaverine was not impaired. Exposure to a free radical-generating system of xanthine plus xanthine oxidase caused a marked and prolonged relaxation in diabetic but not control vessels. Relaxation could not be prevented by the cyclooxygenase inhibitor indomethacin or the lipoxygenase inhibitor nordihydroguaiaretic acid but was attenuated or blocked by catalase. After free radical exposure, aortic rings were washed, reequilibrated, and contracted with a submaximal concentration of norepinephrine. In free radical-exposed vessels, endothelium-dependent relaxation by acetylcholine was reduced by 50% in nondiabetic vessels and abolished in diabetic vessels. Nevertheless, diabetic vessels could still be fully relaxed by nitroglycerin or papaverine. These results suggest selective impairment of endothelium-dependent relaxation in chronic diabetic rat aortas with particular sensitivity to free radical-induced damage.
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Yokoyama, S., R. J. Korthuis, and J. N. Benoit. "Hypoxia-reoxygenation impairs endothelium-dependent relaxation in isolated rat aorta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 5 (May 1, 1996): R1126—R1131. http://dx.doi.org/10.1152/ajpregu.1996.270.5.r1126.
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The effects of hypoxia followed by reoxygenation on endothelium-dependent relaxation in isolated rat aorta were investigated. Acetylcholine (ACh, 3 nM-10 microM) and calcium ionophore A-23187 (3 nM-300 nM)-induced endothelium-dependent vasorelaxation of isolated rate aortic vessel rings was impaired after 15 min of hypoxia followed by 30 min of reoxygenation. Impairment of ACh-induced relaxation was prevented by pretreatment with the combination of superoxide dismutase (200 U/ml) and catalase (1,000 U/ml). Hypoxia-reoxygenation did not affect sodium nitroprusside (0.1 nM-1 microM)-induced endothelium-independent relaxation nor the dissociation constant of ACh to endothelial M3 muscarinic receptors. Propidium iodide staining of the vascular endothelium revealed a significant increase in the number of dead endothelial cells on the aortic vessel rings following hypoxia-reoxygenation, but not on those pretreated with superoxide dismutase and catalase. These results suggest that hypoxia-reoxygenation impairs endothelium-dependent relaxation of rat aorta by a mechanism that involves oxidant-mediated endothelial cell death.
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Sánchez-Pastor, Enrique, Xóchitl Trujillo, Christian Ramos-Flores, Mónica Ríos-Silva, Felipa Andrade, Yolitzy Cárdenas, Elena Castro, Zorayda Urzúa, Oscar Newton-Sánchez, and Miguel Huerta. "Type 2 Diabetes Alters Vascular Cannabinoid Receptor 1 Expression, Phosphorylation Status, and Vasorelaxation in Rat Aorta." Molecules 25, no. 21 (October 26, 2020): 4948. http://dx.doi.org/10.3390/molecules25214948.
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Previous studies have suggested a role of the endocannabinoid system in metabolic diseases, such as diabetes. We investigated the effect of diabetes on cannabinoid receptor type 1 (CB1) expression and cannabinoid-induced vasorelaxation in rat aorta rings. Aortas from healthy rats and from rats with experimentally induced diabetes were used to compare the vasorelaxant effect of the cannabinoid agonist arachidonylcyclopropylamide (ACPA) and CB1 expression and localization. After 4–8 weeks of diabetes induction, CB1 receptor expression and CB1 phosphorylation were higher in aortic rings, in association with greater vasorelaxation induced by the CB1 agonist ACPA compared to healthy rats. The vasorelaxant effect observed in healthy rats is similar throughout the study. Further studies are needed to elucidate the implications of CB1 receptor overexpression in diabetes and its influence on the progression of the cardiovascular complications of this metabolic disease.
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Doğan, Emre. "Vasorelaxant effects of dobutamine and levosimendan on rat aorta rings." Turkish Journal of Thoracic and Cardiovascular Surgery 23, no. 2 (April 15, 2015): 330–35. http://dx.doi.org/10.5606/tgkdc.dergisi.2015.10321.
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Gohar, Michel, Pascal Daleau, Jeffrey Atkinson, and Yves-Michel Gargouil. "Ultradian variations in sensitivity of rat aorta rings to noradrenaline." European Journal of Pharmacology 229, no. 1 (December 1992): 69–73. http://dx.doi.org/10.1016/0014-2999(92)90287-e.
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Carter, Rebecca W., and Nancy L. Kanagy. "Tyrosine kinases regulate intracellular calcium during α2-adrenergic contraction in rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 4 (October 1, 2002): H1673—H1680. http://dx.doi.org/10.1152/ajpheart.01034.2001.
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We have demonstrated enhanced contractile sensitivity to the α2-adrenoreceptor (α2-AR) agonist UK-14304 in arteries from rats made hypertensive with chronic nitric oxide synthase (NOS) inhibition (LHR) compared with arteries from normotensive rats (NR); additionally, this contraction requires Ca2+ entry. We hypothesized that tyrosine kinases augment α2-AR contraction in LHR arteries by increasing Ca2+. The tyrosine kinase inhibitor tyrphostin 23 significantly attenuated UK-14304 contraction of denuded thoracic aortic rings from NR and LHR. However, tyrphostin 23 did not alter UK-14304 contraction in ionomycin-permeabilized aorta, which indicates that tyrosine kinases regulate intracellular Ca2+concentration. The Src family inhibitor PP1 and the epidermal growth factor receptor kinase inhibitor AG-1478 did not alter α2-AR contraction, whereas the mitogen-activated protein kinase extracellular signal-regulated kinase kinase inhibitor PD-98059 attenuated the contraction. Contraction to CaCl2 in ionomycin-permeabilized LHR rings was greater than in NR rings. UK-14304 augmented CaCl2 contraction in ionomycin-permeabilized rings from both groups but to a greater extent in LHR aorta. Together, these data suggest that α2-AR stimulates contraction via two pathways. One, which is enhanced with NOS inhibition hypertension, activates Ca2+ sensitivity and is independent of tyrosine kinases. The other is tyrosine kinase dependent and regulates intracellular Ca2+ concentration.
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Pérez-Guerrero, Concepción, María Álvarez de Sotomayor, Maria Dolores Herrera, and Elisa Marhuenda. "Endothelium Modulates Contractile Response to Simvastatin in Rat Aorta." Zeitschrift für Naturforschung C 55, no. 1-2 (February 1, 2000): 121–24. http://dx.doi.org/10.1515/znc-2000-1-222.
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Simvastatin is an inhibitor of HMG -CoA reductase used in the treatment of hypercholesterolemia. In the present study simvastatin-induced contraction was observed in rat aortic thoracic rings, this effect increased when the endothelium was removed and when NO synthase was blocked by L-NOARG (3 x 10-5 ᴍ) . The contractile effect of simvastatin on intact aortic rings diminished when cyclo-oxygenase was inhibited with indomethacin (10-5 ᴍ). Also in the presence of endothelium, pretreatment with mevalonate (1 mM), the product of HMGCoA reductase activity, significantly inhibited the contraction. In other experiments carried out on endothelium-removed preparations and in medium containing the calcium antagonist, diltiazem (10-5 and 10-6 ᴍ) , the contraction dose-response curves were significantly reduced and the same happened in the presence of the inhibitor of sarcoplasmic reticulum Ca-2+- ATPase, cyclopiazonic acid (CPA) (3 x 10-6 ᴍ) . The results suggest that simvastatin might increase intracellular calcium concentration. This effect could lead to an activation of NO synthase and cyclooxygenase pathways in endothelial cells and to contraction in vascular smooth muscle cells. This rise in Ca2+ concentration could be due to an inhibition of isoprenoid synthesis prevented by mevalonate.
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Alves Filho, Francisco das Chagas, Paulo Marques da Silva Cavalcanti, Rita de Cassia Aleixo Tostes Passaglia, and Gustavo Ballejo. "Long-lasting endothelium-dependent relaxation of isolated arteries caused by an extract from the bark of Combretum leprosum." Einstein (São Paulo) 13, no. 3 (September 2015): 395–403. http://dx.doi.org/10.1590/s1679-45082015ao3242.
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Objective To describe and to characterize the relaxing effect of an extract of the bark of Combretum leprosum on isolated arterial rings from different animals.Methods Rings (3 to 4mm) from rabbit, rat, or porcine arteries rings were suspended in an organ bath (Krebs, 37°C, 95%O2/5%CO2) to record isometric contractions. After the stabilization period (2 to 3 hours) contractions were induced by the addition of phenylephrine (0.1 to 0.3µM) or U46619 (10 to 100nM), and Combretum leprosum extract was added on the plateau of the contractions. Experiments were performed to determine the potency, duration, reversibility, and to get insights on the potential mechanism involved in extract-induced relaxations.Results In all rings tested, Combretumleprosum extract (1.5μg/mL) was able to cause relaxations, which were strictly endothelium-dependent. In rabbit or rat thoracic aorta rings, the relaxations were reversed by vitamin B12a or L-NG-nitroarginine. In porcine right coronary arteries and rabbit abdominal aorta, extract caused both L-NG-nitroarginine-sensitive and L-NG-nitroarginine-resistant relaxations. In rabbit thoracic aorta, the extract was relatively potent (EC50=0.20µg/mL) and caused relaxations; intriguingly the endothelium continued to produce relaxing factors for a long period after removing the extract. The magnitude of extract-induced relaxations was significantly reduced in the absence of extracellular Ca2+; in addition, the TRPs channels blocker ruthenium red (10µM) was able to revert extract-induced relaxations. Phytochemical analyses indicated that the extract was rich in polyphenol-like reacting substances.ConclusionsCombretum leprosum extract contains bioactive compounds capable of promoting Ca2+-dependent stimulation of endothelial cells which results in a prolonged production of relaxing factors.
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Carcillo, Joseph A., and Christopher J. Hough. "Norepinephrine induces expression of c-fos mRNA through the α-adrenoceptor in rat aortic rings." Canadian Journal of Physiology and Pharmacology 73, no. 9 (September 1, 1995): 1281–85. http://dx.doi.org/10.1139/y95-180.
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We examined whether norepinephrine at pharmacologically relevant doses induces increased expression of c-fos mRNA in rat aortic rings, c-fos mRNA was expressed at norepinephrine concentrations known to cause minimum and maximum contraction of rat aorta in vitro. At the concentration known to cause maximum contraction, norepinephrine produced a marked and sustained increase of c-fos mRNA expression. Induction of c-fos was blocked completely by the α1-adrenergic antagonist prazosin, partially by the α2-adrenergic antagonist yohimbine, and not at all by the β-adrenergic antagonist propranolol. A prazosin inhibition curve showed that 1 nmol/L prazosin inhibited 10 μmol/L norepinephrine induced c-fos expression by 40%. At the pharmacologic dose known to cause maximum contraction, norepinephrine induces c-fos mRNA expression through the α-adrenoceptor in rat aortic rings.Key words: vascular smooth muscle contraction, rat aorta, norepinephrine, c-fos mRNA expression, adrenergic receptor, catecholamine.
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Compton, Steven J., John J. McGuire, Mahmoud Saifeddine, and Morley D. Hollenberg. "Restricted ability of human mast cell tryptase to activate proteinase-activated receptor-2 in rat aorta." Canadian Journal of Physiology and Pharmacology 80, no. 10 (October 1, 2002): 987–92. http://dx.doi.org/10.1139/y02-125.
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We investigated the potential of human mast cell tryptase to induce relaxation of rat aorta. Trypsin and the selective PAR2-activating peptide (PAR2-AP) SLIGRL-NH2 stimulated robust relaxation of phenylephrine-precontracted rat aortic rings. However, human lung tryptase (1100 nM) either in the presence or absence of heparin failed to induce any significant relaxation. Notwithstanding, incubation of the aorta with tryptase (100 nM), following the addition of a peptide corresponding to the cleavage/activation sequence of rat PAR2 (rPAR2), resulted in relaxation of precontracted tissue due to the proteolytic release of the PAR2-AP SLIGRL/ from the parent peptide. Thus, tryptase was enzymatically active in the bioassay system. Preincubation of aorta with neuraminidase to remove cell-surface sialic acid unmasked the ability of tryptase to induce relaxation of the aorta, but had no effect on relaxation induced by trypsin, SLIGRL-NH2, or acetylcholine (Ach). Like trypsin and SLIGRL-NH2, the tryptase-induced relaxation was inhibited by either removal of the endothelium or pretreatment of the tissue with NG-nitro-L-arginine methyl ester (L-NAME), suggesting an endothelium-derived nitric oxide mechanism. Interestingly, tryptase in the presence of heparin failed to induce relaxation of precontracted neuraminidase-treated rat aorta. We conclude that tryptase-induced relaxation of rat aorta, most likely via PAR2, is tightly regulated by heparin and cell-surface sialic acid.Key words: tryptase, PAR2, cardiovascular system, protease.
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Carter, Rebecca W., McKenzie Begaye, and Nancy L. Kanagy. "Acute and chronic NOS inhibition enhances α2- adrenoreceptor-stimulated RhoA and Rho kinase in rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 4 (October 1, 2002): H1361—H1369. http://dx.doi.org/10.1152/ajpheart.01101.2001.
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We demonstrated that arteries from rats made hypertensive with chronic nitric oxide (NO) synthase (NOS) inhibition ( N ω-nitro-l-arginine in drinking water, LHR) have enhanced contractile sensitivity to α2-adrenergic receptors (α2-AR) agonist UK-14304 compared with arteries from normotensive rats (NR). NO may regulate vascular tone in part through suppression of RhoA and Rho kinase (ROK). We hypothesized that enhanced RhoA and ROK activity augments α2-AR contraction in LHR aortic rings. Y-27632 eliminated UK-14304 contraction in LHR and NR aortic rings. The order of increasing sensitivity to Y-27632 was the following: endothelium-intact NR, LHR, and endothelium-denuded NR. UK-14304 stimulated RhoA translocation to the membrane fraction in LHR and denuded NR but not in intact NR aorta. Basally, more RhoA was present in the membrane fraction in denuded NR than in intact NR or LHR aorta. Relaxation to S-nitroso- N-acetyl-penicillamine and Y-27632 in denuded ionomycin-permeabilized rings was greater in NR than in LHR. Together these studies indicate α2-AR contraction depends on ROK activity more in NR than LHR aorta. Additionally, endogenous NO may regulate RhoA activation, whereas chronic NOS inhibition appears to cause RhoA desensitization.
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Wright, Gary. "Use-dependent decline in rat aorta sensitivity to contraction by potassium." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 921–28. http://dx.doi.org/10.1139/y91-140.
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Aortic rings excised from rats at 12 weeks of age showed a decrease in responsiveness during repeated contraction by increasing potassium concentration. By comparison, aortic rings obtained from rats at 22 and 26 weeks exhibited less loss or an increase in responsiveness to high potassium concentration during repeated contraction. The decrease in responsiveness to potassium in aortae of young rats was not due to the extended interval of incubation of the tissue in vitro. Aortic rings incubated without stimulation for 4 h following a reference contraction showed no change in contractile response to potassium. However, the magnitude of loss in responsiveness to potassium did appear to be related to the potassium concentration and the length of time the tissues were exposed to the high potassium solutions. Contraction of the tissue at 60 versus 30 mM KCl or extending the interval in depolarizing solution from 15 to 60 min significantly enhanced the decline in tissue responsiveness to potassium. The interruption of a series of potassium-induced contractions by exposure of the tissue to contractile (serotonin, norepinephrine) or relaxant (acetylcholine, isoproterenol) stimuli had no effect on the loss in responsiveness to potassium. However, injection of the calcium channel agonist, Bay K 8644, into the incubation media restored responsiveness to potassium. Concentration–response curves indicated that both sensitivity and the maximal response to potassium were reduced in aortic rings repeatedly contracted with potassium. Bay K 8644 addition immediately following the control contraction significantly increased sensitivity and the maximal response to potassium compared with the control contraction. After tissues had been repeatedly contracted by potassium, Bay K 8644 restored tissue sensitivity and the maximum response to the control level. The results indicate that aortic tissues of young rats are subject to desensitization to potassium stimulation during repeated exposure in vitro. The restoration of tissue sensitivity by Bay K 8644 suggests that this desensitization centers on decreased effectiveness of the voltage-dependent mechanism for increasing intracellular concentration of free calcium and the activation of the contractile protein.Key words: concentration–response, depolarization, vascular smooth muscle, tension.
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Teixeira, Rafaela, Talita Menengat, Gabriel Andrade, Bruno Cotrim, Cristiano Ponte, Wilson C. Santos, and Gabriel Resende. "Microwave Assisted Synthesis of 4-Phenylquinazolin-2(1H)-one Derivatives that Inhibit Vasopressor Tonus in Rat Thoracic Aorta." Molecules 25, no. 6 (March 24, 2020): 1467. http://dx.doi.org/10.3390/molecules25061467.
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Quinazolinones have pharmacological effects on vascular reactivity through different mechanisms. We synthesized 4-phenylquinazolin-2(1H)-one derivatives under microwave irradiation and tested them on the rat thoracic aorta. The prepared compounds 2a–2f were obtained in about 1 h with suitable yields (31–92%). All derivatives produced vasorelaxant effects with IC50 values ranging from 3.41 ± 0.65 µM to 39.72 ± 6.77 µM. Compounds 2c, 2e and 2f demonstrated the highest potency in endothelium-intact aorta rings (IC50 4.31 ± 0.90 µM, 4.94 ± 1.21 µM and 3.41 ± 0.65 µM respectively), and they achieved around 90% relaxation (30 μM). In aorta rings without an endothelium, the effect of compound 2f was abolished. Using the MTT assay to test for cell viability, only compound 2b induced cytotoxicity at the maximum concentration employed (30 µM). The results show that vasorelaxation by 4-phenylquinazolin-2(1H)-one derivatives might depend on the activation of a signalling pathway triggered by endothelium-derived factors.
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Delp, M. D., R. M. McAllister, and M. H. Laughlin. "Exercise training alters endothelium-dependent vasoreactivity of rat abdominal aorta." Journal of Applied Physiology 75, no. 3 (September 1, 1993): 1354–63. http://dx.doi.org/10.1152/jappl.1993.75.3.1354.
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We tested the hypothesis that adaptations in peripheral arterial vasoreactivity are induced by exercise training. Male rats were trained to run on a treadmill at 30 m/min (15 degrees incline) for 1 h/day 5 days/wk for 10–12 wk. Efficacy was indicated by a 51% increase (P < 0.05) in citrate synthase activity in soleus muscle of exercise-trained (ET) rats compared with that of sedentary (SED) control rats. Responses to vasoactive compounds were examined in vitro using rings of abdominal aorta. Maximal isometric contractile tension evoked by KCl, norepinephrine (NE), and phenylephrine were not different between groups; sensitivity to phenylephrine was also not different between groups. However, sensitivity was lower for both KCl and NE in vessels from ET animals. Endothelium removal did not influence KCl sensitivity but did abolish the difference in NE sensitivity of vessel segments between ET and SED animals. Maximal vasodilator responses induced by acetylcholine (ACh; NE or prostaglandin F2 alpha preconstriction) were greater in vessel rings from ET rats. However, dilatory responses by sodium nitroprusside (NE or prostaglandin F2 alpha preconstriction) and forskolin (NE preconstriction) were not different between groups, indicating that the augmented ACh-induced dilatory response resulted from an adaptation of the endothelium. Blockade of nitric oxide synthase activity diminished ACh-induced vasodilation by 79 and 100% in SED and ET rats, respectively. These results indicate that training alters vasomotor function in rat abdominal aortas through adaptations of both endothelium and smooth muscle.
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Silva, Joelmir Lucena Veiga da, Fabiana de Andrade Cavalcante, Tania Maria Sarmento da Silva, Alessandro Elery Ramos, Thárcia Kiara Beserra Oliveira, Schirley Cristina Almeida Pereira, and Bagnólia Araújo da Silva. "Vasorelaxation endothelium-independent of the ethyl acetate phase from aerial parts of Solanum paludosum Moric. envolves channels-calcium L-type blockade." Research, Society and Development 10, no. 1 (January 17, 2021): e31710111845. http://dx.doi.org/10.33448/rsd-v10i1.11845.
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Previous results showed the ethyl acetate phase (SP-AcOEt), obtained from aerial parts of Solanum paludosum, relaxed the aorta isolated in the endothelium-dependent and -independent manner. The vasorelaxant effects of SP-AcOEt was not characterized on aorta rings endothelium-denuded, thus this work aimed to elucidate the mechanisms endothelium-independent vasorelaxation on rat isolated aorta. The aorta was isolated from Wistar rats and mounted in glass baths containing 6 mL of normal Krebs physiological solution with pH at 7.4. The preparation was maintained at 37ºC and bubbled continuously with a mixture of 95% O2 and 5% CO2. Aortic rings were maintained for 1 hour by a resting tension of 1g and next were contracted with phenylephrine after the sustained contraction ACh was added to access the integrity of the endothelium. SP-AcOEt relaxed pre-contracted aorta by KCl-30mM or -80mM in a similar manner, suggesting blockade CaV, but not channel-K+ participating. SP-AcOEt also inhibited the contraction induced by CaCl2 and relaxed pre-contracted aorta by (±)-BayK8644 (EC50 = 16.9±1.3 μg/mL), which confirms the involvement of L-type CaV blockade. SP-AcOEt presented vasorelaxation endothelium-independent that involves L-type CaV blockade.
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Gonzales, Rayna J., Benjimen R. Walker, and Nancy L. Kanagy. "17β-Estradiol increases nitric oxide-dependent dilation in rat pulmonary arteries and thoracic aorta." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 3 (March 1, 2001): L555—L564. http://dx.doi.org/10.1152/ajplung.2001.280.3.l555.
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Past studies have demonstrated that 17β-estradiol (E2β) increases endothelial nitric oxide (NO) synthase (eNOS) activity in uterine, heart, and skeletal muscle and in cultured human endothelial cells. However, little is known about E2β regulation of NO synthesis in the pulmonary vasculature. The present study evaluated E2β regulation of eNOS function in pulmonary arteries and thoracic aortas. We hypothesized that E2β upregulates vascular NO release by increasing eNOS expression. To test this, NO-dependent vasodilation was assessed in isolated perfused lungs and aortic rings from ovariectomized Sprague-Dawley rats treated for 1 wk with 20 μg/24 h of E2β or vehicle. Expression of eNOS was evaluated by Western blot and immunohistochemistry. Also, a RNase protection assay determined eNOS mRNA levels in lung and aortic homogenates from control and treated rats. Vasodilation to ionomycin in lungs from the E2β-treated group was enhanced compared with that in control animals. Endothelium-intact aortic rings from E2β-treated animals also demonstrated augmented endothelium-dependent dilation. Both responses were blocked with NOS inhibition. Immunostaining for eNOS was greater in pulmonary arteries and aortas from E2β-treated compared with control rats. However, mRNA levels did not differ between groups. Thus we conclude that in vivo E2β treatment augments endothelium-dependent dilation in aorta and lung, increasing expression of eNOS independently of sustained augmented gene transcription.
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Zelenkov, P., T. McLoughlin, and R. A. Johns. "Endotoxin enhances hypoxic constriction of rat aorta and pulmonary artery through induction of EDRF/NO synthase." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 4 (October 1, 1993): L346—L354. http://dx.doi.org/10.1152/ajplung.1993.265.4.l346.
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The vascular response to hypoxia in endotoxin (lipopolysaccharide; LPS)-exposed rat pulmonary artery (PA) and thoracic aorta (AO) was investigated and the mechanism of the observed hypoxic responses defined. In isometric tension studies, LPS-treated AO and PA rings, with and without endothelium, demonstrated decreased (P < 0.05) contractile response to phenylephrine (PE EC50), and the dose response was shifted to the right (P < 0.01) compared with non-LPS treated rings. Both vessel types responded to hypoxia with a markedly increased (P < 0.01) and sustained (P < 0.01) constriction when preexposed to LPS. Control non-LPS rings with endothelium intact had a transient vasoconstriction in early hypoxia, which was abolished with removal of the endothelium. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthase, increased the PE EC50 tension in LPS-treated rings, markedly reduced the duration and magnitude of the hypoxic vasoconstriction in LPS-treated rings, and attenuated the transient vasoconstriction seen in endothelium-intact, non-LPS rings (all P < 0.05). L-Arginine reversed the L-NAME effects. Hypoxia decreased guanosine 3',5'-cyclic monophosphate (cGMP) content 54 +/- 4% in all LPS and 33 +/- 4% in the non-LPS intact rings (P < 0.05). L-NAME reduced cGMP content 90 +/- 5% in all LPS rings. Indomethacin inhibited formation of a constriction factor in aortic LPS-treated rings (P < 0.01) that was endothelium dependent and unaffected by the presence of L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)
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Hyvelin, Jean-Marc, Clare O’Connor, and Paul McLoughlin. "Effect of changes in pH on wall tension in isolated rat pulmonary artery: role of the RhoA/Rho-kinase pathway." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 4 (October 2004): L673—L684. http://dx.doi.org/10.1152/ajplung.00331.2003.
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Pulmonary arteries (PA) are resistant to the vasodilator effects of extracellular acidosis in systemic vessels; the mechanism underlying this difference between systemic and pulmonary circulations has not been elucidated. We hypothesized that RhoA/Rho-kinase-mediated Ca2+ sensitization pathway played a greater role in tension development in pulmonary than in systemic vascular smooth muscle and that this pathway was insensitive to acidosis. In arterial rings contracted with the α1-agonist phenylephrine (PE), the Rho-kinase inhibitor Y-27632 (≤3 μM) induced greater relaxation in precontracted PA rings than in aortic rings. In PA rings stimulated by PE, the activation of RhoA was greater than in aorta. Normocapnic acidosis (NA) induced a smaller relaxation in precontracted PA than in aorta. However, in the presence of nifedipine and thapsigargin, when PE-induced contraction was predominantly mediated by Rho-kinase, the relaxant effect of NA was reduced and similar in both vessel types. Furthermore, in the presence of Y-27632, NA induced a greater relaxation in both PA and aorta, which was similar in both vessels. Finally, in α-toxin-permeabilized smooth muscle, PE-induced contraction at constant Ca2+ activity was inhibited by Y-27632 and unaffected by acidosis. These results indicate that Ca2+ sensitization induced by the RhoA/Rho-kinase pathway played a greater role in agonist-induced vascular smooth muscle contraction in PA than in aorta and that tension mediated by this pathway was insensitive to acidosis. The predominant role of the RhoA/Rho-kinase pathway in the pulmonary vasculature may account for the resistance of this circulation to the vasodilator effect of acidosis observed in the systemic circulation.
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Hatano, Y., K. Mizumoto, T. Yoshiyama, M. Yamamoto, and H. Iranami. "Endothelium-dependent and -independent vasodilation of isolated rat aorta induced by caffeine." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 5 (November 1, 1995): H1679—H1684. http://dx.doi.org/10.1152/ajpheart.1995.269.5.h1679.
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Caffeine (10(-4)-10(-3) M) induced concentration-dependent relaxations of phenylephrine-precontracted rat aortic rings with endothelium. Endothelial denudation significantly, but only partially, attenuated caffeine-induced relaxation. Pretreatment with NG-nitro-L-arginine, oxyhemoglobin, and methylene blue attenuated the relaxations to an extent similar to endothelial denudation. Guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP) contents of aortic strips with endothelium increased significantly after exposure to caffeine (10(-3) M). Endothelial denudation attenuated caffeine-induced cGMP increase. Pretreatment with ryanodine (2 x 10(-5) M), which has been shown to combine with receptors on endoplasmic reticulum (ER) of endothelium, attenuated caffeine-induced relaxation and cGMP content increase of rings with endothelium. Pretreatment with caffeine potentiated sodium nitroprusside-induced relaxations and cGMP increase of rings without endothelium. These results demonstrated that caffeine-induced relaxation comprises two components. In the endothelium-dependent mechanism, caffeine promotes nitric oxide synthesis in endothelium by release of Ca2+ from ER through a ryanodine-sensitive Ca2+ channel, and the suppression of cGMP degradation also contributes to the relaxation. In the endothelium-independent mechanism, caffeine acts as a 3',5'-cyclic-nucleotide phosphodiesterase inhibitor.
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Kleschyov, Andrei L., Bernard Muller, Thérèse Keravis, Marie-Elisabeth Stoeckel, and Jean-Claude Stoclet. "Adventitia-derived nitric oxide in rat aortas exposed to endotoxin: cell origin and functional consequences." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (December 1, 2000): H2743—H2751. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2743.
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The role of adventitial cells in bacterial lipopolysaccharide (LPS)-induced vascular nitric oxide (NO) overproduction has been largely ignored. In rat aortas exposed to LPS in vitro or in vivo, it was found that adventitia contained the major part of NO synthase (NOS)-2 protein (Western blot and immunohistochemistry) and generated the largest amount of NO (electron paramagnetic resonance spin trapping). NOS-2 immunoreactive cells were mainly resident macrophages at an early stage (5 h, in vitro or in vivo) and fibroblasts at a later stage (20 h, in vitro). Adventitial NOS-2 activity largely accounted for 1) the relaxing effect of l-arginine in rings exposed to LPS in vivo, 2) generation of an “NO store” revealed by N-acetylcysteine-induced relaxation, and 3) formation of protein-bound dinitrosyl iron complexes in the medial layer of aortic rings exposed to LPS in vitro. In conclusion, the adventitia is a powerful source of NO triggered by LPS in the rat aorta. This novel source of NO has an important impact on smooth muscle function and might be implicated in various inflammatory diseases.
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Zhu, Jiaxuan, Takefumi Mori, Tianjian Huang, and Julian H. Lombard. "Effect of high-salt diet on NO release and superoxide production in rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 2 (February 2004): H575—H583. http://dx.doi.org/10.1152/ajpheart.00331.2003.
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Sprague-Dawley rats were fed either a high-salt (HS) diet (4.0% NaCl) or a low-salt (LS) diet (0.4% NaCl) for 3 days. Nitric oxide (NO) and superoxide production were assessed in the thoracic aorta by evaluating the fluorescence signal intensity from 4,5-diaminofluorescein (DAF-2DA) and dihydroethidine, respectively. Methacholine caused increased NO release in the aortas from rats on a LS but not HS diet. The SOD mimetic tempol restored methacholine-induced NO release in aortas from rats on a HS diet. Methacholine also caused superoxide production in the aortas of rats on a HS diet but not in the aortas of rats on a LS diet. Tempol and NG-monomethyl-l-arginine eliminated methacholine-induced superoxide production in the aortas of rats on a HS diet. Aortic rings from rats on the HS diet showed impaired methacholine-induced relaxation, which was improved by tempol. Tempol alone caused a NO-dependent relaxation of norepinephrine-precontracted aortas that was significantly greater in the aortas of rats on the HS diet than in vessels from rats on the LS diet. These data suggest that a HS diet impairs endothelium-dependent relaxation via reduced NO levels and increased superoxide production.
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Dominiczak, A. F., J. Quilley, and D. F. Bohr. "Contraction and relaxation of rat aorta in response to ATP." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 1 (July 1, 1991): H243—H251. http://dx.doi.org/10.1152/ajpheart.1991.261.1.h243.
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Vascular responses to ATP were studied in aortic rings isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). Low concentrations of ATP (10 nM to 10 microM) caused relaxation and high concentrations (0.1 mM to 10 mM) caused contraction. Both of these responses were accentuated by factors released from the endothelium. The endothelium-derived relaxing factor (EDRF) was blocked by NG-monomethyl-L-arginine (L-NMMA). This is the first time that it has been reported that ATP causes the release of an endothelium-derived contracting factor (EDCF). Its release was diminished but not completely blocked by cyclooxygenase inhibitors. Assays of muscle bath prostanoid composition indicated that ATP stimulation caused the release of prostaglandins I2 and E2 and thromboxane A2 from intact aortic rings. Evidence is presented that neither endothelin nor superoxide anion contributed to the EDCF. No difference was observed between WKY and SHRSP with regard to either the endothelial contributions to the response, or the direct action on vascular smooth muscle of ATP. High concentrations of ATP achieved intravascularly in hypoxia may cause vasospasm by release of endothelial prostanoids.
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Badreck-Amoudi, A., C. K. Patel, T. P. C. Kane, and S. E. Greenwald. "The Effect of Age on Residual Strain in the Rat Aorta." Journal of Biomechanical Engineering 118, no. 4 (November 1, 1996): 440–44. http://dx.doi.org/10.1115/1.2796029.
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Residual stress is observed in many parts of the cardiovascular system and is thought to reduce transmural stress gradients due to intravascular pressure. Its development is closely associated with normal growth and pathological remodeling, although there appear to be few previous reports of the relationship between aging and residual stress. We have estimated residual strain (an indicator of the magnitude of residual stress) at ten sites along the aorta of rats aged 2.5 to 56 weeks by measuring the degree to which rings of vessel spring open when cut (opening angle). At all ages the opening angle decreased along the aorta, reaching a minimum near the renal arteries and increasing toward the aorto-iliac bifurcation, a result that confirms previous studies. During growth, although the unloaded circumference of the aorta increased steadily, the wall thickness and medial surface area fell to a minimum at the age of 6 weeks before continuing a steady increase. Similarly, the opening angle decreased between the ages of 2.5 and 6 weeks, thereafter increasing with age. In the abdominal aorta, a strong correlation between opening angle and wall thickness relative to midwall radius (h/R) was seen; whereas in the thoracic segment, in which no increase in h/R with age occurred, no such relationship was found. These observations are in keeping with a recently proposed hypothesis that residual stress will change in response to growth-related changes in vessel geometry driven by a tendency to minimize the nonuniform stress distribution inevitably found in pressurized thick-walled cylinders.
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Sugiuchi, Noboru, Hidekazu Kinouchi, Osamu Tajiri, Tadashi Aoki, Keizo Takahashi, Ronald Lis, Vladimil Kvetan, David Katz, and Hideo Nagashima. "INFLUENCE OF THIOPENTAL TO ENDOTOXIN TREATED ISOLATED AORTA RINGS IN RAT." Shock 4, Supplement (December 1995): 49. http://dx.doi.org/10.1097/00024382-199512001-00195.
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Li, Su Juan, Fang Li, Jin Yan Yang, Sai Mei Yan, Ying Wang, and Cui Yang. "Vasorelaxation of Rat Aorta Induced by Extract from Clerodendranthus spicatus." Advanced Materials Research 887-888 (February 2014): 537–40. http://dx.doi.org/10.4028/www.scientific.net/amr.887-888.537.
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The isometric tension was measured in rat aortic rings. The extract fromClerodendranthus spicatus(CS) can enhance the relaxation induced by ACh in lower concentration and has a notable difference on SNP-induced relaxation in male and female. The relaxation of CS is also related to the inhibition of intracellular Ca2+increase.
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Şahintürk, Serdar, and Naciye İşbil. "The role of potassium channels on vasorelaxant effects of elabela in rat thoracic aorta." Turkish Journal of Thoracic and Cardiovascular Surgery 30, no. 1 (January 1, 2022): 18–25. http://dx.doi.org/10.5606/tgkdc.dergisi.2022.22756.
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Background: This study aims to investigate the roles of potassium channel subtypes in the vasorelaxant effect mechanism of elabela, which is a recently discovered endogenous apelin receptor ligand. Methods: The vascular rings (4-mm) obtained from the thoracic aortas of 20 male Wistar Albino rats were placed into the isolated tissue bath system. The resting tension was set to 1 g. The aortic rings were contracted with 10-5 molar phenylephrine after the equilibration period (90 min). Elabela was applied cumulatively (10-10-10-6 molar) to the aortic rings in the plateau phase. The experimental protocol was repeated in the presence of specific potassium channel subtype inhibitors to determine the role of potassium channels in the vasorelaxant effect mechanism of elabela. Results: Elabela induced a concentration-dependent vasorelaxation (p<0.001). The maximum relaxation level was approximately 51% according to phenylephrineinduced contraction. Vasorelaxant effect level of elabela statistically significantly decreased after removal of the endothelium (p<0.05). Tetraethylammonium (1 milimolar), 4-Aminopyridine (1 milimolar), glyburide (10 micromolar), and barium chloride (30 micromolar) statistically significantly decreased the vasorelaxant effect level of elabela (p<0.001, p<0.001, p<0.01, and p<0.05 respectively). However, anandamide (10 micromolar) and apamin (100 nanomolar) did not statistically significantly change the vasorelaxant effect level of elabela. Conclusion: Our results suggest that large-conductance calciumactivated, voltage-gated, adenosine triphosphate-sensitive, and inward-rectifier potassium channels are involved in the vasorelaxant effect mechanism of elabela in the rat thoracic aorta.
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Sohn, Ju-Tae, Seong-Ho Ok, Hee-Jin Kim, Seon-Hak Moon, Il-Woo Shin, Heon-Keun Lee, and Young-Kyun Chung. "Inhibitory Effect of Fentanyl on Acetylcholine-induced Relaxation in Rat Aorta." Anesthesiology 101, no. 1 (July 1, 2004): 89–96. http://dx.doi.org/10.1097/00000542-200407000-00015.
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Background Previous study has shown that fentanyl attenuates acetylcholine-induced vasorelaxation. The goal of the current in vitro study was to identify the muscarinic receptor subtype that is mainly involved in the fentanyl-induced attenuation of endothelium-dependent relaxation elicited by acetylcholine. Methods The effects of fentanyl and muscarinic receptor antagonists on the acetylcholine concentration-response curve were assessed in aortic vascular smooth muscle ring preparations precontracted with phenylephrine. In the rings pretreated independently with pirenzepine, 4-diphenylacetoxyl-N-methylpiperidine methiodide, and naloxone, acetylcholine concentration-response curves were generated in the presence and absence of fentanyl. The effect of fentanyl on the concentration-response curve for calcium ionophore A23187 was assessed. Results Fentanyl (0.297 x 10 0.785 x 10 m) attenuated acetylcholine-induced vasorelaxation in ring preparations with or without 10 m naloxone. Pirenzepine (10 to 10 m) and 4-diphenylacetoxyl-N-methylpiperidine methiodide (10 to 10 m) produced a parallel rightward shift in the acetylcholine concentration-response curve. The concentrations (-log M) of pirenzepine and 4-diphenylacetoxyl-N-methylpiperidine methiodide necessary to displace the concentration-response curve of an acetylcholine by twofold were estimated to be 6.886 +/- 0.070 and 9.256 +/- 0.087, respectively. Methoctramine, 10 m, did not alter the acetylcholine concentration-response curve. Fentanyl, 0.785 x 10 m, attenuated acetylcholine-induced vasorelaxation in the rings pretreated with 10 m pirenzepine but had no effect on vasorelaxation in the rings pretreated with 10 m 4-diphenylacetoxyl-N-methylpiperidine methiodide. Fentanyl, 0.785 x 10 m, did not significantly alter calcium ionophore A23187-induced vasorelaxation. Conclusions These results indicate that fentanyl attenuates acetylcholine-induced vasorelaxation via an inhibitory effect at a level proximal to nitric oxide synthase activation on the pathway involving endothelial M3 muscarinic receptor activation in rat aorta.
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Hattori, Y., H. Kawasaki, K. Abe, and M. Kanno. "Superoxide dismutase recovers altered endothelium-dependent relaxation in diabetic rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1086—H1094. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1086.
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Experiments were designed to characterize endothelium-dependent relaxation in thoracic aortic rings obtained from streptozotocin-induced diabetic rats. When the degree of the peak relaxation was compared, the endothelium-dependent relaxant responses to acetylcholine, histamine, or ADP in precontracted aortic rings showed that there was no significant difference between diabetic and control vessels. However, the time courses appeared quite different. The endothelium-dependent relaxant responses in diabetic vessels were more transient than those in control vessels. In addition, the rapid fade of the endothelium-dependent responses observed in diabetic vessels was significantly suppressed by pretreatment with superoxide dismutase. Pretreatment with catalase, deferoxamine, allopurinol, or indomethacin did not prevent the rapid fade of the endothelium-dependent relaxation. The endothelium-independent relaxation induced by nitric oxide also faded more quickly in diabetic vessels; this impairment was less pronounced in the presence of superoxide dismutase. These results suggest that the transient nature of the endothelium-dependent relaxation is more marked in diabetic rat aorta as a result of an enhanced accumulation of superoxide anion.
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St-Louis, Jean, Céline Coderre, and Ernesto L. Schiffrin. "Atrial natriuretic peptide interferes with calcium requirements in vascular tissues of the rat." Canadian Journal of Physiology and Pharmacology 66, no. 7 (July 1, 1988): 963–66. http://dx.doi.org/10.1139/y88-158.
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The inhibitory effect of atrial natriuretic peptide on the myotropic action of phenylephrine on superior mesenteric artery and thoracic aorta rings was studied to test the hypothesis that this peptide interferes with the mobilization of intra- or extra-cellular calcium produced by vasoconstrictor agents. In the absence of calcium in the bathing solution, phenylephrine (10−6 M) produced a residual effect, which was antagonized in a concentration-dependent manner by the atrial peptide in both mesenteric artery and aorta rings. When calcium (2.5 mM) was added to the bathing solution after the response to phenylephrine in the absence of calcium, a further increase in the tonus of the tissue was observed. This effect was also antagonized by atrial natriuretic peptide in a dose-dependent manner in the two tissues. These results suggest that atrial natriuretic peptide inhibits the effect of vasoconstrictor agents by functionally interfering with the mobilization of intra- and extra-cellular calcium produced by these vasoconstrictors.
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Michea, Luis, Verónica Irribarra, I. Annelise Goecke, and Elisa T. Marusic. "Reduced Na-K pump but increased Na-K-2Cl cotransporter in aorta of streptozotocin-induced diabetic rat." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H851—H858. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h851.
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The activities of Na-K-ATPase and Na-K-2Cl cotransporter (NKCC1) were studied in the aorta, heart, and skeletal muscle of streptozotocin (STZ)-induced diabetic rats and control rats. In the aortic rings of STZ rats, the Na-K-ATPase-dependent 86Rb/K uptake was reduced to 60.0 ± 5.5% of the control value ( P < 0.01). However, Na-K-ATPase activity in soleus skeletal muscle fibers of STZ rats and paired control rats was similar, showing that the reduction of Na-K-ATPase activity in aortas of STZ rats is tissue specific. To functionally distinguish the contributions of ouabain-resistant (α1) and ouabain-sensitive (α2 and α3) isoforms to the Na-K-ATPase activity in aortic rings, we used either a high (10−3 M) or a low (10−5M) ouabain concentration during 86Rb/K uptake. We found that the reduction in total Na-K-ATPase activity resulted from a dramatic decrement in ouabain-sensitive mediated 86Rb/K uptake (26.0 ± 3.9% of control, P < 0.01). Western blot analysis of membrane fractions from aortas of STZ rats demonstrated a significant reduction in protein levels of α1- and α2-catalytic isoforms (α1 = 71.3 ± 9.8% of control values, P < 0.05; α2 = 44.5 ± 11.3% of control, P < 0.01). In contrast, aortic rings from the STZ rats demonstrated an increase in NKCC1 activity (172.5 ± 9.5%, P < 0.01); however, in heart tissue no difference in NKCC1 activity was seen between control and diabetic animals. Transport studies of endothelium-denuded or intact aortic rings demonstrated that the endothelium stimulates both Na-K-ATPase and Na-K-2Cl dependent 86Rb/K uptake. The endothelium-dependent stimulation of Na-K-ATPase and Na-K-2Cl was not hampered by diabetes. We conclude that abnormal vascular vessel tone and function, reported in STZ-induced diabetic rats, may be related to ion transport abnormalities caused by changes in Na-K-ATPase and Na-K-2Cl activities.
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Wong, Emily S. W., Ricky Y. K. Man, Kwok F. J. Ng, Susan W. S. Leung, and Paul M. Vanhoutte. "L-arginine and Arginase Products Potentiate Dexmedetomidine-induced Contractions in the Rat Aorta." Anesthesiology 128, no. 3 (March 1, 2018): 564–73. http://dx.doi.org/10.1097/aln.0000000000002032.
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Abstract Background The α2-adrenergic sedative/anesthetic agent dexmedetomidine exerts biphasic effects on isolated arteries, causing endothelium-dependent relaxations at concentrations at or below 30 nM, followed by contractions at higher concentrations. l-arginine is a common substrate of endothelial nitric oxide synthase and arginases. This study was designed to investigate the role of l-arginine in modulating the overall vascular response to dexmedetomidine. Methods Isometric tension was measured in isolated aortic rings of Sprague Dawley rats. Cumulative concentrations of dexmedetomidine (10 nM to 10 μM) were added to quiescent rings (with and without endothelium) after previous incubation with vehicle, Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME; nitric oxide synthase inhibitor), prazosin (α1-adrenergic antagonist), rauwolscine (α2-adrenergic antagonist), l-arginine, (S)-(2-boronethyl)-l-cysteine hydrochloride (arginase inhibitor), NG-hydroxy-l-arginine (arginase inhibitor), urea and/or ornithine. In some preparations, immunofluorescent staining, immunoblotting, or measurement of urea content were performed. Results Dexmedetomidine did not contract control rings with endothelium but evoked concentration-dependent increases in tension in such rings treated with l-NAME (Emax 50 ± 4%) or after endothelium-removal (Emax 74 ± 5%; N = 7 to 12). Exogenous l-arginine augmented the dexmedetomidine-induced contractions in the presence of l-NAME (Emax 75 ± 3%). This potentiation was abolished by (S)-(2-boronethyl)-l-cysteine hydrochloride (Emax 16 ± 4%) and NG-hydroxy-l-arginine (Emax 18 ± 4%). Either urea or ornithine, the downstream arginase products, had a similar potentiating effect as l-arginine. Immunoassay measurements demonstrated an upregulation of arginase I by l-arginine treatment in the presence of l-NAME (N = 4). Conclusions These results suggest that when vascular nitric oxide homeostasis is impaired, the potentiation of the vasoconstrictor effect of dexmedetomidine by l-arginine depends on arginase activity and the production of urea and ornithine.
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Baños, G., F. Martínez, J. I. Grimaldo, and M. Franco. "Adenosine participates in regulation of smooth muscle relaxation in aortas from rats with experimental hypothyroidism." Canadian Journal of Physiology and Pharmacology 80, no. 6 (June 1, 2002): 507–14. http://dx.doi.org/10.1139/y02-064.
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The contribution of adenosine receptors was evaluated in vascular relaxation in experimental hypothyroidism. Hypothyroid aortic rings contracted less than normal controls with noradrenaline, phenylephrine, and KCl; the difference was maintained after incubation with 1,3-dipropyl-8-p-sulfophenylxanthine (an A1 and A2 adenosine receptor blocker). The vascular relaxation induced by acetylcholine or carbachol was similar in normal and hypothyroid aortic rings. However, adenosine, N6-cyclopentyladenosine (an A1 adenosine receptor analogue), and 5'-N-ethylcarbox amidoadenosine (an A2 and A3 adenosine analogue) induced vasodilation that was larger in hypothyroid than in normal aortas. Nω-nitro-L-arginine methyl ester shifted the dose-response curves of adenosine, N6-cyclopentyladenosine, or 5'-N-ethylcarboxamidoadenosine to the right in both normal and hypothyroid vessels. The blocker 1,3-dipropyl-8-p-sulfophenylxanthine significantly reduced adenosine-induced relaxation in the hypothyroid but not in the normal aortic vessels. These results suggest that in hypothyroid aortas, a larger adenosine-mediated vasodilation is observed probably due to an increase in receptor number or sensitivity.Key words: adenosine receptors, nitric oxide, hypothyroidism, smooth muscle, rat aorta.
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Ding, Andrew Q., and John N. Stallone. "Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation." Journal of Applied Physiology 91, no. 6 (December 1, 2001): 2742–50. http://dx.doi.org/10.1152/jappl.2001.91.6.2742.
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Recent studies have established that testosterone (Tes) produces acute (nongenomic) vasorelaxation. This study examined the structural specificity of Tes-induced vasorelaxation and the role of vascular smooth muscle (VSM) K+ channels in rat thoracic aorta. Aortic rings from male Sprague-Dawley rats with (Endo+) and without endothelium (Endo−) were prepared for isometric tension recording. In Endo− aortas precontracted with phenylephrine, 5–300 μM Tes produced dose-dependent relaxation from 10 μM (4 ± 1%) to 300 μM (100 ± 1%). In paired Endo+ and Endo− aortas, Tes-induced vasorelaxation was slightly but significantly greater in Endo+ aortas (at 5–150 μM Tes); sensitivity (EC50) of the aorta to Tes was reduced by nearly one-half in Endo− vessels. Based on the sensitivity (EC50) of Endo− aortas, Tes, the active metabolite 5α-dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate and Tes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone ≫ Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 ± 2% (25–300 μM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors had no effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel.
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Ozer, Erdem Kamil, Miyase Gozde Gunduz, Ahmed El-Khouly, Yildirim Sara, Rahime Simsek, Alper Bektas Iskit, and Cihat Safak. "Synthesis of fused 1,4-dihydropyridines as potential calcium channel blockers." Turkish Journal of Biochemistry 43, no. 6 (June 12, 2017): 578–86. http://dx.doi.org/10.1515/tjb-2016-0247.
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AbstractObjectiveThe aim of this study was to synthesize ten 1,4-dihydropyridine (DHP) derivatives in which substituted cyclohexane rings were fused to the DHP ring and to determine how different ester groups and the benzoyl substituent introduced in 4-phenyl ring affected their calcium channel blocking activity.MethodsA microwave-assisted one-pot method was applied for the synthesis of compound1–5according to a modified Hantzsch reaction. The benzoyl moiety was introduced in the 4-phenyl ring of these dihydropyridines by refluxing with benzoyl chloride in acetone in the presence of anhydrous potassium carbonate. Synthesized products were characterized by elemental analysis, IR,1H-NMR and13C-NMR spectroscopy. The inhibitory actions of compounds1–10on calcium channel blocking activity were tested on isolated rat aorta preparations.ResultsThe obtained pharmacological results showed that although all compounds are potent relaxing agents on isolated rat aorta smooth muscle, introduction of a benzoyloxy substitiuent on the phenyl ring (compound6–10) decreased the relaxant effect of these compunds.ConclusionThe reported 1,4-DHP derivatives have calcium channel blocking activity on rat aorta smooth muscle.
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Samseny, Reine Raïssa Rolande Aworet, Justine Okome Essono, and Sophie Aboughe Angone. "Studies of the Vasorelaxant Properties of Gnetum africanum Welw (Gnetaceae) on Isolated Rat Aorta." Scholars Academic Journal of Biosciences 10, no. 2 (February 28, 2022): 15–21. http://dx.doi.org/10.36347/sajb.2022.v10i02.002.
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High blood pressure is a chronic cardiovascular disease caused by an increase in blood pressure above normal. Poorly treated high blood pressure can damage the arteries of the brain, heart and kidneys, leading to serious complications. Long considered a disease of the rich, hypertension is now a real public health problem in Africa. The treatment of this disease is not only long term, but it is also expensive for many patients. To overcome this, the African populations resort to herbal treatments. Among these plants we have Gnetum africanum which is a food plant from Gabon which has medicinal properties. Our work aims to validate the pharmacological effect of the aqueous extract of Gnetum africanum by a study on the isolated rat aorta. The rings aorta are kept in an oxygenated Mac Ewen solution and maintained at a temperature of 37°C. At the beginning of the experiment, the aortic band is subjected to a tension of 1 g force. We then balance the device for 1 hour to have stable contractile movements. The aqueous extract of the leaves showed a relaxing action on the smooth muscles of the isolated rat aorta. This relaxation of the isolated rat aorta is similar to that obtained by the action of amlodipine. These observations suggest that decoction of Gnetum africanum have a relaxant effect on rat isolated aorta. This justifies its use by traditional therapists in the treatment of arterial hypertension.
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Papadopoulos, Anthony, and Michael D. Delp. "Effects of hindlimb unweighting on the mechanical and structure properties of the rat abdominal aorta." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 439–45. http://dx.doi.org/10.1152/japplphysiol.00734.2002.
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Previous studies have shown that hindlimb unweighting of rats, a model of microgravity, reduces evoked contractile tension of peripheral conduit arteries. It has been hypothesized that this diminished contractile tension is the result of alterations in the mechanical properties of these arteries (e.g., active and passive mechanics). Therefore, the purpose of this study was to determine whether the reduced contractile force of the abdominal aorta from 2-wk hindlimb-unweighted (HU) rats results from a mechanical function deficit resulting from structural vascular alterations or material property changes. Aortas were isolated from control (C) and HU rats, and vasoconstrictor responses to norepinephrine (10−9–10−4 M) and AVP (10−9–10−5 M) were tested in vitro. In a second series of tests, the active and passive Cauchy stress-stretch relations were determined by incrementally increasing the uniaxial displacement of the aortic rings. Maximal Cauchy stress in response to norepinephrine and AVP were less in aortic rings from HU rats. The active Cauchy stress-stretch response indicated that, although maximum stress was lower in aortas from HU rats (C, 8.1 ± 0.2 kPa; HU, 7.0 ± 0.4 kPa), it was achieved at a similar hoop stretch. There were also no differences in the passive Cauchy stress-stretch response or the gross vascular morphology (e.g., medial cross-sectional area: C, 0.30 ± 0.02 mm2; HU, 0.32 ± 0.01 mm2) between groups and no differences in resting or basal vascular tone at the displacement that elicits peak developed tension between groups (resting tension: C, 1.71 ± 0.06 g; HU, 1.78 ± 0.14 g). These results indicate that HU does not alter the functional mechanical properties of conduit arteries. However, the significantly lower active Cauchy stress of aortas from HU rats demonstrates a true contractile deficit in these arteries.
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Mahmoud, Mona Fouad, and Hany Mohamed El Bassossy. "Curcumin attenuates fructose-induced vascular dysfunction of isolated rat thoracic aorta rings." Pharmaceutical Biology 52, no. 8 (March 10, 2014): 972–77. http://dx.doi.org/10.3109/13880209.2013.874465.
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