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1
DiCarlo, S. E., R. W. Blair, V. S. Bishop, and H. L. Stone. "Role of beta 2-adrenergic receptors on coronary resistance during exercise." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2287–93. http://dx.doi.org/10.1152/jappl.1988.64.6.2287.
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The effects of regional alpha- and specific beta 2-adrenergic receptor blockade on measurements of late diastolic coronary resistance (LDCR) and mean coronary blood flow velocity (CBFV) during exercise were examined in 14 conscious adult mongrel dogs. Specific beta 2-adrenergic receptor blockade (ICI 118.551) significantly decreased CBFV and increased LDCR by blockade of beta 2-vasodilator tone independent of alpha-adrenergic receptor-mediated tone and independent of altering myocardial metabolism. alpha-Adrenergic receptor blockade (phentolamine, 1 mg) significantly increased CBFV and decreased LDCR by blocking sympathetically mediated vasoconstrictor tone. There was no significant difference in the magnitude of response between alpha- and beta 2-adrenergic receptor blockade. These results demonstrate that alpha- and beta 2-adrenergic receptors have a significant and evidently equal influence on CBFV and LDCR during exercise. Four weeks of daily exercise and left stellate ganglionectomy (LSGx) prevented phentolamine-induced vasodilation but not ICI 118.551-induced vasoconstriction. This suggests that daily exercise and LSGx significantly decreased the alpha-adrenergic receptor-mediated vasoconstrictor tone on the coronary circulation, resulting in an apparently greater role for the coronary vascular beta 2-adrenergic receptor on the control of CBFV and LDCR during exercise.
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Awad, E. W., and M. Anctil. "IDENTIFICATION OF beta-LIKE ADRENOCEPTORS ASSOCIATED WITH BIOLUMINESCENCE IN THE SEA PANSY RENILLA KOELLIKERI." Journal of Experimental Biology 177, no. 1 (April 1, 1993): 181–200. http://dx.doi.org/10.1242/jeb.177.1.181.
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Previous studies have reported pharmacological and biochemical evidence for the involvement of adrenergic substances in the regulation of neuroeffector activities in the bioluminescent cnidarian Renilla koellikeri (Cnidaria, Anthozoa). Therefore, direct radiobinding assays were developed to identify and characterize beta-adrenergic binding in membrane preparations from this species, using the two beta-antagonists [3H]dihydroalprenolol and [3H]CGP12177 as tracers. In addition, the effect of various beta-adrenergic agents on luminescence was examined. Binding of the radioligands at 25°C was rapid, reversible, saturable and specific. Saturation studies revealed the presence of two different and independent classes of binding site, site1 and site2, in the body of the colony (rachis). In contrast, homogeneous populations of binding sites corresponding to site1 were detected in autozooid polyps and to site2 in the peduncle. The pharmacological profile of beta-adrenergic binding in R. koellikeri membrane preparations displayed properties consistent with the presence of two sites and followed a pattern similar to beta2- and beta1-adrenergic receptor subtypes for site1 and site2, respectively. Bioluminescence in polyps was induced by beta-agonists as well as by one beta1-selective antagonist, atenolol, and was blocked by several beta-blockers including (+/−)CGP12177. The specificity pattern of the physiological effect of beta-adrenergic drugs on luminescence mirrors that of the radioligand interaction with site1. This suggests that radioligand binding to site1 represents binding to the receptor that mediates luminescence excitation in R. koellikeri. Blockade of the luminescent responses to site1 agonists by isotonic MgCl2 indicates that this beta-adrenergic mechanism must rely on interneuronal transmission. Collectively, these results suggest the evolutionary conservation of beta-adrenoceptors and of their dual character from coelenterates to higher vertebrates.
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Jasper, J. R., H. J. Motulsky, L. C. Mahan, and P. A. Insel. "Beta-adrenoceptor metabolism in wild-type, Gs, and protein kinase A-variant S49 cells." American Journal of Physiology-Cell Physiology 259, no. 1 (July 1, 1990): C41—C46. http://dx.doi.org/10.1152/ajpcell.1990.259.1.c41.
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To determine the role of the stimulatory guanine nucleotide-binding protein, Gs, and adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase in the basal metabolism of beta-adrenergic receptors in S49 lymphoma cells, we measured the return of receptor number and function after irreversible blockade of receptors. After inactivation of receptors with the irreversible ligand N8-(bromoacetyl)-N'-[3-(4-indolyoxy)-2-hydroxypropyl]-(2)-1,8-diam ino-p- methane (BIM), beta-adrenergic receptors (defined as [125I]iodocyanopindolol binding sites) reappeared in a biphasic manner, the faster phase having a half-time (t 1/2) of 3-8 h (approximately 50% of the sites) and the slower phase greater than 40 h. Although the slow phase is not readily explained, recovery of binding sites during the first 10 h matched recovery of receptor function after BIM treatment (as measured by stimulation of cAMP accumulation) and recovery of receptor sites after downregulation induced by the agonist isoproterenol. Thus quantifying receptor recovery during the first 10 h after BIM treatment appears to be a reasonable method for examining basal receptor metabolism in S49 cells. Measured in this way, metabolism of beta-adrenergic receptors is very similar in wild-type S49 and the following variant clones: cyc- (absent Gs alpha), UNC and H21a (defective Gs alpha), and kin- (lacking cAMP-dependent protein kinase activity). Although previous data have demonstrated that agonist-promoted downregulation of beta-adrenergic receptors requires functional receptor-Gs coupling, the current data suggest that neither Gs nor cAMP-dependent protein kinase activity plays an important role in the regulation of basal metabolism of beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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Vatner, S. F., D. R. Knight, and T. H. Hintze. "Norepinephrine-induced beta 1-adrenergic peripheral vasodilation in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (July 1, 1985): H49—H56. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h49.
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Norepinephrine (NE) elicits alpha-adrenergic vasoconstriction and beta 1-adrenergic increases in heart rate and myocardial contractility. To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied after recovery from instrumentation for the measurement of cardiac output, arterial pressure, and left ventricular (LV) pressure and calculations of LV dP/dt and total peripheral resistance (TPR). NE, after pretreatment with hexamethonium and phentolamine, reduced mean arterial pressure 40 +/- 5% from 117 +/- 9 mmHg and TPR 60 +/- 5% from 0.058 +/- 0.007 mmHg X ml-1 X min and increased cardiac output 55 +/- 11% from 2,159 +/- 188 ml/min. beta 1-Adrenergic blockade with atenolol reversed the vasodilation induced by NE completely, while at this time isoproterenol was still able to reduce peripheral resistance further, by 67 +/- 7%, indicating that beta 2-adrenergic receptors were not blocked. Administration of phentolamine to intact dogs caused a fall in mean arterial pressure (23 +/- 5%) and TPR (34 +/- 5.4%) and an endogenous increase in plasma NE (2,987 +/- 905 pg/ml) and epinephrine (584 +/- 92 pg/ml). These increases in cardiac output and decreases in TPR were also reversed by atenolol (0.5 mg/kg). Moreover, this dose of atenolol blocked the increases in iliac blood flow induced by local injection of NE in the limb. Thus, in the presence of alpha-adrenergic receptor blockade, either administration of NE or release of endogenous NE elicits potent peripheral vasodilation, which appears to involve a beta 1-adrenergic receptor mechanism.
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Kagiya, T., M. Hori, K. Iwakura, K. Iwai, Y. Watanabe, S. Uchida, H. Yoshida, A. Kitabatake, M. Inoue, and T. Kamada. "Role of increased alpha 1-adrenergic activity in cardiomyopathic Syrian hamster." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (January 1, 1991): H80—H88. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h80.
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We investigated serial changes in myocardial norepinephrine content and myocardial adrenergic receptors during the development of cardiomyopathy in Syrian hamsters (Bio 14.6) and their age-matched healthy controls. We also examined phosphatidylinositide hydrolysis after alpha 1-adrenergic stimulation and the effects of alpha 1-blockade. We found that in the prehypertrophic stage, myocardial norepinephrine content and densities of alpha 1- and beta-adrenergic receptors were significantly higher in the cardiomyopathic hamsters than in the controls. However, in the early heart failure stage, beta-receptor density was 28% lower than that of the age-matched controls, although alpha 1-receptor density remained 55% higher. Norepinephrine-stimulated phosphatidylinositide hydrolysis in the cardiomyopathic hamster in the hypertrophic stage was twice that in the controls, indicating that the increase in alpha 1-adrenergic receptors is coupled with the intracellular signal transduction. Furthermore, selective alpha 1-adrenoceptor blockade by bunazosin in the cardiomyopathic hamsters from 70 to 170 days of age reduced myocardial hypertrophy and focal myocardial necrosis. Thus we conclude that increased alpha 1-adrenergic activity plays an important role in progression of cardiac hypertrophy is cardiomyopathic Syrian hamsters.
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Borst, M. M., R. Marquetant, W. Kubler, and R. H. Strasser. "Beta-blockade reduces effects of adenosine and carbachol by transregulation of inhibitory receptors and Gi proteins." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 4 (April 1, 1997): H1672—H1679. http://dx.doi.org/10.1152/ajpheart.1997.272.4.h1672.
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Chronic blockade of stimulatory beta-adrenergic receptors may decrease inhibitory receptors of the adrenergic signal transduction system. This transregulation process might reduce the negative inotropic response of the myocardium to inhibitory receptor stimulation. Rats were treated for 6 days with the beta-blocker atenolol (2 mg/day). beta-Adrenergic receptors in cardiac plasma membranes increased from 49 +/- 6 to 75 +/- 9 fmol/mg protein (means +/- SE; P = 0.053), whereas muscarinic M2 receptors decreased (155 +/- 15 vs. 105 +/- 10 fmol/mg protein; P < or = 0.05). Moreover, inhibitory G alpha(i) proteins were reduced by 36%. The functional responses of isolated hearts to inhibitory agonists after prestimulation with isoproterenol (3 nmol/l) were significantly blunted. The Ki value for the negative inotropic response of the maximal rise in developed left ventricular pressure (dP/dt(max)) to adenosine (0.1-100 micromol/l) increased from 5.9 +/- 1.7 to 24.0 +/- 2.5 micromol/l (P < or = 0.001). A similar rightward shift of the dose-response curve was observed for the effects of adenosine on developed left ventricular pressure (LVP) and of carbachol (0.01-10 micromol/l) on LVP and dP/dt. Thus chronic beta-blockade leads to a coordinate transregulation of inhibitory receptors and Gi proteins, reducing the effects of inhibitory receptor activation of the heart. This mechanism may contribute to the beneficial effects of beta-blocker therapy in heart failure.
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Kaufman, Beth D., and Robert E. Shaddy. "Beta-adrenergic receptor blockade and pediatric dilated cardiomyopathy." Progress in Pediatric Cardiology 24, no. 1 (November 2007): 51–57. http://dx.doi.org/10.1016/j.ppedcard.2007.08.004.
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Laughlin, M. H., and R. B. Armstrong. "Adrenoreceptor effects on rat muscle blood flow during treadmill exercise." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1465–72. http://dx.doi.org/10.1152/jappl.1987.62.4.1465.
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The purpose of this study was to examine the effects of the adrenergic receptors on the distribution of blood flow within and among skeletal muscles in rats. Blood flow was measured with the radiolabeled microsphere technique before exercise and during treadmill exercise at 15 or 60 m/min. Alpha- (phentolamine) or beta- (propranolol) adrenergic blocking drugs were administered, and then blood flow was measured and results compared with those from saline-treated rats. Before exercise, alpha-blockade caused increases in total muscle blood flow and in all fast-twitch muscles, whereas muscles composed of greater than 20% slow-twitch fibers showed no effect. During exercise at 15 m/min, the normal increase in total muscle blood flow was attenuated by alpha-blockade. Compared with controls, blood flow was less in the high-oxidative (fast and slow) muscle fiber areas of extensor muscles, whereas blood flow to white areas of extensor muscles was increased. beta-Blockade tended to decrease muscle blood flow before exercise and during exercise at 15 m/min with no apparent relationship between the effects of blockade on blood flow and muscle fiber type. These effects of beta-blockade were not apparent during exercise at 60 m/min. We conclude that before exercise alpha-receptor effects are limited to fast muscle, whereas beta-receptor influences are independent of fiber type, beta-receptors contribute to the initial hyperemia of exercise at 15 m/min, and beta-receptor influence is inversely related to metabolic rate.
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Kuleshova, E. V., N. V. Kuzmenko, M. G. Pliss, and V. A. Tsyrlin. "Mechanisms of beta-blockers antihypertensive action." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 27, no. 3 (August 4, 2021): 291–99. http://dx.doi.org/10.18705/1607-419x-2021-27-3-291-299.
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This article presents an analysis of data on the mechanisms of antihypertensive effect of β-adrenergic receptor blockers. The article describes the effectiveness of cardiotropic action of drugs to reduce high blood pressure (BP) with short-term and long-term action of compounds, the effect of blockers on the activity of plasma renin. The influence of β-blockers on the central mechanisms of blood circulation regulation is considered. Information on the effect of β-blockers on myogenic mechanisms of vascular tone regulation is presented. The possibilities of blockade of β-adrenergic receptors of endothelium-dependent hyperpolarization of smooth muscles of resistive arteries, violation of the NO-cGMP pathway and blockade of Ca2+ channel currents as factors providing expansion of resistive vessels and reduction of high BP are analyzed.
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Ferrara, L. Aldo, Teodoro Marotta, Paolo Rubba, Biagio De Simone, Giovanni Leccia, Stefano Soro, and Mario Mancini. "Effects of alpha-adrenergic and beta-adrenergic receptor blockade on lipid metabolism." American Journal of Medicine 80, no. 2 (February 1986): 104–8. http://dx.doi.org/10.1016/0002-9343(86)90168-3.
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Stonestreet, B. S., E. Le, and D. J. Berard. "Circulatory and metabolic effects of beta-adrenergic blockade in the hyperinsulinemic ovine fetus." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1098—H1106. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1098.
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Offspring of women with poorly controlled diabetes exhibit hypoxemia, elevated catecholamine concentration at birth, and an increased incidence of fetal death. Experimental fetal hyperinsulinemia results in increased catecholamine concentration and hemodynamic changes including increased combined ventricular output and vasodilation of select fetal organs. We hypothesized that insulin-induced catecholamine-mediated beta-adrenergic stimulation supports some of these hemodynamic changes in the hyperinsulinemic ovine fetus. To study this, 24 chronically instrumented fetal sheep receiving insulin for 24 h were exposed to beta-(propranolol),beta 1-(metoprolol), and beta 2-(ICI 118,551) adrenergic blockade. Insulin infusion resulted in hyperinsulinemic-hypoglycemia, a surge in epinephrine and norepinephrine concentration, and increases in the combined ventricular output and regional blood flow to the heart, adrenal glands, kidney, gastrointestinal tract, liver, fat, muscle, carcass, and placenta. In the hyperinsulinemic state, beta-adrenergic blockade was associated with significant reductions in the combined ventricular output and blood flow to fat, carcass, lungs, and the placenta; beta 1-blockade was associated with reductions in the combined ventricular output and blood flow to the lungs; and beta 2-adrenergic blockade was associated with reductions in blood flow to muscle and lungs. Because beta-adrenergic blockade was associated with reductions in placental blood flow during hyperinsulinemia, oxygen and glucose metabolism were also compromised. We conclude that in the hyperinsulinemic-hypoglycemic normoxemic ovine fetus, insulin-induced catecholamine-mediated hemodynamic changes are modulated in part by beta-adrenergic receptor stimulation.
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Knight, D. R., and S. F. Vatner. "Calcium channel blockers induce preferential coronary vasodilation by an alpha 1-mechanism." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 3 (September 1, 1987): H604—H613. http://dx.doi.org/10.1152/ajpheart.1987.253.3.h604.
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The effects of nitrendipine were evaluated on coronary and systemic dynamics in conscious dogs. Nitrendipine (8 micrograms X kg-1 X min-1) decreased late diastolic left circumflex coronary resistance (62 +/- 1.3%) significantly more (P less than 0.01) than total peripheral resistance (54 +/- 1.8%). After propranolol (1 mg/kg) and atropine methyl bromide (0.1 mg/kg) to eliminate reflex increases in myocardial metabolic demand, nitrendipine still reduced late diastolic coronary resistance (56 +/- 1.5%) significantly more (P less than 0.01) than total peripheral resistance (46 +/- 1.4%). However, after adding alpha 1-adrenergic receptor blockade with prazosin (1 mg/kg) to beta-adrenergic and cholinergic receptor blockades, nitrendipine no longer reduced late diastolic coronary resistance (40 +/- 2.7%) more than total peripheral resistance (45 +/- 2.1%) and, in fact, reduced late diastolic coronary resistance less than prior to prazosin. Nifedipine and diltiazem also reduced late diastolic coronary resistance more than total peripheral resistance prior to, but not after, alpha 1-adrenergic receptor blockade. In contrast, sodium nitroprusside reduced late diastolic coronary resistance more (P less than 0.01) than total peripheral resistance both before and after alpha 1-adrenergic receptor blockade. Thus calcium channel blockers preferentially dilate the coronary bed in comparison with the systemic circulation. Since the preferential effects were abolished by prazosin, an alpha 1-adrenergic mechanism is implicated.
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Claustre, J., S. Brechet, P. Plaisancie, JA Chayvialle, and JC Cuber. "Stimulatory effect of beta-adrenergic agonists on ileal L cell secretion and modulation by alpha-adrenergic activation." Journal of Endocrinology 162, no. 2 (August 1, 1999): 271–78. http://dx.doi.org/10.1677/joe.0.1620271.
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Postprandial release of peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) from L cells results from both nutrient transit in the ileal lumen and neural drive of endocrine cells. The adrenosympathetic system and its effectors have been shown to induce secretion of L cells in vivo or in vitro. Because these transmitters act through three receptors, beta, alpha1, alpha2, coupled to different intracellular pathways, we evaluated the responses of L cells to specific agonists, using the model of isolated vascularly perfused rat ileum. General stimulation of adrenergic receptors with epinephrine (10(-7) M) induced significant GLP-1 and PYY secretions (94+/-38 and 257+/-59 fmol/8 min respectively) which were abolished upon propranolol (10(-7) M) pretreatment and strongly decreased upon infusion with 10(-8) M prazosin. Blockade of alpha2-receptors with idazoxan (10(-8) M) did not alter epinephrine-induced peptide secretion. The beta-adrenergic agonist isoproterenol (10(-6) M) infused for 30 min induced a transient release of GLP-1 and PYY (integrated release over the 8 min of the peak secretion: 38+/-16 and 214+/-69 fmol for GLP-1 and PYY respectively, P<0.05). Because terbutaline but not dobutamine or BRL 37,344 (10(-5) M) induced significant GLP-1 and PYY secretions (135+/-30 and 305+/-39 fmol/8 min respectively), isoproterenol-induced secretions are suggested to result mainly from stimulation of the beta2-isoreceptor type. In contrast, the alpha1-agonist phenylephrine (10(-7) M) did not stimulate peptide release. When co-infused with 10(-6) M or 10(-7) M isoproterenol, 10(-7) M phenylephrine raised GLP-1 release to 174+/-53 and 108+/-28 fmol/8 min respectively (vs 38+/-16 and 35+/-10 fmol/8 min for isoproterenol alone, P<0.05) whereas PYY secretion was not significantly increased. Clonidine (10(-7) M), an alpha2-agonist, induced a moderate and delayed increase of GLP-1 and PYY but abolished the isoproterenol-induced peptide secretion. Our results showed that general stimulation of adrenergic receptors stimulates the secretory activity of ileal endocrine L cells. The net peptide secretion results from the activation of the beta2-isoreceptor type. Additionally, GLP-1 and PYY secretions are positively modulated by alpha1-receptor stimulation and inhibited by alpha2-receptor activation upon beta-receptor occupation.
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McIntyre, R. C., A. Banerjee, D. D. Bensard, E. C. Brew, A. R. Hahn, and D. A. Fullerton. "Adenosine A1-receptor mechanisms antagonize beta-adrenergic pulmonary vasodilation in hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 6 (December 1, 1994): H2179—H2185. http://dx.doi.org/10.1152/ajpheart.1994.267.6.h2179.
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Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we investigated 1) the effect of hypoxia and exogenous Ado on beta-AR-mediated pulmonary vasodilation, 2) the intracellular site of dysfunctional beta-AR-mediated pulmonary vasodilation in hypoxia, and 3) the Ado receptor subtype responsible for dysfunction of beta-AR-mediated pulmonary vasodilation. Hypoxia attenuated normal beta-AR-mediated pulmonary vasodilation to isoproterenol (97.5 +/- 0.8 vs. 71.5 +/- 2.3%, P < 0.01). In contrast, forskolin induced the same vasorelaxation in hypoxic pulmonary rings as controls (P = 0.09). Incubation of normoxic rings with Ado attenuated the vasorelaxation response induced by beta-AR stimulation (71.5 +/- 5.9%, P < 0.01), similar to the effect observed in hypoxia. Both nonspecific Ado receptor blockade (8-sulfophenyl-theophylline) and specific A1-receptor blockade (8-cyclopentyl-1,3-dimethylxanthine) restored the vasorelaxation response of hypoxic rings induced by beta-AR stimulation (93.3 +/- 2.3 and 92.2 +/- 2.8%, P < 0.01). The effects of hypoxia and Ado were reproduced by a specific A1 agonist (2-chloro-N6-cyclopentyladenosine), demonstrating impaired vasorelaxation induced by beta-AR stimulation in normoxia (70.6 +/- 4.5%, P < 0.01). From these data, we conclude that hypoxia antagonizes beta-AR-mediated pulmonary vasodilation via an Ado A1-receptor mechanism.
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Inderwies, Tyra, Johannes Riedl, Evangelos Kiossis, and Rupert M. Bruckmaier. "Effects of α- and β-adrenergic receptor stimulation and oxytocin receptor blockade on milking characteristics in dairy cows before and after removal of the teat sphincter." Journal of Dairy Research 70, no. 3 (July 21, 2003): 289–92. http://dx.doi.org/10.1017/s0022029903006289.
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Alpha (α)- and beta (β)-adrenergic receptors in the bovine mammary gland are mainly present in the teat muscles and in the region where large milk ducts reach the cisternal cavities. The aim of the study was to test the hypothesis that the region of the large mammary ducts is the most important location of α- and β-adrenergic receptor stimulation affecting milk ejection and milk removal. Effects of α- and β-adrenergic receptor stimulation and of oxytocin (OT) receptor blockade on milking characteristics were tested in six cows. Milk flow was measured before and after the distal part of one teat, including the teat canal and teat sphincter, had been partly amputated. Before the operation, milk yield and peak flow rate decreased during α-adrenergic receptor stimulation and during the OT receptor blockade, and increased during β-adrenergic stimulation. After removal of the teat tip, relations of milk yield and peak flow rates after administration of α- and β-agonists and after application of an OT receptor blocking agent were similar to those before operation. Only total milk yield had decreased in the teat-amputated quarter owing to unhindered flow of cisternal milk before cluster attachment. Since responses to α- and β-adrenergic receptor stimulation as well as to OT receptor blockade do not differ with or without the teat sphincter, it is concluded that milk flow is mainly influenced by the muscle tone of the large mammary ducts.
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Stagner, J. I., and E. Samols. "Role of intrapancreatic ganglia in regulation of periodic insular secretions." American Journal of Physiology-Endocrinology and Metabolism 248, no. 5 (May 1, 1985): E522—E530. http://dx.doi.org/10.1152/ajpendo.1985.248.5.e522.
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The regulatory system responsible for insulin oscillations from the in vitro pancreas is unknown. To test the hypothesis that intrapancreatic ganglia are the pacemaker or driver of the oscillations, combined nicotinic, muscarinic, and adrenergic antagonists were infused. Combined muscarinic, alpha- and beta-adrenergic, and presynaptic nicotinic receptor blockade (beta-bungarotoxin) was without effect on oscillations. The infusion of the postsynaptic nicotinic receptor antagonists, hexamethonium, alpha-bungarotoxin (ATX), or curarine, significantly altered the preinfusion oscillatory pattern of insulin release by reducing the period. Nicotine-stimulated insulin release was inhibited by ATX on a background of atropine, phentolamine, and beta-bungarotoxin. Propranolol decreased nicotine-stimulated insulin release, which was further reduced by ATX. These data support the theory that nicotinic receptors may be present pre- and postsynaptically at the ganglionic level and presynaptically on sympathetic nerve axons. We propose that ganglionic nicotinic receptors may be regulatory and that ganglia may serve as the pacemaker to regulate pancreatic hormone oscillations.
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McDonald, J. V., L. W. Gonzales, P. L. Ballard, J. Pitha, and J. M. Roberts. "Lung beta-adrenoreceptor blockade affects perinatal surfactant release but not lung water." Journal of Applied Physiology 60, no. 5 (May 1, 1986): 1727–33. http://dx.doi.org/10.1152/jappl.1986.60.5.1727.
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We induced beta-adrenergic receptor blockade at 28 days gestation in the fetal rabbit with an irreversible beta-antagonist, bromace-tylalprenolomenthane (BrAlp). There was a marked decrease in concentration of available receptors in lung with increasing doses of BrAlp. BrAlp treatment decreased isoproterenol, but not prostaglandin, stimulated adenosine 3′,5′-cyclic monophosphate (cAMP) generation in lung minces, and had no effect on activation of adenylate cyclase through non-beta-receptor-mediated components of the cyclase system in particulate preparations. Phospholipid recovery via lung lavage was significantly less from treated fetuses than from controls in groups delivered by cesarean section at 30 days (-31%) or vaginally at 31 days (-34%) and not allowed to air breathe. However, if fetuses from either group were allowed to air breathe, the difference was abolished. BrAlp treatment did not affect the phospholipid composition in lavage fluid, the rate of phosphatidylcholine synthesis, or tissue content of total or saturated phosphatidylcholine. Beta-adrenergic receptor blockade did not produce a significant change in lung water content either at or after birth regardless of the route of delivery. These data indicate that endogenous catecholamines play a role in surfactant secretion in both the fetal and newborn rabbit. We found no effects of BrAlp treatment on lung water, suggesting perhaps a less important role of endogenous catecholamines or that fewer receptors are required for this response than remained after treatment.
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Granneman, J. G., and K. N. Lahners. "Regulation of mouse beta 3-adrenergic receptor gene expression and mRNA splice variants in adipocytes." American Journal of Physiology-Cell Physiology 268, no. 4 (April 1, 1995): C1040—C1044. http://dx.doi.org/10.1152/ajpcell.1995.268.4.c1040.
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This study examined the regulation of murine beta 3-receptor mRNA and determined whether the recently described mRNA splice variants are differentially regulated by agents that alter total beta 3-receptor mRNA levels. In vivo treatment of mice with the beta 3-receptor agonist BRL-26830 reduced total beta 3-transcripts by 64% in white adipose tissue but did not alter the mRNA splicing pattern. Further analysis in cultured 3T3-F442A adipocytes showed that isoproterenol, dexamethasone, or phorbol 12-myristate 13-acetate also greatly reduced beta 3-receptor mRNA levels without selectively altering poly-U-containing transcripts. Blockade of transcription with actinomycin D produced a rapid loss of beta 3-receptor mRNA, which was prevented by blockade of mRNA translation with cycloheximide. However, neither actinomycin D nor cycloheximide altered the splicing pattern of beta 3-receptor mRNA. Analysis of transcription rate by nuclear run-off assay indicated that 8-bromoadenosine 3',5'-cyclic monophosphate and phorbol 12-myristate 13-acetate reduce beta 3-receptor gene transcription and that suppression of transcription is sufficient to account for the reduction in beta 3-receptor mRNA levels by these agents.
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Maman, Stephan R., Alvaro F. Vargas, Tariq Ali Ahmad, Amanda J. Miller, Zhaohui Gao, Urs A. Leuenberger, David N. Proctor, and Matthew D. Muller. "Beta-1 vs. beta-2 adrenergic control of coronary blood flow during isometric handgrip exercise in humans." Journal of Applied Physiology 123, no. 2 (August 1, 2017): 337–43. http://dx.doi.org/10.1152/japplphysiol.00106.2017.
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During exercise, β-adrenergic receptors are activated throughout the body. In healthy humans, the net effect of β-adrenergic stimulation is an increase in coronary blood flow. However, the role of vascular β1 vs. β2 receptors in coronary exercise hyperemia is not clear. In this study, we simultaneously measured noninvasive indexes of myocardial oxygen supply (i.e., blood velocity in the left anterior descending coronary artery; Doppler echocardiography) and demand [i.e., rate pressure product (RPP) = heart rate × systolic blood pressure) and tested the hypothesis that β1 blockade with esmolol improves coronary exercise hyperemia compared with nonselective β-blockade with propranolol. Eight healthy young men received intravenous infusions of esmolol, propranolol, and saline on three separate days in a single-blind, randomized, crossover design. During each infusion, subjects performed isometric handgrip exercise until fatigue. Blood pressure, heart rate, and coronary blood velocity (CBV) were measured continuously, and RPP was calculated. Changes in parameters from baseline were compared with paired t-tests. Esmolol (Δ = 3296 ± 1204) and propranolol (Δ = 2997 ± 699) caused similar reductions in peak RPP compared with saline (Δ = 5384 ± 1865). In support of our hypothesis, ΔCBV with esmolol was significantly greater than with propranolol (7.3 ± 2.4 vs. 4.5 ± 1.6 cm/s; P = 0.002). This effect was also evident when normalizing ΔCBV to ΔRPP. In summary, not only does selective β1 blockade reduce myocardial oxygen demand during exercise, but it also unveils β2-receptor-mediated coronary exercise hyperemia. NEW & NOTEWORTHY In this study, we evaluated the role of vascular β1 vs. β2 receptors in coronary exercise hyperemia in a single-blind, randomized, crossover study in healthy men. In response to isometric handgrip exercise, blood flow velocity in the left anterior descending coronary artery was significantly greater with esmolol compared with propranolol. These findings increase our understanding of the individual and combined roles of coronary β1 and β2 adrenergic receptors in humans.
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Philipsen, E. K., J. Myhre, S. Larsen, M. Damkjær Nielsen, J. J. Holst, and J. Hilsted. "The relationship between some beta-adrenergic mediated responses and plasma concentrations of adrenaline and cyclic AMP in man." Acta Endocrinologica 122, no. 1 (January 1990): 115–20. http://dx.doi.org/10.1530/acta.0.1220115.
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Abstract To test the hypothesis that increments in plasma cyclic AMP during beta-adrenergic stimulation reflect integrated second messenger function of the tissues activated by the angonist, graded adrenaline infusion resulting in plasma adrenaline concentrations within the physiological range was performed in 8 healthy subjects with and without concomitant beta-adrenoceptor blockade by iv propranolol. A significant correlation was found between increments in plasma adrenaline and plasma cyclic AMP in the experiments without beta-blockade; during concomitant beta-blockade the increase in plasma cyclic AMP concentrations at low adrenaline infusion rates was prevented, whereas a small increase in cyclic AMP was found at high adrenaline infusion rates, probably owing to incomplete beta-receptor blockade. Likewise, the adrenaline-induced increments in blood substrates (glucose, lactate, glycerol and betahydroxy butyric acid) were significantly reduced but not completely prevented by beta-blockade. We conclude that an altered relationship between beta-agonist concentrations and plasma cyclic AMP may provide evidence for the existence of differences in beta-adrenergic sensitivity in man.
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Shen, Y. T., D. E. Vatner, H. E. Gagnon, and S. F. Vatner. "Species differences in regulation of alpha-adrenergic receptor function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1110—R1116. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1110.
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The effects of alpha-adrenergic receptor stimulation with norepinephrine and phenylephrine after beta-adrenergic and muscarinic receptor blockades were compared in conscious baboons, calves, dogs, and rats in which left ventricular (LV) pressure. LV maximum rate of pressure development (dP/dt), and heart rate were measured. Autonomic receptor density was examined in crude sarcolemmal preparations from the hearts. The major physiological differences were observed in rats, where alpha 1-adrenergic receptor stimulation resulted in the greatest (P less than 0.05) increases in LV dP/dt (29 +/- 2%) in response to phenylephrine, 5.0 micrograms/kg, in comparison with responses in dogs (12 +/- 4%), calves (3 +/- 3%), and baboons (1 +/- 2%). This was associated with the greatest (P less than 0.05) alpha 1-adrenergic receptor density in the rat heart (73 +/- 5 fmol/mg) compared with values in the baboon (6 +/- 1 fmol/mg), calf (21 +/- 3 fmol/mg), or dog (10 +/- 3 fmol/mg) myocardium. Thus there are major differences among mammalian species in alpha-adrenergic receptor density and physiological responsiveness to alpha-adrenergic agonists.
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Hamdad, N., Z. Ming, R. Parent, and M. Lavallee. "Beta 2-adrenergic dilation of conductance coronary arteries involves flow-dependent NO formation in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (November 1, 1996): H1926—H1937. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h1926.
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The contribution of nitric oxide (NO) formation to the dilation of large epicardial coronary arteries to beta 1- and beta 2-adrenergic receptor stimulation was investigated in conscious dogs. After beta 1-adrenergic blockade (atenolol, 1.0 mg/kg iv), selective beta 2-adrenergic receptor activation with intracoronary bolus injections of pirbuterol (50 ng/kg) increased coronary blood flow (CBF) by 95 +/- 19% from 48.5 +/- 8.4 ml/min and external epicardial coronary diameter (CD) by 0.14 +/- 0.03 from 3.23 +/- 0.31 mm. After intracoronary N omega-nitro-L-arginine methyl ester (L-NAME, 50 micrograms.kg-1.min-1 x 12 min) was administered, baseline CD decreased but CBF was not altered. After L-NAME, bolus injections of pirbuterol resulted in smaller (P < 0.01) CBF responses (40 +/- 12%), and increases in CD were abolished. When pirbuterol (500 ng.kg-1.min-1) was given as a continuous infusion, CBF increased by 36 +/- 5% from 55.4 +/- 5.8 ml/min and CD by 0.16 +/- 0.03 mm from 3.44 +/- 0.16 mm. L-NAME abolished CD increases and limited (P < 0.01) CBF responses to 9 +/- 3%. When increases in CBF caused by pirbuterol before L-NAME were prevented by arterial constriction, CD increases were suppressed. In contrast, CBF and CD responses to beta 1-adrenergic stimulation were maintained after L-NAME. Thus beta 2-adrenergic dilation of epicardial conductance arteries is primarily a flow-dependent process involving NO formation. In contrast, beta 1-adrenergic activation produces epicardial coronary dilation independent of an L-NAME-sensitive mechanism.
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laccarino, G., V. Trimarco, F. Lanni, E. Cipolletta, R. Izzo, G. F. Di Renzo, L. Annunziato, and B. Trimarco. "BETA ADRENERGIC RECEPTOR POLYMORPHISMS AND METABOLIC ADVERSE EVENTS TO ANTIHYPERTENSIVE BETA BLOCKADE TREATMENT." Journal of Hypertension 22, Suppl. 2 (June 2004): S291—S292. http://dx.doi.org/10.1097/00004872-200406002-01011.
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Tucker, B. J., C. A. Mundy, and R. C. Blantz. "Effects of beta 1-adrenergic blockade on glomerular dynamics and angiotensin II response." American Journal of Physiology-Renal Physiology 257, no. 2 (August 1, 1989): F225—F230. http://dx.doi.org/10.1152/ajprenal.1989.257.2.f225.
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Adrenergic activity regulates renal function by several mechanisms. Renal nerves not only exert vasoconstrictor functions but also may influence glomerular hemodynamics by beta-adrenergic activity, especially via the effects on renin angiotensin activity. Little is known of the specific glomerular hemodynamic alterations resulting from beta 1-adrenergic blockade. Current studies examined the effects of 4-6 days of treatment with atenolol (50 mg/kg), a beta 1-selective adrenergic antagonist, on glomerular hemodynamics in plasma volume-expanded Munich-Wistar rats. Atenolol treatment reduced blood pressure both in the awake state and during micropuncture. This reduction in blood pressure contributed to a decrease in nephron filtration rate (48 +/- 1 in untreated rats vs. 40 +/- 1 nl.min-1.g kidney wt-1 in the atenolol-treated group, P less than 0.05) by reduction in nephron plasma flow (182 +/- 2 vs. 154 +/- 4 nl.min-1.g kidney wt-1 in the atenolol-treated rats). No other determinant of glomerular ultrafiltration was influenced by atenolol treatment. Since beta 1-adrenergic blockade may influence the generation of angiotensin II, the response to angiotensin II infusion was assessed and found not to differ from control untreated animals. These studies demonstrate that beta 1-receptor blockade reduced nephron filtration rate by decreasing mean arterial blood pressure and nephron plasma flow without significant modifications in vascular resistance and the glomerular hydrostatic pressure gradient.
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Friedman, D. B., G. A. Ordway, and R. S. Williams. "Exercise-induced functional desensitization of canine cardiac beta-adrenergic receptors." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1721–23. http://dx.doi.org/10.1152/jappl.1987.62.4.1721.
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To test the hypothesis that the high levels of endogenous catecholamines associated with strenuous exercise produce functional desensitization of cardiac beta-adrenergic receptors, we measured the bolus chronotropic dose of isoproterenol necessary to produce a 25-beats/min increase in heart rate (CD25) in the resting state and after the return of heart rate to resting levels after 60 min of treadmill running in 13 normal dogs. Immediately after exercise, 12 of 13 dogs were less sensitive to the chronotropic effects of beta-adrenergic receptor stimulation: mean CD25 increased from 1.16 +/- 0.17 to 3.50 +/- 0.98 micrograms (P less than 0.02). A similar reduction in isoproterenol sensitivity was evident regardless of whether testing was performed in the presence or absence of vagal blockade with atropine. By 3 h after exercise, CD25 had returned to the preexercise level, with no further change noted 24 h after exercise. There was no change in the CD25 when measured serially in three unexercised dogs. We conclude that a single bout of dynamic exercise is sufficient to produce a significantly decreased chronotropic responsiveness to isoproterenol. This phenomenon may represent an acute but transient desensitization of cardiac beta-adrenergic receptors.
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Bonham, A. C., D. D. Gutterman, J. M. Arthur, M. L. Marcus, G. F. Gebhart, and M. J. Brody. "Electrical stimulation in perifornical lateral hypothalamus decreases coronary blood flow in cats." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 3 (March 1, 1987): H474—H484. http://dx.doi.org/10.1152/ajpheart.1987.252.3.h474.
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Based on evidence implicating the central nervous system in the regulation of coronary vascular resistance and the knowledge that the hypothalamus is a central site for integration of cardiovascular control, studies were undertaken to determine if electrical stimulation in the hypothalamus produced coronary vasoconstriction. In anesthetized cats, following beta-adrenergic receptor blockade, stimulation in perifornical lateral hypothalamus produced a transient decrease in coronary blood flow velocity (30 +/- 5%), a small pressor effect (7 +/- 2 mmHg), and an initial decrease in hindquarter blood flow velocity (51 +/- 5%). The decrease in coronary flow velocity, which had an onset latency of 1-3 s and a duration of 5-15 s, was abolished by ipsilateral stellate ganglionectomy and by intravenous and intracoronary prazosin. The coronary vasoconstriction produced by hypothalamic stimulation was not different from that produced by cardioaccelerator nerve stimulation. These results suggest that electrical stimulation of a hypothalamic site produces an alpha-adrenergic receptor-mediated decrease in coronary blood flow that is unmasked by beta-adrenergic receptor blockade, requires the integrity of ipsilateral cardiac sympathetic innervation, and mimics the coronary response to cardioaccelerator nerve stimulation.
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Hatton, D. C., K. E. Scrogin, D. Levine, D. Feller, and D. A. McCarron. "Dietary calcium modulates blood pressure through alpha 1-adrenergic receptors." American Journal of Physiology-Renal Physiology 264, no. 2 (February 1, 1993): F234—F238. http://dx.doi.org/10.1152/ajprenal.1993.264.2.f234.
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To investigate the role of adrenergic receptor activity in dietary calcium-induced alterations in blood pressure, weanling spontaneously hypertensive rats (SHR) were placed on either high-calcium (2.0%) or low-calcium (0.1%) diets for 1-2 wk. Baseline blood pressure was higher and pressor responses to exogenous norepinephrine (NE) were greater in the SHR on low-calcium diets than high-calcium diets. There was no difference between diet groups in circulating NE or in the pressor response to angiotensin II. The difference in basal blood pressure was eliminated by the alpha 1-adrenergic receptor blockers phentolamine and prazosin but was not altered by alpha 2-, beta 1-, or beta 2-adrenergic receptor blockade (idazoxan, metoprolol, and butoxamine, respectively). Furthermore, hypotension produced by either calcitonin gene-related peptide, captopril, or nitroprusside failed to eliminate the diet-induced difference in blood pressure. The results suggest the possibility that diet-induced differences in alpha 1-adrenergic activity may be responsible, in part, for variations in blood pressure on different calcium diets.
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Cooper, G., R. L. Kent, P. McGonigle, and A. M. Watanabe. "Beta adrenergic receptor blockade of feline myocardium. Cardiac mechanics, energetics, and beta adrenoceptor regulation." Journal of Clinical Investigation 77, no. 2 (February 1, 1986): 441–55. http://dx.doi.org/10.1172/jci112323.
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Naden, R. P., and C. R. Rosenfeld. "Role of alpha-receptors in estrogen-induced vasodilation in nonpregnant sheep." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 3 (March 1, 1985): H339—H344. http://dx.doi.org/10.1152/ajpheart.1985.248.3.h339.
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Estradiol-17 beta (E2) produces vasodilation in several systemic vascular beds, but most extensively in the nonpregnant uterus. It has been postulated that E2 induces this vasodilation via blockade of vascular alpha-adrenergic receptors. This hypothesis was tested in six chronically instrumented, nonpregnant sheep by comparing the systemic and uterine hemodynamic responses to intravenous E2, to an alpha-adrenergic receptor blocker, phentolamine, and to both agents given together. Uterine blood flow (UBF) increased significantly after E2 administration, from 20 +/- 7 to 233 +/- 37 (SE) ml/min. In contrast, phentolamine had no detectable effect on UBF or on the UBF response to E2 when both were given together. Similar contrasting responses were observed in the effects of E2 and/or phentolamine on the systemic vasculature. When responses to alpha-agonists were evaluated, there was no evidence of alpha-blockade following E2 despite the substantial vasodilation; in contrast, alpha-blockade was present during phentolamine administration when no vasodilation was noted. Therefore, we conclude that E2-induced vasodilation in chronically instrumented sheep is not mediated through blockade of vascular alpha-adrenergic receptors.
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van Wylen, D. G., and L. G. D'Alecy. "Regional blood flow distribution during the Cushing response: alterations with adrenergic blockade." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 1 (January 1, 1985): H98—H108. http://dx.doi.org/10.1152/ajpheart.1985.248.1.h98.
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Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood flow (CBF) decreased 50%, coronary blood flow (CoBF) increased 120%, and peripheral tissue blood flow was reduced only in the kidneys (18%) and the intestines (small 22%, large 35%). Blood flow to the other viscera, skin, and skeletal muscle was unchanged. CO (16%) and heart rate (HR, 38%) decreased, and total peripheral resistance (TPR, 68%) and stroke volume (SV, 38%) increased. In BB, CBF decreased 50%, CoBF decreased 20%, and blood flow was reduced 40-80% in all peripheral tissues. CO (69%) and HR (62%) decreased, TPR increased 366%, and SV was unchanged. We conclude that the Cushing response in UB animals combines an alpha-receptor-mediated vasoconstriction with a beta-receptor cardiac stimulation. The beta-mechanism is neither necessary nor sufficient for the hypertension. However, the combination of alpha- and beta-adrenergic mechanisms maintains cardiac output and peripheral tissue blood flow relatively constant while producing a systemic hypertension.
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Deschamps, A., and S. Magder. "Effects of heat stress on vascular capacitance." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 5 (May 1, 1994): H2122—H2129. http://dx.doi.org/10.1152/ajpheart.1994.266.5.h2122.
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In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core temperatures. We repeated the measurements at high core temperatures with ganglionic blockade, alpha-adrenergic receptor blockade, or beta-adrenergic receptor blockade to determine the efferent neurohumoral pathway. When core temperature was increased from 37.8 +/- 0.2 to 41.9 +/- 0.1 degrees C, total splanchnic blood volume decreased 23% (4.6 +/- 1.4 ml/kg) and splanchnic unstressed volume decreased 38.5%. None of the other determinants of venous return changed. Ganglionic blockade shifted the total and unstressed splanchnic blood volume during heat stress back to normothermic values. However, beta- and alpha-blockade did not affect splanchnic volumes. We conclude that a decrease in splanchnic unstressed volume is an important factor for the increased venous return during heat stress. Although mediated through sympathetic ganglions, this decrease is not abolished by alpha- or beta-receptor blockade.
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Lee, H. T., C. I. Thompson, J. Linden, and F. L. Belloni. "Differential sensitization of cardiac actions of adenosine in rats after chronic theophylline treatment." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (May 1, 1993): H1634—H1643. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1634.
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To determine the effect of chronic adenosine receptor blockade on atrial responsiveness, we administered theophylline to rats in their drinking water (0.6 mg/ml) for 2 wk. Inotropic and chronotropic responses to the adenosine receptor agonists N6-cyclopentyladenosine (CPA) and 5'-(N-ethylcarboxamido)-adenosine (NECA) were then measured in isolated atria from treated and control animals. The indirect (antiadrenergic) actions of CPA and NECA on force and rate, measured during beta-adrenergic receptor stimulation by isoproterenol, were markedly sensitized (2- to 10-fold reductions in the agonist concentration needed to obtain a half-maximal response) after theophylline. The sensitization was homologous because inotropic and chronotropic responses to carbachol were not affected by theophylline. The direct negative inotropic and chronotropic actions of CPA and NECA, measured without concomitant beta-adrenergic stimulation, were not sensitized after theophylline. The number of atrial A1-receptors, measured by antagonist radioligand binding (maximum specific binding at saturation), was increased by 22% in theophylline-treated rats [66.2 +/- 3.4 vs. 54.3 +/- 1.9 (control) fmol/mg protein, P < 0.05]. Competition binding indicated that the fraction of coupled (high-affinity) receptors was unchanged. The number of ventricular A1-receptors was increased to a similar extent without any change in coupling. Thus chronic dietary theophylline upregulated cardiac A1-adenosine receptors without changing coupling state or affinity and sensitized rat atria to the indirect, antiadrenergic, inhibitory inotropic and chronotropic actions of adenosine receptor agonists.
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Porcelli, R. J., and M. V. Cutaia. "Pulmonary vascular reactivity to biogenic amines during acute hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 2 (August 1, 1988): H329—H334. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h329.
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The effects of acute hypoxia on the pressor responses to five biogenic amines were studied in isolated blood-perfused cat lungs. Hypoxia (Po2 = 46 +/- 2 Torr) reduced the pressor responses to phenylephrine while changing the pressor responses to epinephrine and norepinephrine to vasodilation. Hypoxia reduced the pressor responses to histamine, and these reductions were preceded by small but significant vasodilations. Hypoxia had no effect on the pressor responses to serotonin. These changes in pulmonary vasoactivity were reversed on reoxygenation, independent of changes in base-line tone and not correlated with circulating catecholamines. We also examined the effects of hypoxia on the pressor responses to norepinephrine during beta-blockade with propranolol and then alpha-blockade with dibenzyline. The vasodilation produced during hypoxia by norepinephrine was blocked by propranolol, and vasoconstriction reappeared. When alpha-blockade was then established, vasodilation to norepinephrine reemerged during hypoxia. These results demonstrate that hypoxia produces changes in pulmonary vascular responsiveness that are acute in nature and reversible. Although the cellular nature of these changes is unknown, the data suggest that hypoxia produces acute shifts in antagonistic adrenergic receptor activity by either 1) reducing alpha- or increasing beta-receptor activity or 2) acutely changing adrenergic receptor conformation, affinity, or efficacy, such that beta-activity prevails.
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Hooper, S. B., and R. Harding. "Effect of beta-adrenergic blockade on lung liquid secretion during fetal asphyxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 4 (October 1, 1989): R705—R710. http://dx.doi.org/10.1152/ajpregu.1989.257.4.r705.
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The hypothesis tested in this study was that beta-adrenergic stimulation is responsible for the inhibition of fetal lung liquid production during moderate fetal asphyxia. In chronically catheterized fetal sheep, net lung liquid production rates were measured over three consecutive periods: a control period, a period of reduced uterine blood flow (RUBF) or epinephrine infusion, and periods of RUBF or epinephrine infusion in the presence of the beta-adrenergic receptor antagonist propranolol. The net production rate of fetal lung liquid was decreased from a mean control value of 7.7 +/- 1.0 to 1.5 +/- 0.4 ml/h (P less than 0.001) by RUBF; the administration of propranolol had no further effect on these liquid production rates (1.1 +/- 0.5 ml/h). In other experiments epinephrine infusion reduced the net production rate of fetal lung liquid from a mean control value of 7.2 +/- 1.4 to 1.7 +/- 1.8 ml/h (P less than 0.025); the addition of propranolol reversed this inhibition (secretion rate 6.1 +/- 1.4 ml/h, P less than 0.005). We conclude that the inhibition of fetal lung liquid production induced by moderate fetal asphyxia does not solely result from catecholamine stimulation of pulmonary beta-receptors.
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Hargrove, D. M., G. J. Bagby, C. H. Lang, and J. J. Spitzer. "Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism." American Journal of Physiology-Endocrinology and Metabolism 255, no. 5 (November 1, 1988): E629—E635. http://dx.doi.org/10.1152/ajpendo.1988.255.5.e629.
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Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.
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Takahashi, Toshiyuki, Toshihisa Anzai, Tsutomu Yoshikawa, Yuichiro Maekawa, Keitaro Mahara, Michikado Iwata, H. Kirk Hammond, and Satoshi Ogawa. "Angiotensin receptor blockade improves myocardial beta-adrenergic receptor signaling in postinfarction left ventricular remodeling." Journal of the American College of Cardiology 43, no. 1 (January 2004): 125–32. http://dx.doi.org/10.1016/j.jacc.2003.07.036.
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Cogswell, T. L., G. A. Bernath, H. Raff, R. G. Hoffmann, and H. S. Klopfenstein. "Total peripheral resistance during cardiac tamponade: adrenergic and angiotensin roles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 5 (November 1, 1986): R916—R922. http://dx.doi.org/10.1152/ajpregu.1986.251.5.r916.
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During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was calculated as the conscious euvolemic animals underwent cardiac tamponade induced by intrapericardial saline infusion at 20 ml/min. Six dogs underwent cardiac tamponade in the control condition (no medications) and during independent alpha- and beta-adrenergic and angiotensin-converting enzyme (ACE) inhibition. PRA and angiotensin II (ANG II) were measured during control tamponade. We found that TPR increased continuously to levels of greater than 200% of base line as IPP rose during cardiac tamponade (P less than 0.01). This increase in TPR was unaffected by beta-adrenergic or ACE blockade but was blunted by alpha-adrenergic blockade. PRA and ANG II increased only at decompensated tamponade (P less than 0.05) when arterial blood pressure had fallen by 30%. These changes in PRA and ANG II during tamponade were not altered by beta-blockade in six separate animals. We conclude that cardiac tamponade stimulates renin release and ANG II generation by a non-beta-receptor-mediated mechanism. The increase in TPR during cardiac tamponade is primarily dependent on alpha-adrenergic mechanisms, with a limited late contribution from the renin-angiotensin system.
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Sato, N., Y. T. Shen, K. Kiuchi, R. P. Shannon, and S. F. Vatner. "Splenic contraction-induced increases in arterial O2 reduce requirement for CBF in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 2 (August 1, 1995): H491—H503. http://dx.doi.org/10.1152/ajpheart.1995.269.2.h491.
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We investigated the extent to which sympathomimetic amines induced splenic contraction and associated increases in arterial O2 content (CaO2) and how these mechanisms affected control of the coronary circulation by sympathomimetic amines in conscious dogs. Blood hemoglobin (Hb) and CaO2 increased by 16 +/- 2 and 18 +/- 2%, respectively, during norepinephrine (NE, 0.8 micrograms.kg-1.min-1 iv) in the intact, conscious state after splenic contraction. Phenylephrine (PE) induced similar effects. After either alpha 1-adrenergic-receptor blockade or splenectomy, these effects were abolished. Isoproterenol (Iso) also decreased splenic thickness, which was abolished after ganglionic, alpha-, or beta 1/beta 2-adrenergic-receptor blockade. Direct infusions of NE and PE into the splenic artery decreased splenic thickness and increased Hb and CaO2, whereas Iso had no effect. After splenectomy, NE did not increase CaO2, but coronary blood flow (CBF) increased more (73 +/- 6%) vs. before splenectomy (49 +/- 7%) without any differences before and after splenectomy in the responses of pressures, contractility, and myocardial O2 consumption (MVO2). In contrast, renal, mesenteric, and iliac artery blood flows were not significantly different in response to sympathomimetic amines before and after splenectomy. These data indicate that sympathomimetic amines induced splenic contraction either directly or reflexly via alpha-adrenergic-receptor stimulation. The consequent increase in Hb and CaO2 allows for equivalent increases in MVO2, but at a smaller increase in CBF.
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Hryniewicz, Katarzyna, Aleksandr Yasskiy, Jeffrey R. Bender, Lynn O'Donnell, and Stuart D. Katz. "Vascular endothelial effects of chronic beta-adrenergic receptor blockade in heart failure." Journal of Cardiac Failure 10, no. 4 (August 2004): S46. http://dx.doi.org/10.1016/j.cardfail.2004.06.099.
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Zeman, R. J., Y. Zhang, and J. D. Etlinger. "Clenbuterol, a beta 2-agonist, retards wasting and loss of contractility in irradiated dystrophic mdx muscle." American Journal of Physiology-Cell Physiology 267, no. 3 (September 1, 1994): C865—C868. http://dx.doi.org/10.1152/ajpcell.1994.267.3.c865.
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Treatment with the adrenergic beta 2-receptor agonist clenbuterol prevented, in dystrophic muscle from mdx mice, a pronounced loss of contractile strength that is observed after blockade of muscle regeneration with gamma irradiation. In addition, muscle mass and myosin content were greater (62-109%) in irradiated hindlimbs from clenbuterol-treated mdx mice, whereas the effects of the beta 2-agonist were relatively smaller (12-21%) in the nonirradiated hindlimbs. Together, these results suggest that beta 2-agonists can antagonize degenerative processes occurring in muscle fibers lacking dystrophin.
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Arici, Aylin, Sule Kalkan, Omer Demir, Nil Hocaoglu Aksay, Sedef Gidener, and Yesim Tuncok. "Does adenosine A1 receptor stimulation causes beta adrenergic receptor blockade in amitriptyline-induced QRS prolongation?" Toxicology Letters 180 (October 2008): S126. http://dx.doi.org/10.1016/j.toxlet.2008.06.737.
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Ririe, Douglas G., John F. IV Butterworth, Roger L. Royster, Drew A. MacGregor, and Gary P. Zaloga. "Triiodothyronine Increases Contractility Independent of β-Adrenergic Receptors or Stimulation of Cyclic-3',5'-Adenosine Monophosphate." Anesthesiology 82, no. 4 (April 1, 1995): 1004–12. http://dx.doi.org/10.1097/00000542-199504000-00025.
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Background Triiodothyronine regulates cardiac contractility; however, the mechanisms by which it produces its acute contractile effects remains unknown. We compared the acute effects of thyroid hormones (triiodothyronine [T3] and thyroxine [T4]) and of isoproterenol on the contractility of isolated rat hearts. In addition, we sought to determine whether the acute inotropic effects of thyroid hormones were mediated by beta-adrenergic receptors or by increased production of cyclic-3',5'-adenosine monophosphate (cAMP). Methods A Langendorff heart preparation harvested from euthyroid male Sprague-Dawley rats was used. Drugs were administered through an aortic perfusion catheter. A pressure-transduced left-ventricular balloon catheter measured pressure and heart rate changes. Changes in the maximum positive rate of change in pressure (dP/dT) and maximum negative dP/dT were determined. Responses to varying doses of T3, T4, and isoproterenol were assessed in the presence and absence of beta-adrenergic receptor blockade with propranolol. cAMP production, measured by radioimmunoassay, was determined in myocardial cell suspensions after incubation with T3 or isoproterenol. Results T3 0.74 nmol rapidly and significantly increased maximum dP/dT by 335 +/- 38 mmHg/s within 30 s after bolus injection; however, contractility was unchanged after as much as 12.9 nmol T4. The maximal increase in dP/dT after 0.8 nmol isoproterenol was comparable to that produced by T3. However, the cardiotonic actions of isoproterenol were significantly slower to develop (peaking at 60 vs. 15 s) and lasted longer than those of T3. Pretreatment with propranolol 1 mumol diminished the contractile effects of isoproterenol but had no effect on those of T3. Concentrations of isoproterenol that increase contractility also significantly increased cAMP production in isolated rat myocardial cells. However, T3 failed to increase cAMP production. Conclusions These results demonstrate that the acute inotropic effects of T3 are not shared by T4 and appear unrelated to beta-adrenergic receptor mechanisms or to generation of cAMP. Thus, T3 acutely stimulates cardiac contraction by mechanisms that differ from those of the more commonly used beta-adrenergic receptor agonists and phosphodiesterase inhibitors. Further studies are needed to identify the mechanisms underlying the acute contractile effects of T3 and to determine whether T3 will prove useful for increasing ventricular function in patients.
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Lang, C. H. "Beta-adrenergic blockade attenuates insulin resistance induced by tumor necrosis factor." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 5 (May 1, 1993): R984—R991. http://dx.doi.org/10.1152/ajpregu.1993.264.5.r984.
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The macrophage secretory product tumor necrosis factor (TNF) impairs insulin action on peripheral glucose uptake and hepatic glucose output. Because circulating catecholamines are also elevated by TNF, the present study was performed to determine the role of the adrenergic system in eliciting the insulin resistance. Human recombinant TNF (1 microgram.h-1.kg-1) was infused intravenously into chronically catheterized fasted rats for approximately 18 h. Before TNF, an infusion of either saline, propranolol (nonselective beta-antagonist), atenolol (selective beta 1-antagonist), or phentolamine (alpha-antagonist) was started and continued throughout the experimental protocol. Infusion of either the alpha- or beta-receptor antagonist failed to prevent the TNF-induced increase in basal glucose uptake or hepatic glucose output. Under euglycemic hyperinsulinemic conditions, whole body glucose disposal was lower in TNF-infused rats than in control animals. This resulted from a decreased rate of insulin-stimulated glucose uptake by skeletal muscle, skin, and intestine. In propranolol-infused rats, but not in those receiving atenolol or phentolamine, the TNF-induced decrease in whole body glucose uptake was partially prevented. Propranolol attenuated the development of peripheral insulin resistance by selectively preventing the decrease in glucose uptake by skeletal muscle but not by skin and ileum. Propranolol was also able to ameliorate the hepatic insulin resistance produced by TNF. These results suggest that beta-adrenergic stimulation, probably mediated by a beta 2-adrenergic mechanism, is partially responsible for the development of both peripheral and hepatic insulin resistance in animals infused with TNF.
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Badgett, Robert G., Valerie A. Lawrence, and Steven L. Cohn. "Variations in Pharmacology of β-Blockers May Contribute to Heterogeneous Results in Trials of Perioperative β-Blockade." Anesthesiology 113, no. 3 (September 1, 2010): 585–92. http://dx.doi.org/10.1097/aln.0b013e3181e73eea.
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Background Randomized controlled trials and meta-analyses provide conflicting guidance on the role of beta-adrenergic receptor blockers (beta-blockers) in reducing perioperative complications. We hypothesize that variability in trial results may be due in part to heterogeneous properties of beta-blockers. First, we propose that the extent of beta-blocker metabolism by cytochrome P-450 and the time available to titrate the dosage before surgery (titration time) may interact; dependence on P-450 may be most harmful when titration time is short. Second, beta-blockers vary in their selectivity for the beta-1 receptor and reduced selectivity may contribute to cerebral ischemia. Methods We used meta-analysis and meta-regression of existing trials to explore the role of these pharmacological properties. Results We found that both of these pharmacological factors are significantly associated with reduced efficacy of beta-blockers. Conclusions Pharmacological properties of beta-blockers may contribute to heterogeneous trial results. Many trials have used metoprolol, which is extensively metabolized by cytochrome P450 and is less selective for the beta-1 receptor. For these two reasons, the efficacy of metoprolol to prevent perioperative cardiac complications should be compared with the efficacy of other beta-blockers.
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Wakamatsu, Hiroki, Toshiki Watanabe, Yoshiyuki Sato, Shinya Takase, Sadao Omata, and Hitoshi Yokoyama. "Selective Beta-1 Receptor Blockade Further Reduces the Mechanically Stabilized Target Coronary Artery Motion during Beating Heart Surgery." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 5, no. 5 (September 2010): 349–54. http://dx.doi.org/10.1097/imi.0b013e3181f6536b.
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Objective Adequate stabilization of anastomosis sites during off-pump coronary artery bypass is essential to obtain excellent graft patency. We examined the effect of beta-1 adrenergic receptor blockade on the target coronary artery motion by three-dimensional (3D) digital motion capture and reconstruction technology. Methods Eight pigs underwent a sternotomy. Reflection markers were attached to the surface coronary arteries, followed by a mechanical stabilizer application. Two high-speed digital cameras captured two-dimensional (2D) motion of the markers from different angles. These 2D data were reconstructed into 3D data points, representing the motion of each coronary artery. Landiolol hydrochloride, a novel selective beta-1 receptor blocker, was infused intravenously after acquisition of control data. Results Beta-1 receptor blockade decreased heart rate (105 ± 16 vs. 90 ± 9 beat/min; P = 0.007) without decreasing arterial blood pressure. The 3D distance moved (millimeter) during one cardiac cycle was significantly reduced on the left anterior descending (9.6 ± 2.8 vs. 6.6 ± 1.9 mm; P = 0.003), left circumflex (10.5 ± 6.3 vs. 6.4 ± 2.6 mm; P = 0.038), and right coronary (8.3 ± 3.6 vs. 6.5 ± 2.1 mm; P = 0.028) arteries. Reduction in the maximal velocity, maximal acceleration, and maximal deceleration of the anastomosis site in all coronary arteries was also found in a quantitative fashion. Conclusions Selective beta-1 receptor blockade significantly reduces the 3D motion at anastomosis sites on the beating heart, with stable systemic blood pressure. Further quantitative investigations of pharmacological stabilization are warranted to achieve better outcome of the patients undergoing off-pump coronary artery bypass surgery.
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Hintze, T. H., F. L. Belloni, J. E. Harrison, and G. C. Shapiro. "Apparent reduction in baroreflex sensitivity to adenosine in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 3 (September 1, 1985): H554—H559. http://dx.doi.org/10.1152/ajpheart.1985.249.3.h554.
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Relative effects of equihypotensive doses (-35 mmHg) of adenosine (5.0 mumol/kg) and nitroglycerin (25 micrograms/kg) on heart rate and, therefore, baroreflex sensitivity were studied in conscious dogs. Nitroglycerin increased heart rate 133 +/- 24% from 78 +/- 5.5 beats/min, whereas adenosine increased heart rate only 79 +/- 16% from 78 +/- 5.2 beats/min (P less than 0.01). Injection of nitroglycerin during combined beta-adrenergic and muscarinic receptor blockades caused arterial pressure to fall 38 +/- 3.4% from 107 +/- 3.2 mmHg without any significant change in heart rate (3.8 +/- 3.8 from 162 +/- 9.2 beats/min). During combined beta-adrenergic and muscarinic receptor blockades adenosine also reduced arterial pressure 45 +/- 2.7% from 106 +/- 2.9 mmHg but unexpectedly reduced heart rate as well by 37 +/- 1.7% from 160 +/- 9.7 beats/min. This bradycardia reflected an effect on the sinoatrial (SA) node rather than an induction of heart block, since the R-R interval increased by 70 +/- 7.8% from 371 +/- 20 ms (P less than 0.01), while the P-R interval increased only 13 +/- 2.3% from 97 +/- 7.2 ms (P less than 0.05) with no electrocardiographic evidence of nonconducted beats. Arterial plasma adenosine levels were 43 +/- 5 nmol/ml at this time. Adenosine also caused bradycardia during muscarinic blockade alone (-43 +/- 3.4% from 201 +/- 6.4 beats/min) and following bilateral vagal section (-33 +/- 1.9% from 151 +/- 5.9 beats/min). In summary, adenosine appears to alter normal baroreflex function in the conscious dog by reducing the tachycardia that normally follows a fall in systemic arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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Fujii, A. M., and S. F. Vatner. "Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 4 (October 1, 1987): H728—H736. http://dx.doi.org/10.1152/ajpheart.1987.253.4.h728.
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To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the complicating inotropic effects of the agonists studied. Norepinephrine (0.2 microgram/kg bolus) increased mean arterial pressure by 30 +/- 3 mmHg, total peripheral resistance by 51 +/- 4 mmHg . l-1 . min-1, and decreased heart rate by 26 +/- 3 beats/min. After arterial baroreceptor denervation, norepinephrine increased mean arterial pressure by 69 +/- 8 mmHg, total peripheral resistance by 48 +/- 6 mmHg . l-1 . min-1, and heart rate did not change. After ganglionic blockade (hexamethonium 40 mg/kg), norepinephrine increased mean arterial pressure by 76 +/- 3 mmHg, total peripheral resistance by 47 +/- 4 mmHg X l-1 X min-1, and heart rate did not change. Only after elimination of the buffering by heart rate by use of cholinergic receptor blockade (atropine 0.1 mg/kg) or ventricular pacing could buffering of the vasoconstrictor responses to alpha-adrenergic receptor agonists be demonstrated. Thus in conscious dogs the primary mechanism for buffering increases in arterial pressure induced by alpha-adrenergic receptor agonists is compensatory changes in heart rate and cardiac output with little buffering of total peripheral resistance.
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Nganele, D. M., and T. H. Hintze. "Cardiac chemical reflex control of preload in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 4 (April 1, 1990): H1055—H1063. http://dx.doi.org/10.1152/ajpheart.1990.258.4.h1055.
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The purpose of our study was to determine the effects of cardiac chemical reflexes on left ventricular (LV) preload in conscious dogs. Adult mongrel dogs were instrumented to measure LV pressure and, with ultrasonic dimension crystals, to measure LV internal diameter. A catheter was inserted in the left circumflex coronary artery for the administration of increasing doses of veratridine, arachidonic acid (AA), and prostacyclin (PGI2). LV end-diastolic diameter (EDD) and end-diastolic pressure (EDP) were used as indexes of preload. Veratridine (0.4 micrograms/kg) reduced EDD 3.0 +/- 0.5% from 36.6 +/- 1.7 mm and EDP 24 +/- 5.0% from 6.1 +/- 0.5 mmHg (P less than 0.05). AA (100 micrograms/kg) reduced EDD by 3.7 +/- 0.5% from 37 +/- 1.1 mm and EDP by 25 +/- 4.4% from 7.0 +/- 0.6 mmHg (P less than 0.05). PGI2 (0.5 micrograms/kg) also reduced EDD by 3.3 +/- 0.5% from 37 +/- 0.5 mm and EDP by 25 +/- 6.0% from 7.8 +/- 0.3 mmHg (P less than 0.05). Although holding heart rate constant by pacing or combined beta-adrenergic and muscarinic receptor blockades did not reduce the preload responses to veratridine, AA, or PGI2, alpha 1-adrenergic blockade or vagotomy abolished them. Systemic arterial barodenervation markedly potentiated the reduction in myocardial size after stimulation of cardiac chemical receptors. Stimulation of inhibitory cardiac receptors, therefore, reduces preload via a vagal reflex by withdrawing peripheral alpha-adrenergic tone to capacitance vessels in the conscious dog.
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Mandic, Danijela, Lana Nezic, and Ranko Skrbic. "Severe hyperkalemia induced by propranolol." Medical review 67, no. 5-6 (2014): 181–84. http://dx.doi.org/10.2298/mpns1406181m.
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Introduction. Hyperkalemia secondary to beta-adrenergic receptor blockade occurs in 1-5% of patients and is likely to develop with non-cardio-selective beta-blockers. Case Report. We have described hyperkalemia in a patient with angina pectoris receiving propranolol, clinically manifested as weakness, tightness behind the sternum and numbness in the limbs. Laboratory tests showed hyperkalemia (6.6 mmol/L), peaked T wave and a corrected QT interval of 510 ms. After discontinuation of propranolol, decline in potassium level, normalisation of electrocardiographic changes and clinical improvement were achieved. Causal relationship of drug related hyperkalemia has been confirmed as probable/likely according to Naranjo Adverse Drug Reaction Probability Score of 7 and the World Health Organization Uppsala Monitoring Centre Probability Scale. Conclusion. Hyperkalemia can be unpredictable and life-threatening complication of propranolol or a non-selective adrenergic beta blocker treatment, and requires timely identification of cause and implementation of therapeutic measures.
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Kruse, P., J. Ladefoged, U. Nielsen, P. E. Paulev, and J. P. Sorensen. "beta-Blockade used in precision sports: effect on pistol shooting performance." Journal of Applied Physiology 61, no. 2 (August 1, 1986): 417–20. http://dx.doi.org/10.1152/jappl.1986.61.2.417.
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In a double-blind cross-over study of 33 marksmen (standard pistol, 25 m) the adrenergic beta 1-receptor blocker, metoprolol, was compared to placebo. Metoprolol obviously improved the pistol shooting performance compared with placebo. Shooting improved by 13.4% of possible improvement (i.e., 600 points minus actual points obtained) as an average (SE = 4%, 2P less than 0.002). The most skilled athletes demonstrated the clearest metoprolol improvement. We found no correlation between the shooting improvement and changes in the cardiovascular variables (i.e., changes of heart rate and systolic blood pressure) and no correlation to the estimated maximum O2 uptake. The shooting improvement is an effect of metoprolol on hand tremor. Emotional increase of heart rate and systolic blood pressure seem to be a beta 1-receptor phenomenon.