Articles de revues : « Pharmacology, Norepinephrine »

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Carcillo, Joseph A., et 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, n^o 9 (1 septembre 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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Mitchell, Heather A., et David Weinshenker. « Good night and good luck : Norepinephrine in sleep pharmacology ». Biochemical Pharmacology 79, n^o 6 (mars 2010) : 801–9. http://dx.doi.org/10.1016/j.bcp.2009.10.004.

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Forrest, Christopher R., Ning Xu et Cho Y. Pang. « Evidence for nicotine-induced skin flap ischemic necrosis in the pig ». Canadian Journal of Physiology and Pharmacology 72, n^o 1 (1 janvier 1994) : 30–38. http://dx.doi.org/10.1139/y94-006.

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There is clinical and experimental evidence to indicate that cigarette smoking may increase the risk of skin ischemic necrosis in flap surgery but the pathogenic mechanism remains unclear. The objectives of this project were to investigate the potential deleterious effects and mechanism of action of nicotine, a major by-product of cigarette smoking, in skin flap surgery in the pig. It was observed that 4–5 weeks of intramuscular nicotine injections (4 mg/kg; twice daily) significantly (p < 0.05) decreased the skin flap capillary blood flow and the length and area of skin flap viability in the pig. This nicotine treatment also induced a 1.6-fold increase in skin flap tissue content of norepinephrine compared with the saline-treated control. The estimated mean wet skin tissue content of norepinephrine (5 × 10−7 M) was much higher than the circulating level of norepinephrine (1.8 × 10−9 M) in nicotine-treated pigs. This level of norepinephrine (5 ×10−7 M) was seen to induce a significant vasoconstrictor effect (75% increase over basal perfusion pressure) in isolated perfused pig skin flaps. It was also observed that the vasoconstrictor effect of norepinephrine was significantly (p < 0.05) enhanced in the presence of 10−4 M Nω-monomethyl-L-arginine or NG-nitro-L-arginine, an endothelium-derived relaxing factor – nitric oxide (EDRF/NO) synthesis inhibitor. This vasoconstrictor effect was further enhanced in the presence of NG-nitro-L-arginine and 10−5 M indomethacin, a cyclooxygenase inhibitor. Taken together, these observations indicate that 4–5 weeks of nicotine treatment significantly reduced the skin capillary blood flow and viability in skin flap surgery in the pig and this deleterious effect was likely to be mediated, at least in part, by locally released norepinephrine induced by nicotine treatment. Furthermore, norepinephrine also induced skin flap local release of EDRF/NO and a vasodilating prostanoid that in turn attenuated norepinephrine's vasoconstrictor effect in the skin vasculature. We speculate that skin vasculature with compromised endothelial cell function as a result of trauma or disease is more susceptible to the vasoconstrictor effect of norepinephrine released by nicotine.Key words: chronic nicotine, norepinephrine, skin vasoconstriction, flap surgery.

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Li, Peter P., David Sibony et Jerry J. Warsh. « Pharmacologic characterization of cirazoline-activated inositol phospholipid hydrolysis in rat brain cortical slices ». Canadian Journal of Physiology and Pharmacology 66, n^o 11 (1 novembre 1988) : 1460–63. http://dx.doi.org/10.1139/y88-238.

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Interaction of cirazoline, an imidazoline derivative, with α1-adrenoceptor coupled inositol phospholipid hydrolysis was characterized in rat brain cortical slices. Norepinephrine, a full α1-agonist, and phenylephrine, a partial α1-agonist, on inositol phospholipid hydrolysis were included for comparison. Norepinephrine produced a fourfold stimulation of inositol phospholipid hydrolysis, whereas cirazoline and phenylephrine caused only submaximal responses (40–60%) when compared with norepinephrine. The stimulation of inositol phospholipid hydrolysis by cirazoline was completely blocked by the α1-adrenoceptor antagonist prazosin, but not by selective α2- or β-adrenoceptor antagonists. Furthermore, the norepinephrine dose–response curve was shifted to the right in the presence of cirazoline, without affecting the maximal response. These results suggest that cirazoline behaves as a partial agonist at brain α1-adrenoceptors linked to inositol phospholipid hydrolysis.

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Stahl, Stephen M., Meghan M. Grady, Chantal Moret et Mike Briley. « SNRIs : The Pharmacology, Clinical Efficacy, and Tolerability in Comparison with Other Classes of Antidepressants ». CNS Spectrums 10, n^o 9 (septembre 2005) : 732–47. http://dx.doi.org/10.1017/s1092852900019726.

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AbstractThe class of serotonin and norepinephrine reuptake inhibitors (SNRIs) now comprises three medications: venlafaxine, milnacipran, and duloxetine. These drugs block the reuptake of both serotonin (5-HT) and norepinephrine with differing selectivity. Whereas milnacipran blocks 5-HT and norepinephrine reuptake with equal affinity, duloxetine has a 10-fold selectivity for 5-HT and venlafaxine a 30-fold selectivity for 5-HT. All three SNRIs are efficacious in treating a variety of anxiety disorders. There is no evidence for major differences between SNRIs and SSRIs in their efficacy in treating anxiety disorders. In contrast to SSRIs, which are generally ineffective in treating chronic pain, all three SNRIs seem to be helpful in relieving chronic pain associated with and independent of depression. Tolerability of an SNRI at therapeutic doses varies within the class. Although no direct comparative data are available, venlafaxine seems to be the least well-tolerated, combining serotonergic adverse effects (nausea, sexual dysfunction, withdrawal problems) with a dose-dependent cardiovascular phenomenon, principally hypertension. Duloxetine and milnacipran appear better tolerated and essentially devoid of cardiovascular toxicity.

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Vadiei, Nina, Mitchell J. Daley, Manasa S. Murthy et Carrie S. Shuman. « Impact of Norepinephrine Weight-Based Dosing Compared With Non–Weight-Based Dosing in Achieving Time to Goal Mean Arterial Pressure in Obese Patients With Septic Shock ». Annals of Pharmacotherapy 51, n^o 3 (25 novembre 2016) : 194–202. http://dx.doi.org/10.1177/1060028016682030.

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Background: Currently, a lack of standardization exists in norepinephrine dosing units, the first-line vasopressor for septic shock. Timely achievement of goal mean arterial pressure (MAP) is dependent on optimal vasopressor dosing. Objective: To determine if weight-based dosing (WBD) of norepinephrine leads to earlier time to goal MAP compared with non-WBD in obese patients with septic shock. Methods: This was a retrospective, multicenter cohort study. Patients had a body mass index (BMI) ≥30 kg/m2 and received norepinephrine for septic shock with either a non-WBD strategy (between December 2009 and January 2013) or WBD strategy (between January 2013 and December 2015). The primary outcome was time to goal MAP. Secondary outcomes were norepinephrine duration, dose requirements, and development of treatment-related complications. Results: A total of 287 patients were included (WBD 144; non-WBD 143). There was no difference in median time to goal MAP (WBD 58 minutes, interquartile range [IQR] = 16.8-118.5, vs non-WBD 60 minutes, IQR = 17.5-193.5; P = 0.28). However, there was a difference in median cumulative norepinephrine dose (WBD 12.6 mg, IQR = 4.9-45.9, vs non-WBD 10.5 mg, IQR = 3.9-25.6; P = 0.04) and time to norepinephrine discontinuation (WBD 33 hours, IQR = 15-69, vs non-WBD 27 hours, IQR = 12-51; P = 0.03). There was no difference in rates of atrial fibrillation (WBD 15.3% vs non-WBD 23.7%; P = 0.07) or mortality (WBD 23.6% vs non-WBD 23.1%; P = 0.92). Conclusion: WBD of norepinephrine does not achieve time to goal MAP earlier in obese patients with septic shock. However, WBD may lead to higher norepinephrine cumulative dose requirements and prolonged time until norepinephrine discontinuation.

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Tatsuno, Tohru, Terufumi Kato, Michiko Katsuyama et Mitsutaka Nakamura. « Chronic effects of L-threo-dihydroxyphenylserine, a precursor of (-)-norepinephrine, in norepinephrine-deficient mice ». Japanese Journal of Pharmacology 49 (1989) : 302. http://dx.doi.org/10.1016/s0021-5198(19)56743-9.

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Dong, Erdan, Akito Yatani, Amy Mohan et Chang-seng Liang. « Myocardial β-adrenoceptor down-regulation by norepinephrine is linked to reduced norepinephrine uptake activity ». European Journal of Pharmacology 384, n^o 1 (novembre 1999) : 17–24. http://dx.doi.org/10.1016/s0014-2999(99)00652-4.

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Lang, Chim C., Abdul R. Rahman, David J. K. Balfour et Allan D. Struthers. « The differential effects of circulating norepinephrine and neuronally released norepinephrine on sodium excretion in humans ». Clinical Pharmacology and Therapeutics 54, n^o 5 (novembre 1993) : 514–22. http://dx.doi.org/10.1038/clpt.1993.183.

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Stein, C. M., R. Nelson, H. B. He, M. Wood et A. J. J. Wood. « Effects of Epinephrine on Norepinephrine Release ». Clinical Pharmacology & ; Therapeutics 59, n^o 2 (février 1996) : 139. http://dx.doi.org/10.1038/sj.clpt.1996.55.

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Prommer, Eric. « Aripiprazole ». American Journal of Hospice and Palliative Medicine® 34, n^o 2 (10 juillet 2016) : 180–85. http://dx.doi.org/10.1177/1049909115612800.

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Delirium is a palliative care emergency where patients experience changes in perception, awareness, and behavior. Common features include changes in the sleep–wake cycle, emotional lability, delusional thinking, and language and thought disorders. Delirium results from neurotransmitter imbalances involving several neurotransmitters such as dopamine, glutamate, norepinephrine, acetylcholine, gamma-aminobutyric acid, and serotonin. Untreated delirium causes significant morbidity and mortality. Nonpharmacologic and pharmacologic approaches treat delirium. Current pharmacologic management of delirium involves using agents such as haloperidol or second-generation antipsychotics. Third-generation atypical antipsychotic drugs have emerged as a potential choice for delirium management. Aripiprazole is a third-generation antipsychotic with a dopamine receptor-binding profile distinct from other second-generation antipsychotics. Aripiprazole acts as partial agonist at dopamine D2 and 5-hydroxytryptamine (5-HT)1A receptors, stabilizing the dopamine receptor leading to improvement in symptoms. The article reviews the pharmacology, pharmacodynamics, metabolism, and evidence of clinical efficacy for this new antipsychotic agent. This article explores possible roles in palliative care.

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Kato, Terufumi, Michiko Katsuyama, Nobuyuki Karai, Mitsutaka Nakamura et Junki Katsube. « Central effect of a norepinephrine precursor, L-threo-DOPS in norepinephrine-depleted mice : Behavior and biochemistry. » Japanese Journal of Pharmacology 39 (1985) : 181. http://dx.doi.org/10.1016/s0021-5198(19)63526-2.

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Bredhold, Benjamin E., Shauna D. Winters, John C. Callison, Robert E. Heidel, Lauren M. Allen et Leslie A. Hamilton. « Impact of the Sequence of Norepinephrine and Vasopressin Discontinuation in Patients Recovering From Septic Shock ». Hospital Pharmacy 55, n^o 1 (5 décembre 2018) : 26–31. http://dx.doi.org/10.1177/0018578718817469.

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Background: Septic shock is a serious medical condition affecting millions of people each year and guidelines direct vasopressor use in these patients. However, there is little information as to which vasopressor should be discontinued first. Objective: The objective of this study was to assess the impact of the sequence of norepinephrine and vasopressin discontinuation on intensive care unit (ICU) length of stay. Methods: This was a single-center retrospective cohort study conducted at The University of Tennessee Medical Center in Knoxville, Tennessee. Patients included in this study were adults 18 years of age and older with a diagnosis of septic shock who received norepinephrine in combination with vasopressin. Patients were excluded if norepinephrine or vasopressin were not the last 2 vasoactive agents used or if the patient expired or care was withdrawn. Measurements and Main Results: A total of 86 patients were included in this study, with 34 patients in the norepinephrine discontinued first group (NDF) and 52 in the vasopressin discontinued first group (VDF). For the primary outcome of ICU length of stay, no statistically significant difference was found between the NDF and the VDF groups (9.38 days vs 11.07 days, P = .313). The secondary outcome of the dose of norepinephrine at which vasopressin was initiated was also found to not be significant between the NDF and VDF groups (22 µg/min vs 31.1 µg/min, P = .11). The rates of hypotension within 24 hours of discontinuation of the first agent were also not significant between the NDF and VDF groups (17% vs 31%, P = .38). Conclusions: Based on the results of this study, there was significant no difference in ICU length of stay based on the sequence of discontinuation between norepinephrine and vasopressin in patients recovering from septic shock.

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Vatta, M. S., L. G. Bianciotti, A. S. Locatelli, M. L. Papouchado et B. E. Fernández. « Monophasic and biphasic effects of angiotensin II and III on norepinephrine uptake and release in rat adrenal medulla ». Canadian Journal of Physiology and Pharmacology 70, n^o 6 (1 juin 1992) : 821–25. http://dx.doi.org/10.1139/y92-110.

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Angiotensin II and III have hypertensive effects. They induce vascular smooth muscle constriction, increase sodium reabsorption by renal tubules, stimulate the anteroventral third ventricle area, increase vasopressin and aldosterone secretions, and modify catecholamine metabolism. In this work, angiotensin II and III effects on norepinephrine uptake and release in rat adrenal medulla were investigated. Both angiotensins decreased total and neuronal norepinephrine uptake. Angiotensin II showed a biphasic effect only on evoked neuronal norepinephrine release (an earlier decrease followed by a later increase), while increasing the spontaneous norepinephrine release only after 12 min. On the other hand, angiotensin III showed a biphasic effect on evoked and spontaneous neuronal norepinephrine release. Both angiotensins altered norepinephrine distribution into intracellular stores, concentrating the amine into the granular pool and decreasing the cytosolic store. The results suggest a physiological biphasic effect of angiotensin II as well as angiotensin III that may be involved in the modulation of sympathetic activity in the rat adrenal medulla.Key words: angiotensin II, angiotensin III, norepinephrine uptake, norepinephrine release, adrenal medulla.

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Schafferhans, K., D. Grimm, E. Heidbreder et A. Heidland. « Norepinephrine Induced Renal Failure ». Journal of Cardiovascular Pharmacology 8, n^o 6 (novembre 1986) : 1329. http://dx.doi.org/10.1097/00005344-198611000-00208.

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Richardt, Doreen, Andreas Dendorfer, Ralph Tölg, Peter Dominiak et Gert Richardt. « Inhibition of nonexocytotic norepinephrine release by desipramine reduces myocardial infarction size ». Canadian Journal of Physiology and Pharmacology 84, n^o 11 (novembre 2006) : 1185–89. http://dx.doi.org/10.1139/y06-066.

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During myocardial ischemia, a substantial accumulation of norepinephrine occurs in the ischemic zone due to a local nonexocytotic release of norepinephrine. Norepinephrine release is driven by the neuronal monoamine transporter (NET), which reverses its usual transmembrane transport direction. We investigated whether this local accumulation of norepinephrine contributes to irreversible myocardial injury in an in vivo model of myocardial infarction. Male, anaesthetized Wistar rats were subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. Five minutes prior to coronary occlusion, the NET inhibitor desipramine was administered intravenously. Infarct size (IS) was determined by TTC-staining and was related to the area at risk (AAR). The influence of desipramine on cardiac norepinephrine release was investigated in isolated perfused hearts with 30 min of regional ischemia. Norepinephrine was measured in the effluent from the hearts by HPLC and electrochemical detection. Desipramine (0.1–0.8 mg/kg) dose-dependently reduced infarct size (IS/AAR) from 0.54 to 0.21 and suppressed postischemic norepinephrine release from 245 to 108 pg/mL. In summary, the data indicate that nonexocytotic release of norepinephrine in myocardial ischemia exaggerates acute ischemic damage, because suppression of ischemia-induced release of norepinephrine by the tricyclic antidepressant desipramine effectively reduces infarct size in an in vivo model of myocardial ischemia.

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Baines, Andrew DeWitt, Rosa Drangova et Patrick Ho. « Neural stimulation of gluconeogenesis in isolated pyruvate-perfused rat kidneys ». Canadian Journal of Physiology and Pharmacology 66, n^o 1 (1 janvier 1988) : 106–11. http://dx.doi.org/10.1139/y88-020.

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To estimate peritubular norepinephrine concentration during renal nerve stimulation, we compared gluconeogenic responses in isolated pyruvate-perfused rat kidneys with electrical nerve stimulation and exogenous norepinephrine. During 2 and 4 Hz stimulation, venous norepinephrine was 1.7 ± 0.4 and 2.7 ± 0.9 nmol/L, respectively. Intra-arterial norepinephrine infusion of 60 pmol/min for 20 min (an amount corresponding to that released during 4 Hz stimulation) resulted in venous norepinephrine levels of 3.6 ± 0.6 nmol/L. Electrical stimuli (1, 2, and 4 Hz) sustained increases in vascular resistance of 2, 5, and 11% during 20 min of stimulation, while the norepinephrine infusion increased resistance gradually by 8% and a bolus (12.5 nmol/L) transiently increased resistance by 2%. All electrical and norepinephrine interventions, except 1 Hz, decreased fractional Cl excretion. Decreased glomerular filtration rate was observed only during 4 Hz stimulation. Gluconeogenesis transiently increased during stimulation at 2 or 4 Hz (12% (p = 0.056) and 15% (p = 0.028)). The 5% increase in gluconeogenesis during norepinephrine infusion did not differ from the increase during 4 Hz stimulation (p = 0.45). An exogenous norepinephrine bolus (12.5 nmol/L) increased gluconeogenesis 60% for 15 min, four times more than the response to 4 Hz nerve stimulation (p = 0.012). Therefore, we conclude that nerve stimulation sufficient to produce sustained vasoconstriction and antinatriuresis raised norepinephrine concentration less than 12 nmol/L on the peritubular surface of the S1 proximal tubule, thus accounting for the small gluconeogenic response.

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Sato, Koichi, Miho Sawada, Masayoshi Kojima et Yasuaki Dohi. « Biphasic pressor responses to norepinephrine in humans ». Clinical Pharmacology & ; Therapeutics 58, n^o 5 (novembre 1995) : 583–87. http://dx.doi.org/10.1016/0009-9236(95)90178-7.

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Dazzi, Laura, Emanuele Seu, Giulia Cherchi et Giovanni Biggio. « Antagonism of the stress-induced increase in cortical norepinephrine output by the selective norepinephrine reuptake inhibitor reboxetine ». European Journal of Pharmacology 476, n^o 1-2 (août 2003) : 55–61. http://dx.doi.org/10.1016/s0014-2999(03)02130-7.

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Lorbar, Mojca, Eugene S. Chung, Arash Nabi, Katarina Skalova, Richard A. Fenton, James G. Dobson, Jr. et Theo E. Meyer. « Receptors subtypes involved in adenosine-mediated modulation of norepinephrine release from cardiac nerve terminals ». Canadian Journal of Physiology and Pharmacology 82, n^o 11 (1 novembre 2004) : 1026–31. http://dx.doi.org/10.1139/y04-108.

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The objective of this study was to determine which adenosine receptor subtypes were involved in the modulation of norepinephrine release from cardiac nerve terminals. In addition, the persistence of adenosine-mediated effects was evaluated. Rat hearts attached to the stellate ganglion were isolated and perfused. The ganglion was electrically stimulated twice (S1 and S2), allowing 10 min between the stimulations. To determine adenosine receptor subtypes, selective and nonselective adenosine agonists and antagonists were infused following S1 and until the end of S2. To evaluate the persistence of adenosine-mediated effect on norepinephrine release, the stellate ganglion was stimulated a third (S3) and fourth (S4) time. Coronary effluents were collected to determine norepinephrine content. Adenosine and a selective A1 receptor agonist, CCPA, inhibited norepinephrine release by 49% and 54%, respectively. This effect was reversed by simultaneous infusion of nonspecific (8-SPT) and specific (DPCPX) A1 receptor antagonists. Selective A2A (CGS 21680) and A3 (AB-MECA) receptor agonists had no discernible effect on norepinephrine release. Similarly, adenosine A2A receptor antagonists CSC and DMPX did not alter the dose-response relation between norepinephrine release and adenosine. Finally, the inhibitory effects of adenosine on norepinephrine release did not persist 10 min subsequent to the removal of adenosine. Adenosine inhibited norepinephrine release primarily via the adenosine A1 receptor. This effect of adenosine was of short duration. Adenosine A2A and A3 receptors were either absent or functionally insignificant in the regulation of norepinephrine release in the rat heart.Key words: adenosine, norepinephrine, receptor, rat, neurotransmitters.

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Yamaguchi, Nobuharu, Richard Briand et Martine Brassard. « Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output ». Canadian Journal of Physiology and Pharmacology 67, n^o 5 (1 mai 1989) : 499–505. http://dx.doi.org/10.1139/y89-079.

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This study reports on the major source of circulating norepinephrine that is known to increase, progressively, during sustained hypoglycemia induced by intravenous insulin administration. Plasma concentrations of epinephrine, norepinephrine, and dopamine were simultaneously determined for adrenal venous and aortic blood in dogs anesthetized with sodium pentobarbital. The model used allowed us to perform a functional adrenalectomy (ADRX), while continuously monitoring the adrenal medullary secretory function. Under basal conditions, the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine were 0.169 ± 0.074, 0.067 ± 0.023, and 0.011 ± 0.003, respectively. Plasma concentrations (ng/mL) of aortic epinephrine, norepinephrine, and dopamine were 0.132 ± 0.047, 0.268 ± 0.034, and 0.034 ± 0.009. Following insulin injection (0.15 IU/kg, i.v.), the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine increased gradually (p < 0.05), reaching the values of 0.918 ± 0.200, 0.365 ± 0.058, and 0.034 ± 0.007 30 min after insulin administration. Similarly, aortic epinephrine, norepinephrine, and dopamine concentrations (ng/mL) increased significantly (p < 0.05) to 0.702 ± 0.144, 0.526 ± 0.093, and 0.066 ± 0.024. The aortic glucose concentration (mg/dL) was diminished from 81.8 ± 4.1 to 36.9 ± 3.4 (p < 0.01). After taking the blood sample at 30 min following insulin administration, ADRX was immediately performed. Five minutes after the onset of ADRX, the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine increased further to 1.707 ± 0.374 (p < 0.05), 0.668 ± 0.139 (p < 0.05), and 0.052 ± 0.017. By contrast, aortic epinephrine, norepinephrine, and dopamine concentrations rapidly diminished (p < 0.05) to their initial control levels reaching 0.051 ± 0.014, 0.252 ± 0.023, and 0.031 ± 0.005 ng/mL, 5 min after ADRX. The present results indicate that during the early phase of insulin-induced hypoglycemia, circulating norepinephrine in aortic blood significantly increases due, primarily, to the enhanced adrenal norepinephrine output.Key words: insulin, plasma norepinephrine, adrenal catecholamines, functional adrenalectomy, hypoglycemia.

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Portoghese, Philip S. « Could DAA modulate norepinephrine storage function ? » Trends in Pharmacological Sciences 8, n^o 1 (janvier 1987) : 18–19. http://dx.doi.org/10.1016/0165-6147(87)90025-3.

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Inoue, Kazuhide, et James G. Kenimer. « Mechanism of muscarinic receptor-stimulated norepinephrine release ». Japanese Journal of Pharmacology 46 (1988) : 254. http://dx.doi.org/10.1016/s0021-5198(19)57603-x.

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Ubeda, M., F. Fenoy, L. F. Carbonell, F. J. Salazar, J. García-Estañ, M. G. Salom et T. Quesada. « Effect of captopril on norepinephrine vascular contractility ». General Pharmacology : The Vascular System 16, n^o 3 (janvier 1985) : 303–6. http://dx.doi.org/10.1016/0306-3623(85)90091-6.

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Swann, Alan C., Marijn Lijffijt, Scott D. Lane, Blake Cox, Joel L. Steinberg et F. Gerard Moeller. « Norepinephrine and impulsivity : effects of acute yohimbine ». Psychopharmacology 229, n^o 1 (6 avril 2013) : 83–94. http://dx.doi.org/10.1007/s00213-013-3088-7.

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Malootian, A., G. S. Friedrichs et G. F. Merrill. « Flow-dependent antiarrhythmic properties of ammonia during catecholamine-driven ventricular tachycardia ». Canadian Journal of Physiology and Pharmacology 70, n^o 1 (1 janvier 1992) : 94–99. http://dx.doi.org/10.1139/y92-013.

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Fifteen mongrel dogs weighing 22–34 kg were instrumented to investigate the antiarrhythmic effects of ammonia (0.1 – 0.2 mmol/min ammonium hydroxide), adenosine (1.87 μmol/min), and saline (0.9% NaCl) during norepinephrine-driven ventricular tachycardia, under conditions of controlled and natural coronary blood flow. Under natural flow conditions, the severe ectopy caused by norepinephrine (100–800 ng∙kg−1∙min−1) was reduced by 42 ± 4% after 30 s of ammonia infusion. Adenosine infusion reduced percent ectopy by 97 ± 2% at 30 s. Ammonia also significantly increased coronary blood flow by 26 ± 4%, while adenosine increased blood flow by 72 ± 14%. Saline infusion had no significant effect on either the severity of ventricular tachycardia or coronary blood flow. Norepinephrine consistently caused coronary functional hyperemia as previously reported. When coronary blood flow was controlled by a peristaltic pump to match natural coronary blood flow and to prevent norepinephrine-induced coronary functional hyperemia, the antiarrhythmic effects of ammonia were lost while those of adenosine were unaffected. Additionally, increasing coronary blood flow manually during norepinephrine-induced ventricular tachycardia, to a level seen with combined norepinephrine and ammonia under natural flow conditions, appeared to worsen the venticular arrhythmias. We conclude that the antiarrhythmic properties of ammonia against norepinephrine-driven ventricular tachycardia might be dependent on coronary blood flow, while those of adenosine are independent of coronary blood flow.Key words: coronary flow, ammonium hydroxide, cardiac, norepinephrine.

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Engler, Mary B. « Effect of omega-3 fatty acids, docosahexaenoic and eicosapentaenoic, on norepinephrine-induced contractions ». Canadian Journal of Physiology and Pharmacology 70, n^o 5 (1 mai 1992) : 675–79. http://dx.doi.org/10.1139/y92-086.

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The relaxant responses of the rat thoracic aorta to omega-3 fatty acids, docosahexaenoic and eicosapentaenoic, on norepinephrine- and potassium-induced contractions were investigated. Relaxation was enhanced in vessels contracted with norepinephrine. Docosahexaenoic acid at concentrations as low as 1, 3, and 10 μM evoked significant relaxant responses (15, 23, 30%) in norepinephrine-contracted vessels as compared with responses (5, 9, 12%) in potassium-contracted vessels. Results for eicosapentaenoic acid under similar conditions were 3, 8, and 19% in norepinephrine-contracted vessels and 3, 3, and 8% in potassium-contracted vessels. Pretreatment with eicosapentaenoic (10 μM) or docosahexaenoic acids (1–10 μM) decreased the contractile response to physiologic concentrations of norepinephrine. In the presence of calcium-free medium, the omega-3 fatty acids (1–30 μM) significantly abolished sustained norepinephrine contractions but did not reduce the phasic contractions when incubated prior to norepinephrine contraction. Comparatively, the effects of docosahexaenoic acid were greater than eicosapentaenoic acid. These findings suggest that the relaxant effects of the omega-3 fatty acids are specific to the mode of contraction, i.e., α-adrenoceptor stimuli. This effect may be related to intracellular calcium mechanisms, since both fatty acids reversed norepinephrine-induced sustained contractions in the absence of extracellular calcium.Key words: omega-3 polyunsaturated fatty acids, eicosapentaenoic acid, docosahexaenoic acid, vascular responses, fish oils.

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Vatta, M. S., L. G. Bianciotti et B. E. Fernández. « Influence of atrial natriuretic factor on uptake, intracellular distribution, and release of norepinephrine in rat adrenal medulla ». Canadian Journal of Physiology and Pharmacology 71, n^o 3-4 (1 mars 1993) : 195–200. http://dx.doi.org/10.1139/y93-030.

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Several studies have demonstrated that atrial natriuretic factor can bind to adrenal medulla cells. Furthermore, atrial natriuretic factor immunoreactivity has been identified in chromaffin cells. The aim of the present work was to investigate atrial natriuretic factor effects on the uptake, intracellular distribution, and release of norepinephrine in the rat adrenal medulla. Results showed that 100 nM atrial natriuretic factor induced a rapid increase of norepinephrine uptake during the first minute of the incubation period. This increase was maintained for up to 60 min. In addition, only neuronal norepinephrine uptake was increased by the natriuretic factor; non-neuronal norepinephrine uptake was unaltered. Atrial natriuretic factor modified the intracellular distribution of the amine store: the granular fraction of norepinephrine increased, while the cytosolic fraction decreased. On the other hand, different concentrations (10, 50, and 100 nM) of the atrial factor decreased spontaneous [3H]norepinephrine output in a concentration-dependent manner. Furthermore, atrial natriuretic factor (10 nM) also reduced high potassium solution evoked secretion of norepineprhine. These results suggest that atrial natriuretic factor modulates sympathetic activity in the rat adrenal medulla. These effects of atrial natriuretic factor may be related to the catecholamine peripheral mechanism involved in the regulation of arterial blood pressure, smooth muscle tone, metabolic activity, etc.Key words: adrenal medulla, atrial natriuretic factor, intracellular norepinephrine distribution, norepinephrine release, norepineprhine uptake.

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Xue, Rui, Ying Li, Xin-Hua He, Zeng-Liang Jin, Shi-Yong Fan, Ting-Ting Zhang, Nuo-Min Li et al. « Pharmacokinetic profiles contribute to the differences in behavioral pharmacology of 071031B enantiomers as novel serotonin and norepinephrine reuptake inhibitors ». Journal of Psychopharmacology 31, n^o 3 (14 décembre 2016) : 377–86. http://dx.doi.org/10.1177/0269881116681456.

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Our previous study indicated that a chiral compound 071031B was a novel serotonin and noradrenaline reuptake inhibitor with superior antidepressant activity compared to duloxetine. The present study aimed to investigate chiral pharmacology differences of 071031B enantiomers, S-071031B and R-071031B, and disclose mechanisms underlying the behavioral differences based on target profiles and pharmacokinetic profiles. In vivo behavioral tests indicated that S-071031B was more potent than R-071031B in two depression models (the forced swimming test in mice and rats) and two pain models (the acetic acid-induced writhing and formalin tests in mice). In vitro assays revealed that both S-071031B and R-071031B showed high affinity for human serotonin transporters and norepinephrine transporters with equal potency, and showed consistently equipotent inhibitory effects on serotonin and norepinephrine uptake. Pharmacokinetic studies demonstrated that oral availability and hepatic metabolism, rather than pH stability, intestinal transport, and plasma binding, contributed to enantiomers’ behavioral differences. Based on these findings, it is suggested that S-071031B is a more active enantiomer, and the differential pharmacokinetic profiles, but not target affinity, contribute to differences of S-071031B and R-071031B in behavioral pharmacology. Moreover, current PK-PD study may provide positive exploration for chiral antidepressants development.

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Han, Mingming, Fang Kang, Chengwei Yang, Mingyu Zhai, Kesong Zheng, Ting Wang, Ziyou Liu et Juan Li. « A comparative study of serotonin and norepinephrine as adjuncts to improve cutaneous antinociception of mexiletine in response to skin pinpricks in rats ». International Journal of Immunopathology and Pharmacology 35 (janvier 2021) : 205873842110161. http://dx.doi.org/10.1177/20587384211016129.

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As adrenaline, serotonin and norepinephrine are two other vasoconstrictors and both of which have been proved to increase the quality and duration of local anesthetics when added as adjuvants. However, the difference in the improvement of the nociception of local anesthetics between the two adjuvants remains unclear. The purpose of this study was to assess the cutaneous nociception of mexiletine by coadministration with serotonin and norepinephrine. Subcutaneous injection of drugs or combinations includes mexiletine 0.6, 1.8, 6.0 μmol, serotonin 1.6500 μmol, noradrenaline 0.8895 nmol, saline, mexiletine 1.8 and 6.0 μmol, respectively combined with serotonin 0.4125, 0.8250, 1.6500 μmol and noradrenaline 0.0356, 0.1779, 0.8895 nmol, with each injection dose of 0.6 ml. The nociception of mexiletine alone and mexiletine coadministered with serotonin and norepinephrine was assessed after subcutaneous injection. Subcutaneous injections of mexiletine elicited dose-related cutaneous antinociception ( P < 0.05, 0.01, or 0.001). Compared with mexiletine (1.8 μmol), adding norepinephrine (except for lowest dose) and serotonin to mexiletine (1.8 μmol) solutions for skin nociceptive block potentiated and prolonged the action ( P < 0.01 or 0.001). Mexiletine (6.0 μmol) combined with norepinephrine and serotonin extended the duration of cutaneous antinociception when compared with mexiletine (6.0 μmol) alone ( P < 0.05, 0.01, or 0.001). Both serotonin and norepinephrine improve the sensory block and enhances the nociceptive block duration of mexiletine, and serotonin is superior to that of norepinephrine.

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Sofuoglu, Mehmet, et R. Andrew Sewell. « Norepinephrine and stimulant addiction ». Addiction Biology 14, n^o 2 (avril 2009) : 119–29. http://dx.doi.org/10.1111/j.1369-1600.2008.00138.x.

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Kawai, Yasuaki, Shigeaki Kobayashi et Toshio Ohhashi. « Existence of two types of postjunctional α-adrenoceptors in the isolated canine internal carotid artery ». Canadian Journal of Physiology and Pharmacology 66, n^o 5 (1 mai 1988) : 655–59. http://dx.doi.org/10.1139/y88-102.

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The pharmacological characteristics of postjunctional α-adrenoceptors in isolated canine internal carotid arteries were investigated by the use of selective agonists and antagonists for α1 and α2-adrenoceptors. Norepinephrine, phenylephrine, and xylazine caused concentration-dependent contractions in the helical strips. The contraction induced by 10−4 M xylazine was significantly smaller than that produced by 10−4 M norepinephrine or 10−4 M phenylephrine. The contraction induced by 10−4 M phenylephrine was almost the same value as that induced by 10−4 M norepinephrine. Phentolamine (10−8 and 10−7 M) caused a parallel shift to the right of the concentration–response curve to norepinephrine. The contractile responses to low concentrations of norepinephrine were significantly suppressed by pretreatment with an α2-antagonist such as yohimbine (10−9 and 10−8 M) or DG 5128(10−7 and 10−6 M). On the other hand, the responses to higher concentrations of norepinephrine were mainly reduced by low concentrations of an α1-antagonist, prazosin (3 × 10−10 and 3 × 10−9 M). These results suggest that both α1- and α2-adrenoceptors are located on the plasma membrane of smooth muscle cells in canine internal carotid arteries and that the norepinephrine-induced contractions at low and high concentrations are mainly mediated by activation of α2- and α1-adrenoceptors, respectively.

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Van Moffaert, Myriam, et Michel Dierick. « Noradrenaline (Norepinephrine) and Depression ». CNS Drugs 12, n^o 4 (1999) : 293–305. http://dx.doi.org/10.2165/00023210-199912040-00004.

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Haan, Bradley J., Megan L. Cadiz et Allycia M. Natavio. « Efficacy and Safety of Vasopressin as First-Line Treatment of Distributive and Hemorrhagic Shock States ». Annals of Pharmacotherapy 54, n^o 3 (18 octobre 2019) : 213–18. http://dx.doi.org/10.1177/1060028019882035.

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Background: Norepinephrine remains the first-line option to manage patients with circulatory shock. Limited evidence exists evaluating noncatecholamine compounds as first-line monotherapy for managing noncardiogenic shock. Objective: To compare vasopressin monotherapy with norepinephrine monotherapy for reversal of distributive and hemorrhagic shock. Methods: This was a retrospective cohort study including adult patients who were diagnosed with hypovolemic or septic shock, received fluids, and received norepinephrine or vasopressin monotherapy for at least 1 hour. Patients excluded lacked a clear diagnosis, were initiated on 2 or more vasopressors at once, or underwent cardiac surgery. The primary outcome was time to shock reversal. Secondary outcomes included mortality, lengths of stay, and safety end points. A multivariable Cox proportional hazards model was performed incorporating baseline and treatment variables. Results: A total of 85 and 160 patients were treated with vasopressin and norepinephrine, respectively. A decrease in time to shock reversal was observed in the vasopressin group (58.32 hours [95% CI, 50.88-66.00] vs 74.64 hours [95% CI, 60.96-88.32], P = 0.004). Mortality was lower in the vasopressin group (25% vs 41%, P = 0.01), and intensive care unit length of stay was longer (13 days [interquartile range, IQR = 7-19] vs 7 days [IQR = 5-9], P = 0.006). Remaining secondary outcomes were similar. The multivariable analysis revealed no difference in time to shock reversal. Conclusion and Relevance: First-line vasopressin exhibited faster time to distributive shock reversal in the unadjusted analysis but failed to maintain this difference in the multivariable analysis. These findings support safe use of vasopressin as first-line therapy or as an alternative to norepinephrine in distributive shock.

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Siri, Francis M., et Richard M. Smith. « Effects of plasma norepinephrine elevation on the heart's adaptation to chronic aortic constriction in rats ». Canadian Journal of Physiology and Pharmacology 64, n^o 7 (1 juillet 1986) : 934–39. http://dx.doi.org/10.1139/y86-161.

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Chronically elevated plasma norepinephrine has the potential for supporting function of diseased hearts, yet may also initiate harmful biochemical and (or) structural changes in the myocardium. The present study investigated the dosage-related effects of chronic norepinephrine infusion on markers of myocardial damage and then tested the influence of a relatively low norepinephrine infusion rate (0.05 μg∙kg−1∙min−1) on the heart's adaptation to pressure overload in aortic constricted rats. Norepinephrine infusion at 0.50 μg∙kg−1∙min−1 led to significantly increased myocardial hydroxyproline concentration and significant mortality. A rate of 0.25 μg∙kg−1∙min−1 increased myocardial hydroxyproline concentration and mortality in aortic constricted rats but had no such effects on sham-operated rats. The lowest rate tested (0.05 μg∙kg−1∙min−1) significantly increased mean arterial pressure and lung weight of aortic constricted rats, without affecting the degree of left ventricular hypertrophy. This infusion rate and aortic constriction each increased plasma norepinephrine and impaired cardiac performance during rapid preloading, although their combination did not cause further impairment. Thus, it appears that even modest plasma norepinephrine elevation has a negative effect on the heart's adaptation to sustained pressure overload.

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McAllister, Susan F., et John D. Cleary. « Blue Digits : Cyanosis Resulting from Norepinephrine Treatment ». Annals of Pharmacotherapy 39, n^o 2 (février 2005) : 383–84. http://dx.doi.org/10.1345/aph.1e241.

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Quan, Ashley Thompson, et Fanny Li. « Hyperinflation of Vasopressors (Vasopressin, Norepinephrine, Ephedrine, etc) ». Journal of Pharmacy Practice 31, n^o 4 (24 juin 2018) : 399–402. http://dx.doi.org/10.1177/0897190018770062.

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Purpose: Hyperinflation refers to the increasing cost of drugs which occurs due to continued drug shortages and rebranding. Hyperinflation has significant implications in increasing overall healthcare costs with reduced reimbursement, increased patient acuity, and an aging population, but published strategies to reduce costs and minimize waste are limited. Objective: To describe the hyperinflation and cost mitigation strategies of three vasopressor medications, vasopressin, epinephrine, and ephedrine. Conclusion: The steep increase in medications is expected to continue, and mitigation strategies to reduce waste and select the most cost effective therapy to offset the price increase is crucial for healthcare systems.

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Yoshitake, Kiyonobu, Sei Kobayashi, Katsuya Hirano et Hideo Kanaide. « The Ca2+-force relationship during norepinephrine-induced contraction. » Japanese Journal of Pharmacology 55 (1991) : 251. http://dx.doi.org/10.1016/s0021-5198(19)39141-3.

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Ikeda, Tetsurou, Shigeo Kitayama, Katsuya Morita et Toshihiro Dohi. « Regulation of rat norepinephrine transporter in PC12 cells ». Japanese Journal of Pharmacology 82 (2000) : 231. http://dx.doi.org/10.1016/s0021-5198(19)48386-8.

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Rapoport, Robert M., et Anita K. Campbell. « Norepinephrine-induced phosphatidylcholine hydrolysis in intact rat aorta ». European Journal of Pharmacology : Molecular Pharmacology 208, n^o 1 (septembre 1991) : 89–92. http://dx.doi.org/10.1016/0922-4106(91)90057-o.

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Carvalho, Ana Franky, Arith-Ruth S. Reyes, Robert C. Sterling, Ellen Unterwald et Elisabeth J. Van Bockstaele. « Contribution of limbic norepinephrine to cannabinoid-induced aversion ». Psychopharmacology 211, n^o 4 (3 juillet 2010) : 479–91. http://dx.doi.org/10.1007/s00213-010-1923-7.

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Blakely, R. D., L. J. De Felice et H. C. Hartzell. « Molecular physiology of norepinephrine and serotonin transporters. » Journal of Experimental Biology 196, n^o 1 (1 novembre 1994) : 263–81. http://dx.doi.org/10.1242/jeb.196.1.263.

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Cocaine- and antidepressant-sensitive norepinephrine and serotonin transporters (NETs and SERTs) are closely related members of the Na+/Cl- transporter gene family, whose other members include transporters for inhibitory amino acid transmitters, neuromodulators, osmolytes and nutrients. Availability of cloned NET and SERT cDNAs has permitted rapid progress in the definition of cellular sites of gene expression, the generation of transporter-specific antibodies suitable for biosynthetic and localization studies, the examination of structure-function relationships in heterologous expression systems and a biophysical analysis of transporter function. In situ hybridization and immunocytochemical studies indicate a primary expression of NET and SERT genes in brain by noradrenergic and serotonergic neurons, respectively. Both NET and SERT are synthesized as glycoproteins, with multiple glycosylation states apparent for SERT proteins in the brain and periphery. N-glycosylation of NET and SERT appears to be essential for transporter assembly and surface expression, but not for antagonist binding affinity. Homology cloning efforts have revealed novel NET and SERT homologs in nonmammalian species that are of potential value in the delineation of the precise sites for substrate and antagonist recognition, including a Drosophila melanogaster SERT with NET-like pharmacology. Electrophysiological recording of human NETs and SERTs stably expressed in HEK-293 cells reveals that both transporters move charge across the plasma membrane following the addition of substrates; these currents can be blocked by NET-and SERT-selective antagonists as well as by cocaine.

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Doe, S., B. Woods et A. M. Perks. « Effects of norepinephrine on lung liquid production by in vitro lungs from fetal guinea pigs ». Canadian Journal of Physiology and Pharmacology 76, n^o 10-11 (1 octobre 1998) : 967–74. http://dx.doi.org/10.1139/y98-110.

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Lungs from near-term fetal guinea pigs (61 ± 2 days of gestation) were supported in vitro for 3 h; lung liquid production was monitored by a dye dilution method. Untreated control preparations produced fluid at 1.38 ± 0.30 mL·kg-1 body weight·h-1, with no significant change (ANOVA; regression analysis); those given 1.24 × 10-9 or 1.24 × 10-8 M norepinephrine during the middle hour showed no significant change, but those given concentrations between 5.24 × 10-8 and 1.24 × 10-5 M all showed significant reductions or fluid reabsorption (based on 42 fetuses). The responses showed a linear relationship with the log concentration (r = 0.97). They appeared to involve alpha-adrenoreceptors, since responses to 10-7 M norepinephrine were unaffected by 10-6 M propranolol, but those to 10-7 and 1.24 × 10-6 M norepinephrine were abolished by 10-6 and 1.78 × 10-5 M phentolamine, respectively (based on 48 fetuses). Activation was through alpha2-adrenoreceptors, since responses to 10-7 and 10-5 M norepinephrine were abolished by 10-4 M yohimbine, but not by 10-5 M prazosin (based on 60 fetuses). The results show that norepinephrine is able to reduce lung liquid production when at plasma levels present at birth, and that it can produce reabsorption; unlike epinephrine, there was no reduction in responses at high concentrations. This work reintroduces a neglected factor, norepinephrine, into possible controls of lung liquid reabsorption, and opens up the potential for neural controls.Key words: fetus, norepinephrine, adrenoreceptors, lung liquid.

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Lorbar, Mojca, Richard A. Fenton et James G. Dobson, Jr. « ATP as a source of interstitial adenosine in the rat heart ». Canadian Journal of Physiology and Pharmacology 77, n^o 8 (1 septembre 1999) : 579–88. http://dx.doi.org/10.1139/y99-056.

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The contribution of neuronal ATP to interstitial adenosine levels was investigated in isolated perfused rat hearts. Ventricular surface transudates, representing interstitial fluid, were analyzed for norepinephrine, ATP, and adenosine. Exocytotic release of norepinephrine was induced by electrical stimulation of cardiac efferents emanating from the stellate ganglion. Ganglion stimulation increased contractility, interstitial norepinephrine, ATP, and adenosine. Interstitial adenosine was 11- to 27-fold higher than interstitial ATP, suggesting that the released ATP is unlikely the only source of adenosine. In the presence of AOPCP (α,β-methyleneadenosine 5'-diphosphate), an ecto-5'-nucleotidase inhibitor, the ganglion-stimulated increase in interstitial ATP and adenosine reached levels similar to those in the absence of AOPCP, also suggesting that adenosine does not derive from extracellular ATP. The perfusate Ca2+ was raised from 1 to 4 mM to determine the importance of the enhanced contractile function on the levels of norepinephrine, ATP, and adenosine. The results were increases in contractility and interstitial norepinephrine, ATP, and adenosine, which were not suppressed with atenolol, indicating a norepinephrine-independent release of ATP and adenosine. Reserpine treatment and administration of guanethidine depleted the catecholamine stores and diminished the catecholamine release, respectively. However, neither agent altered Ca2+-induced increases in ATP and adenosine. It is concluded that the amount of neuronal-derived ATP is low and most likely does not contribute significantly to interstitial levels of adenosine. Furthermore, elevations in interstitial norepinephrine, ATP, and adenosine are associated with neuronal-independent increases in contractile function.Key words: perfused heart, stellate ganglion, co-transmission, calcium, and contractility.

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PYKE, ROBERT E., et H. SCOTT GREENBERG. « Norepinephrine Challenges in Panic Patients ». Journal of Clinical Psychopharmacology 6, n^o 5 (octobre 1986) : 279???285. http://dx.doi.org/10.1097/00004714-198610000-00004.

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Gladstone, David J., et Sandra E. Black. « Enhancing Recovery after Stroke with Noradrenergic Pharmacotherapy : A New Frontier ? » Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 27, n^o 2 (mai 2000) : 97–105. http://dx.doi.org/10.1017/s0317167100052173.

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ABSTRACT:Despite much progress in stroke prevention and acute intervention, recovery and rehabilitation have traditionally received relatively little scientific attention. There is now increasing interest in the development of stroke recovery drugs and innovative rehabilitation techniques to promote functional recovery after completed stroke. Experimental work over the past two decades indicates that pharmacologic intervention to enhance recovery may be possible in the subacute stage, days to weeks poststroke, after irreversible injury has occurred. This paper discusses the concept of “rehabilitation pharmacology” and reviews the growing literature from animal studies and pilot clinical trials on noradrenergic pharmacotherapy, a new experimental strategy in stroke rehabilitation. Amphetamine, a monoamine agonist that increases brain norepinephrine levels, is the most extensively studied drug shown to promote recovery of function in animal models of focal brain injury. Further research is needed to investigate the mechanisms and clinical efficacy of amphetamine and other novel therapeutic interventions on the recovery process.

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Harley, Carolyn W. « A role for norepinephrine in arousal, emotion and learning ? : Limbic modulation by norepinephrine and the kety hypothesis ». Progress in Neuro-Psychopharmacology and Biological Psychiatry 11, n^o 4 (janvier 1987) : 419–58. http://dx.doi.org/10.1016/0278-5846(87)90015-7.

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Buu, Nguyen T., Johanne Duhaime, Karoly Racz, Otto Kuchel et Gunther Schlager. « L-Dopa metabolism in genetically hypertensive mice : effect of pargyline ». Canadian Journal of Physiology and Pharmacology 65, n^o 12 (1 décembre 1987) : 2390–95. http://dx.doi.org/10.1139/y87-379.

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This study on the role of the sympathetic nervous system in the development of hypertension involves the measurement of dopamine and norepinephrine accumulation in various tissues of the hypertensive and random-bred normotensive strains of mice at basal levels, and following a pargyline–L-dopa treatment. Under such a treatment, designed to suppress the homeostatic action of monoamine oxidase and to better expose the relationship between dopamine and norepinephrine, the brain and heart of the hypertensive mice accumulated more dopamine than the normotensive mice. There was a significantly lower norepinephrine accumulation in the heart of the hypertensive mice in spite of comparable dopamine-β-hydroxylase activity in this tissue between the two strains of mice. Under the pargyline–L-dopa treatment, the brain and heart of the older mice in both hypertensive and normotensive strains accumulated significantly (p < 0.05) more dopamine than those of their younger counterparts, while their norepinephrine accumulation remained unchanged. The results demonstrated different patterns of response of dopamine and norepinephrine in the development of hypertension.

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Lautt, W. Wayne, Leslie K. Lockhart et Dallas J. Legare. « Adenosine modulation of vasoconstrictor responses to stimulation of sympathetic nerves and norepinephrine infusion in the superior mesenteric artery of the cat ». Canadian Journal of Physiology and Pharmacology 66, n^o 7 (1 juillet 1988) : 937–41. http://dx.doi.org/10.1139/y88-152.

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Vasoconstriction induced by sympathetic nerve stimulation and by norepinephrine infusion in the superior mesenteric artery of cats anesthetized with pentobarbital was inhibited by adenosine infusions in a dose-related way. The responses to nerve stimulation were not inhibited to a greater extent than the responses to norepinephrine, thus suggesting no presynaptic modulation of sympathetic nerves supplying the resistance vessels of the feline intestinal vascular bed. Blockade of adenosine receptors using 8-phenyltheophylline did not alter the degree of constriction induced by nerve stimulation or norepinephrine infusion, indicating that in the fasted cat, endogenous adenosine co-released or released subsequent to constriction does not affect the peak vasoconstriction reached. Isoproterenol caused similar degrees of vasodilation as adenosine but did not show significant antagonism of the pooled responses to nerve stimulation or norepinephrine infusion; there was no tendency for the degree of dilation induced by isoproterenol to correlate with the inhibition of constrictor responses. Thus, the effect of adenosine on nerve- and norepinephrine-induced constriction is not secondary to nonspecific vasodilation.

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Gazis, Diana, Genevieve Gonzalez et Milton Mendlowitz. « Adrenergic interactions in uterus and vascular smooth muscle in rats in vivo ». Canadian Journal of Physiology and Pharmacology 67, n^o 12 (1 décembre 1989) : 1586–90. http://dx.doi.org/10.1139/y89-254.

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Simultaneous blood pressure and uterine responses to norepinephrine infusions were recorded in urethane-anesthetized, pentolinium–indomethacin treated rats in natural estrus under conditions in which no blockers or blockers of α1-, α2-, and β-adrenergic receptors or of "reuptake" of norepinephrine were present. The contributions of α1- and α2-adrenergic receptors to the blood pressure response were similar during the initial portion of the response. At later times, however, α1-adrenergic receptors were responsible for the major portion of the response. The tachyphylaxis of the pressor response that occurs during norepinephrine infusion could be prevented by preventing norepinephrine "reuptake" with imipramine. In the uterus, the initial small α-adrenergic contractile response (seen only at the lowest infusion rate) was quickly overwhelmed by a β-adrenergic relaxing component. Administration of the β-adrenergic receptor blocker, propranolol, during norepinephrine infusion caused similar increases in blood pressure in control, yohimbine-, and prazosin-treated rats. Uterine contractions, in contrast, were only significantly elevated during β-adrenergic receptor blockade when yohimbine or imipramine had also been administered.Key words: uterus, vascular smooth muscle, adrenergic receptors, rats.

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