Drugs online research references
Eur J Pharmacol. 1989 Nov 21;171(2-3):219-28.
Renal hemodynamic responses to 5-hydroxytryptamine (5-HT): involvement of the 5-HT receptor subtypes in the canine kidney.
Shoji T, Tamaki T, Fukui K, Iwao H, Abe Y.
Department of Pharmacology, Kagawa Medical School, Japan.
The study was designed to define the serotonin (5-HT) receptor subtypes in the canine kidney. An intrarenal infusion of 5-HT at a dose of 5 micrograms/min in anesthetized dogs resulted in a biphasic response of renal blood flow which decreased transiently then increased above the control level during prolonged infusion. The decrease of renal blood flow was abolished by infusion of methysergide but not by ketanserin, and the subsequent increase was abolished by infusion of either ketanserin or methysergide. Terazosin, an alpha1-adrenoceptor antagonist, did not modify the renal action of 5-HT. These findings suggest that the renal blood flow response induced by 5-HT did not depend on an indirect effect via the sympathetic nervous system, the initial vasoconstriction was mediated via a 5-HT1-like receptor, and that the latter vasodilatation was mediated via a 5-HT2 receptor. The infusion of 5-HT also increased urine flow and urinary excretion of sodium. These increases were reversed by pretreatment with ketanserin and abolished by methysergide. We propose that 5-HT may exert its antidiuretic action via a 5-HT1-like receptor in the tubules but that the renal hemodynamic changes induced by 5-HT may overcome its antidiuretic action. The present results suggest the existence of a 5-HT1-like and 5-HT2 receptor in the renal vasculature and a 5-HT1-like receptor in the renal tubules.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2576001&dopt=Abstract
J Pharmacol Exp Ther. 1985 Apr;233(1):87-93.
Comparison of the cardiovascular actions of dopamine and epinine in the dog.
Itoh H, Kohli JD, Rajfer SI, Goldberg LI.
The effects of i.v. infusions of 3 and 6 micrograms/kg/min of dopamine (DA) and epinine on heart rate, arterial blood pressure, regional blood flows and vascular resistances in the renal, mesenteric and femoral vascular beds were compared in pentobarbital-anesthetized dogs. At the 3 micrograms/kg/min infusion rate, neither DA nor epinine changed blood pressure, whereas at the higher infusion rate both increased blood pressure by about 20 mm Hg. DA increased renal blood flow significantly at both infusion rates; whereas, epinine did not change renal blood flow. After administration of phenoxybenzamine, both epinine and DA decreased blood pressure; upon adding propranolol, the vasodepressor effect of epinine, but not of DA, was abolished. However, propranolol did not inhibit epinine-mediated vasodilation in the renal or mesenteric vascular beds, but a marked increase in femoral vascular resistance was observed. The addition of (R)-sulpiride, a DA antagonist, abolished DA and epinine-induced vasodilation in the mesenteric and renal vascular beds. Experiments in animals treated with hexamethonium to block ganglion transmission and propranolol to block beta adrenoceptors revealed that both selective alpha-1 (terazosin) and alpha-2 (rauwolscine) adrenoceptor antagonists inhibited the vasopressor response to DA to a greater degree than the responses to epinine. Thus, although DA and epinine possess significant DA1 activity, the consistent increase in renal blood flow observed with DA is not seen with epinine because of the more potent alpha adrenoceptor activity of the latter, which is mediated by both alpha-1 and alpha-2 adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2858584&dopt=Abstract
Hypertension. 1986 May;8(5):407-14.
Alpha 1-adrenergic blockade and cardiovascular pressor responses in essential hypertension.
Beretta-Piccoli C, Ferrier C, Weidmann P.
The effects of selective alpha 1-adrenergic blockade with terazosin on blood pressure and cardiovascular pressor responsiveness were assessed in 17 subjects with mild to moderate essential hypertension (mean age, 48 +/- 2 [SEM] years). As compared with a 2-week placebo period, 8 weeks of terazosin treatment (mean dose, 10.5 +/- 1.7 mg/day) caused a fall of supine (from 153/103 +/- 3/2 to 143/96 +/- 4/2 mm Hg; p less than 0.025) and upright (from 145/106 +/- 4/2 to 131/94 +/- 5/3 mm Hg; p less than 0.01) arterial pressure; a marked blunting of cardiovascular pressor responsiveness to norepinephrine, as judged from the pressor dose (from 73 +/- 9 to 2156 +/- 496 ng/kg/min; p less than 0.02) and from the rightward shift (p less than 0.01) of the plasma concentration-blood pressure response curve; and a slight increase in plasma norepinephrine concentration (from 37.7 +/- 3.3 to 52.2 +/- 7.8 ng/dl; p less than 0.01). Heart rate, body weight, exchangeable sodium, blood volume, and norepinephrine plasma clearance; plasma epinephrine, renin, angiotensin II, and aldosterone levels; the relationships between angiotensin II-induced increases in arterial pressure or plasma aldosterone and the concomitant increments of plasma angiotensin II; and heart rate responsiveness to isoproterenol did not change significantly after terazosin treatment. These findings suggest that the fall of arterial pressure induced by selective alpha 1-adrenergic blockade in subjects with essential hypertension is associated with, and probably explained by, inhibition of alpha 1-mediated, noradrenergic-dependent vasoconstriction. alpha 1-Adrenergic receptor antagonism did not modify body sodium concentration, the adrenomedullary component of the sympathetic nervous system, angiotensin II levels, or beta-adrenergic dependent mechanisms.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2870984&dopt=Abstract
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