Drugs online research references
Fundam Clin Pharmacol. 1994;8(6):546-52.
Effects of oxodipine and elgodipine on (+)-[3H]-isradipine binding to cardiac and vascular membranes: cardiovascular selectivity.
Rakotoarisoa L, Lepretre N, Mironneau J, Galiano A, Mironneau C.
Laboratoire de Physiologie Cellulaire et Pharmacologie Moleculaire, URA CNRS 1489, Universite de Bordeaux II, France.
We studied the effects of six dihydropyridines on the specific binding of (+)-[3H]-isradipine to vascular (portal vein) and cardiac isolated membranes to achieve the relative cardiovascular selectivity of these compounds. Elgodipine, (+)-oxodipine and nifedipine had a significantly higher affinity for the vascular L-type calcium channel than for the cardiac calcium channel while nicardipine showed opposite properties. The other dihydropyridines (nitrendipine and (+)-isradipine) had similar affinities for the cardiac and vascular calcium channels. As the membrane potential of isolated membranes is about 0 mV, these results suggest that the differences in binding of these dihydropyridines to L-type calcium channels in vascular and cardiac cells may be attributed to differences in the molecular structure of these calcium channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7721232&dopt=Abstract
Eur J Pharmacol. 1997 Sep 24;335(2-3):193-8.
Cardiovascular effects of elgodipine and nifedipine compared in anaesthetized rats.
Valdivielso JM, Macias JF, Lopez-Novoa JM.
Instituto Reina Sofia de Investigacion Nefrologica, Departamento de Fisiologia y Farmacologia, Facultad de Medicina, Universidad de Salamanca, Spain.
The cardiovascular effects of elgodipine were studied and compared with those of nifedipine in the presence or absence of ganglion blockade. A bolus of elgodipine (5-25 microg/kg) or nifedipine (60-120 microg/kg) was given and sequential cardiovascular effects in rats were recorded. Both dihydropyridines induced a dose-dependent decrease in mean arterial pressure but, whereas nifedipine induced reflex tachycardia, elgodipine induced a dose-dependent bradycardia. Both substances induced decreases in left ventricular d P/dt(max) without significant changes in central venous pressure. Good linear correlation was observed between the elgodipine-induced decrease in mean arterial pressure and those of heart rate and left ventricular dP/dt(max). The profile of the decrease in mean arterial pressure in animals pretreated with hexametonium chloride (20 mg/kg) was the same but the nifedipine-induced tachycardia was abolished without changes in elgodipine-induced bradycardia. These characteristics of elgodipine makes this dihydropyridine a potentially beneficial therapeutic agent in the case of severe hypertension accompanied by obstructive coronopathy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9369373&dopt=Abstract
Hypertension. 1995 Dec;26(6 Pt 2):1035-40.
Prostacyclin synthesis elicited by endothelin-1 in rat aorta is mediated by an ETA receptor via influx of calcium and is independent of protein kinase C.
Wright HM, Malik KU.
Department of Pharmacology, College of Medicine, University of Tennessee, Memphis 38163, USA.
The purpose of this study was to characterize the receptor(s) and second messenger systems involved in prostacyclin (prostaglandin [PG] I2) synthesis elicited by endothelin (ET)-1 in the rat aorta. PGI2 synthesis, measured as immunoreactive 6-keto-PGF1 alpha, was assessed in aortic rings exposed to endothelin receptor agonists in the presence and absence of selective ETA and ETB receptor antagonists. ET-1, which has equal affinity for both endothelin receptor subtypes, and ET-3, a preferential ETB receptor agonist, enhanced 6-keto-PGF1 alpha synthesis in a time- and concentration-dependent manner. ET-1 was more potent than ET-3 in increasing 6-keto-PGF1 alpha synthesis. Moreover, the selective ETB receptor agonists IRL-1620 and sarafotoxin S6c did not significantly increase 6-keto-PGF1 alpha synthesis. Furthermore, ET-1-induced 6-keto-PGF1 alpha synthesis was attenuated by an ETA receptor antagonist, BQ-123, in a dose-dependent manner but not by an ETB receptor antagonist, BQ-788. Depletion of extracellular Ca2+ or addition of Ca2+ channel blockers (nifedipine, verapamil, SK&F 96365) attenuated ET-1-mediated 6-keto-PGF1 alpha synthesis, while a Ca2+ channel agonist, S(-)-Bay K 8644, potentiated this effect of ET-1. Selective protein kinase C inhibitors (bisindolylmaleimide I, calphostin C) did not alter ET-1-induced 6-keto-PGF1 alpha synthesis. These data suggest that PGI2 synthesis elicited by ET-1 in the rat aorta is mediated primarily through influx of extracellular Ca2+ via activation of an ETA receptor and is independent of protein kinase C.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7498963&dopt=Abstract
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