Drugs online research references
Br J Pharmacol. 1990 Aug;100(4):669-76.
Mechanisms of long-lasting effects of benidipine on Ca current in guinea-pig ventricular cells.
Yamamoto M, Gotoh Y, Imaizumi Y, Watanabe M.
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
1. Benidipine (KW-3049), a new derivative of 1,4-dihydropyridine (DHP), showed dose-dependent inhibition of Ca current (ICa) which was elicited by depolarization from -40 mV to +10 mV at 0.2 Hz in single cardiac cells isolated from guinea-pig ventricle under whole cell voltage clamp. Half inhibition doses (IC50) of benidipine and nifedipine for the peak ICa at +10 mV were 2.7 nM and 63.1 nM, respectively. 2. A change in holding potential from -40 to -75 mV partially removed the block induced by both 10 nM benidipine and 100 nM nifedipine. The block of ICa by benidipine strongly depended upon holding potentials as did that induced by nifedipine. 3. The effect of 100 nM nifedipine was mostly removed when the cells were kept quiescent at holding potentials negative to -75 mV for 5 min after withdrawal of nifedipine. In contrast, hyperpolarization for several minutes did not significantly accelerate the removal of benidipine-induced block after withdrawal of the drug. Effects of 10 nM benidipine could not be washed out for up to 30 min regardless of the holding potentials. 4. It is suggested that the dissociation of benidipine from the DHP binding site, like that of nifedipine, is greatly accelerated by hyperpolarization. Benidipine but not nifedipine may have an additional interaction with the channel or lipid membrane and cannot be washed away even after the dissociation. Alternatively, the dissociation of benidipine from the DHP binding site may be too slow to occur substantially during the limited period of hyperpolarization in the present study (less than 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2169935&dopt=Abstract
J Cardiovasc Pharmacol. 1985 Nov-Dec;7(6):1127-33.
Nifedipine and nimodipine: effect on blood pressure and regional cerebral blood flow in conscious normotensive and hypertensive rats.
Grabowski M, Johansson BB.
The dose-dependent reduction of mean arterial pressure (MAP) in conscious spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) was more pronounced after intravenous nimodipine than nifedipine administration. Nimodipine (5 micrograms/kg) followed by infusion of 0.75 microgram/kg/min lowered the blood pressure by 10% in both normotensive and hypertensive rats; the same dose schedule of nifedipine did not lower MAP. Neither drug altered the regional cerebral blood flow (rCBF) in this dose. After 50 micrograms/kg nimodipine were administered, followed by 7.5 micrograms/kg/min nimodipine, MAP dropped 38% in WKY and 46% SHR; corresponding figures for nifedipine were 13 and 17%. In spite of the reduction in MAP and a concomitant decrease in PaCO2, rCBF increased significantly in 19 of 23 regions studied after nifedipine and in 15 regions after nimodipine in SHR. The increase in rCBF in WKY was slight and insignificant in most areas. Thus, both calcium entry blockers reduced the cerebrovascular resistance more in SHR than in WKY.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2418299&dopt=Abstract
Eur J Clin Pharmacol. 1989;37(5):443-7.
Comparison of haemodynamic effects of nifedipine and molsidomine in patients with coronary artery disease.
Kyriakidis M, Vyssoulis G, Sfikakis P, Kyriakidis C, Pitsavos C, Valsamis K, Nomikos V, Toutouzas P.
Hippokration Hospital, University of Athens, Greece.
The haemodynamic effects of oral nifedipine 20 mg and molsidomine 4 mg were compared in 24 patients with coronary artery disease. Molsidomine unlike nifedipine caused a significant fall in mean pulmonary artery pressure and left ventricular end-diastolic pressure. Both drugs caused a significant and comparable reduction in systolic and diastolic blood pressure. Although only nifedipine significantly reduced systemic vascular resistance the difference between the drugs was not significant. The heart rate was significantly increased by nifedipine but not by molsidomine. The ejection phase indices were all increased by molsidomine and the increment in the mean normalized systolic ejection rate was significantly greater than that due to nifedipine. The left ventricular end-systolic volume index decreased significantly after molsidomine but not nifedipine. Neither drug significantly affected left ventricular end diastolic volume index, stroke volume index, maximal rate of rise of left ventricular pressure or left ventricular stroke work index.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2598982&dopt=Abstract
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