Drugs online research references
Biol Pharm Bull. 1997 Feb;20(2):196-200.
Spasmolytic effect of efonidipine hydrochloride in isolated canine coronary artery: comparison with the effects of nifedipine and nisoldipine.
Jin H, Sato R, Higashino R, Fukuda Y, Kurimoto T, Tamaki H.
Central Research Laboratories, Zeria Pharmaceutical Co., Ltd., Saitama, Japan.
Spasmolytic effects of efonidipine hydrochloride (efonidipine) on high K(+)-, U46619- and 3,4-diaminopyridine (3,4-DAP)-induced contractions were evaluated in isolated canine coronary, artery, and were compared with the effects of nifedipine and nisoldipine. Efonidipine (0.3-30 nM), nifedipine (1-300 nM) and nisoldipine (0.1-100 nM) each relaxed the contractions induced by high K+ and U46619. However, relaxation produced by efonidipine was slower than that produced by nifedipine or nisoldipine. The rank order of potency of these drugs for U46619-induced contraction was efonidipine > or = nisoldipine > nifedipine, whereas in high K(+)-induced contraction, it was nisoldipine > efonidipine > nifedipine. Thus, the relaxing effect of efonidipine on U46619-induced contraction appeared to be more potent than its effect on high K(+)-induced contractions, when compared with the effects of nifedipine and nisoldipine. These three drugs also suppressed 3,4-DAP-induced rhythmic contractions. However, a marked time-dependent increase in potency was only observed for efonidipine, and was similar to its time-dependent effect on high K(+)- and U46619-induced contractions. Efonidipine did not change the contraction cycle length whilst suppressing the peak contractions. On the other hand, lower concentration of nifedipine at 3 nM and nisoldipine at 1 nM significantly shortened the cycle length. These results suggest that efonidipine may be an effective agent for the treatment of angina pectoris. The high potency of efonidipine for U46619-induced contractions will provide some advantages in the clinical use of this compound on thromboxane A2-mediated coronary vasoconstriction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9057986&dopt=Abstract
J Cardiovasc Pharmacol. 1997 May;29(5):624-30.
Inhibitory effects of efonidipine hydrochloride on contraction induced by several vasoconstrictors in porcine coronary artery: comparison with effects of nifedipine and nisoldipine.
Higashino R, Sato R, Jin H, Inoue N, Fukuta Y, Kurimoto T, Tamaki H.
Central Research Laboratories, Zeria Pharmaceutical Co., Ltd., Saitama, Japan.
We studied the effects of efonidipine hydrochloride (efonidipine), a 1,4-dihydropyridine derivative, on contractions induced by high-K+ solution (high K+), serotonin (5-HT), U46619, which is a stable analog of thromboxane A2, and endothelin-1 (ET-1) in comparison with those of nifedipine and nisoldipine in porcine coronary arteries. The effects of the drugs were compared after 1- and 3-h incubations. Efonidipine, nifedipine, and nisoldipine each inhibited the contractions induced by these vasoconstrictors. The inhibition of high-K(+)- and 5-HT-induced contractions by efonidipine, but not by nifedipine and nisoldipine, increased when the incubation time was prolonged, whereas the inhibition of U46619- and ET-1-induced contractions was not altered. The potency of efonidipine on U46619- and ET-1-induced contractions was greater than that of nifedipine and equivalent to that of nisoldipine. Thus the inhibitory effect of efonidipine on U46619- and ET-1-induced contractions seems to be stronger than its effects on high-K(+)- or 5-HT-induced contractions, in contrast to the effects of other dihydropyridines. In an additional series of experiments, efonidipine did not inhibit U46619-induced contractions in Ca2(+)-free solution or in the presence of nifedipine. Moreover, efonidipine did not inhibit the specific binding of [3H]SQ 29,548, a thromboxane A2 antagonist, to porcine coronary arterial membrane. Therefore we think that the inhibitory effect of efonidipine on contractions induced by vasoconstrictors was caused by blockade of Ca2+ influx through L-type Ca2+ channels. However, some unknown mechanism(s) in addition to this effect on Ca2+ channels may contribute to the effect of efonidipine on U46619- and ET-1-induced contractions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9213205&dopt=Abstract
Jpn Heart J. 1978 Nov;19(6):904-12.
Effects of anti-anginal agents on cyclical reductions of coronary blood flow.
Uchida Y, Yoshimoto N, Murao S.
The effects of coronary vasodilating agents and alpha- and beta-adrenergic blocking agents on cyclical reductions of blood flow in the partially constricted coronary artery of anesthetized dogs were examined. Intravenous injections of nitroglycerin (50 microgram/Kg), SG 75 (150 microgram/Kg), papaverine (1 mg/Kg), and nicotinic acid (10 mg/Kg) eliminated both cyclical reductions of flow and ST elevation (group 1). Nifedipine (10 microgram/Kg), verapamil (500 microgram/Kg), diltiazem (500 microgram/Kg), and propranolol (500 microgram/Kg) suppressed ST elevation, but they could not eliminate cyclical reductions of flow (group 2). Dipyridamole (1 mg/Kg) and phenotolamine (500 microgram/Kg) augmented both ST elevation and cyclical reductions of flow (group 3). The results indicate that ST elevation due to cyclical reductions of coronary blood flow was eliminated by spasmolytic actions of group 1 on coronary artery, was suppressed by negative chronotropic and/or inotropic actions of group 2, and was augmented by peripheral actions of group 3.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=35631&dopt=Abstract
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