Interactions of H Ions, Ca-Antagonistic Drugs and Cardiac Glycosides with Excitation-Contraction Coupling of Vascular Smooth Muscle

Fleckenstein, A.; Nakayama, Kouji; Fleckenstein-Grün, G.; Byon, Y. K.

doi:10.1007/978-3-642-66427-4_24

Cited by 51 publications

(27 citation statements)

References 4 publications

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“…It has been sug gested that in islets of Langerhans, verapamil inhibits the glucose-induced insulin secretion by interfering with the transmembrane influx of calcium ion (26 , 33). As shown in the present experiments, among the calcium-antagonists tested, nifedipine (11,27,28) produced the most potent inhibitory effect on insulin secretion, while the effect of verapamil was similar to, or somewhat more potent than that of diltiazem.…”

Section: Discussionsupporting

confidence: 69%

Effect of Diltiazem on Insulin Secretion I. Experiments in Vitro

Yamaguchi

Akimoto

Nakajima

et al. 1977

Japanese Journal of Pharmacology

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Section: Discussionsupporting

confidence: 69%

Effect of Diltiazem on Insulin Secretion I. Experiments in Vitro

Yamaguchi

Akimoto

Nakajima

et al. 1977

Japanese Journal of Pharmacology

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“…[5][6][7] Although the precise mechanism whereby hyperventilation induces coronary spasm is still unclear, alkalosis caused by hyperventilation may increase intracellular calcium ion, which results in contraction of the coronary vascular smooth muscle. 5,8,9 The role of magnesium in cardiac disease was recently reviewed.10-13 Experimental studies in vitro have shown that depletion of magnesium from the superfusate medium potentiates contractile responses of small and large coronary arteries to various stimuli.14 Magnesium also may be a physiologic calcium antagonist and thus may prevent the contraction of the vascular smooth muscle. [13][14][15]ever, to date, no clinical study concerning the effect of magnesium on coronary spasm has been performed.…”

Section: Effect Of Magnesium On Anginal Attack Induced By Hyperventilmentioning

confidence: 99%

Effect of magnesium on anginal attack induced by hyperventilation in patients with variant angina.

et al. 1989

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To examine whether or not magnesium suppresses coronary spasm, the effect of magnesium infusion on anginal attacks induced by hyperventilation was studied in 20 patients with variant angina. In all patients, anginal attacks associated with ischemic ST segment changes on the electrocardiogram were repeatedly induced by hyperventilation. The study was performed in the early morning successively for 3 days. On days 1 and 3 (control studies), 50 minutes before the hyperventilation test, a 5% glucose solution was infused as a placebo. On day 2 (magnesium study), 50 minutes before the hyperventilation test, magnesium sulfate (0.27 mM/kg body wt) was infused during a 20-minute period. During the control studies, anginal attack was induced by hyperventilation in all 20 patients, whereas during the magnesium study, anginal attack was induced by hyperventilation in only six (30%) of the 20 patients (p < 0.001 vs. control studies). The changes in arterial blood pH and Pco2 caused by hyperventilation were not significant between the control study and the magnesium study. Mean serum magnesium concentration increased from 2.2+0.2 to 6.0±0.5 mg/dl immediately after infusing magnesium and was 4.5+0.6 mg/dl before the hyperventilation test during the magnesium study. We conclude that magnesium suppresses anginal attacks induced by hyperventilation in patients with variant angina. (Circulation 1989;79:597-602) P revious studies have shown that variant angina is caused by spasm of a large coronary artery,1-4 and hyperventilation has been used to induce coronary spasm in patients with variant angina.5-7 Although the precise mechanism whereby hyperventilation induces coronary spasm is still unclear, alkalosis caused by hyperventilation may increase intracellular calcium ion, which results in contraction of the coronary vascular smooth muscle.5,8,9The role of magnesium in cardiac disease was recently reviewed.10-13 Experimental studies in vitro have shown that depletion of magnesium from the superfusate medium potentiates contractile responses of small and large coronary arteries to various stimuli.14 Magnesium also may be a physiologic calcium antagonist and thus may prevent the contraction of the vascular smooth muscle.

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“…In contrast to dipyridamole, a coronary vaso dilator, verapamil reduces the contractile force of the mammalian myocardium (2), and the mechanism of the action underlying the negative inotropic and vasodilator actions has been generally attributed to a calcium-antagonistic inhibition of the excitation-contraction coupling in the cardiac muscle and vascular smooth muscle fibers (3,4). A recently-developed coronary vasodilator, nifedipine also exerts a negative inotropic effect on the mammalian myocardium (5,6,7) and its mechanism of action has also been ascribed to the calcium antagonism (4, 7).…”

mentioning

confidence: 99%

Simultaneous Assessment of Effects of Coronary Vasodilators on the Coronary Blood Flow and the Myocardial Contractility by Using the Blood-Perfused Canine Papillary Muscle

Himori

Ono

Taira

1976

Japanese Journal of Pharmacology

113

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Abstract-Effects of 6 coronary vasodilators on the coronary blood flow and the con tractile force of the ventricular muscle were examined simultaneously by injecting these drugs to the arterially blood-perfused canine papillary muscle preparation.All com pounds produced a dose-dependent increase in blood flow rate, and relative potencies determined on the basis of doses producing a 100 increase in blood flow rate, ED100, were in the descending order : nifedipine---verapamil---diltiazem; dilazep--,dipyrida mole>carbochromen, and approximately I : 1 12 : 1;'26 : 1 100: 1/300 : 1;'500. All drugs except for dipyridamole caused a dose-dependent decrease in the developed tension of the papillary muscle, although nifedipine and diltiazem in low doses produced a slight increase. Relative potencies determined on the basis of doses producing a 50°0 decrease in developed tension, ID50, were as follows : nifedinine (1), verapanil (1/13), diltiazem (1/40), dilazep (1 100), and carbochromen (1,'270). Ratios of the 1D50 to ED100 were as follows : diltiazem (5.2), nifedipine (3.5), verapamil (3.5), dilazep (2.5), and carbochromen (1.8). The higher the value the more predominant on the coronary vascular bed or the less depressant on the myocardial contractility were their actions.A coronary vasodilator, dipyridamole has no cardiodepressant action, but does increase the venous return and the cardiac output in the dog (1). This suggests that dipyridamole may have rather a cardiostimulant action. In contrast to dipyridamole, a coronary vaso dilator, verapamil reduces the contractile force of the mammalian myocardium (2), and the mechanism of the action underlying the negative inotropic and vasodilator actions has been generally attributed to a calcium-antagonistic inhibition of the excitation-contraction coupling in the cardiac muscle and vascular smooth muscle fibers (3, 4). A recently-developed coronary vasodilator, nifedipine also exerts a negative inotropic effect on the mammalian myocardium (5, 6, 7) and its mechanism of action has also been ascribed to the calcium antagonism (4, 7).The negative isotropic action of these calcium-antagonistic vasodilators is considered to be favorable for the treatment of ischemic heart disease as the reduction in the myocardial contractile force leads to the decreased myocardial oxygen consumption (4). However, an excess of the negative inotropic action is one of the untoward effects as it produces the congestive heart failure. Thus, it is of value to obtain precise information about the potency producing coronary vasodilation and that affecting the myocardial contractility in each coronary vasodilator.Investigators studying the effects of coronary vasodilators on the coronary circulation

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Interactions of H Ions, Ca-Antagonistic Drugs and Cardiac Glycosides with Excitation-Contraction Coupling of Vascular Smooth Muscle

Cited by 51 publications

References 4 publications

Effect of Diltiazem on Insulin Secretion I. Experiments in Vitro

Effect of Diltiazem on Insulin Secretion I. Experiments in Vitro

Effect of magnesium on anginal attack induced by hyperventilation in patients with variant angina.

Simultaneous Assessment of Effects of Coronary Vasodilators on the Coronary Blood Flow and the Myocardial Contractility by Using the Blood-Perfused Canine Papillary Muscle

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