The antihypertensive effects of verapamil and propranolol were evaluated in 62 patients with mild to moderate systemic hypertension. We also studied the change of 24 hours urinary catecholamines. 31 cases received verapamil and 31 others were treated by propranolol for 4 weeks. Before treating, there were no statistically significant differences (ECG, echocardiology, blood pressure...) noted between the two groups. Conclusions: 1) Blood pressure and heart rate were controlled by verapamil as well as by propranolol. 2) 24 hours urinary catecholamines were reduced by verapamil but not by propranolol
Hypertension ; Verapamil

The Na+ -K+ -activated ATPase is required to maintain osmotic balance and stabilize cell volume. The Na+ -K+ -ATPase has a more direct role in regulating cell volume; it controls the solute concentrations inside the cell, thereby regulating the osmotic forces that can make a cell swell or shrink. The impotance of the Na+ -K+ -ATPase in controlling cell volume is indicated by the observation that animal cells swell, and may burst, if they are treated with ouabain, which, inhibits the Na+ -K+ -ATPase. The present experiment was designed and carried out to determine the effect of verapamil, a calcium blocker, on the activity of Na+ -K+ -ATPase prepared from renal medulla in the normal rabbit. It was reported that verapamil, a well known coronary vasodilator, possessed negative inotropic effects. The mechanism of action of verapamil was initially thought to be due to coronary vasodilation and blockade of myocardial B-adrenergic receptors. 1t was termed such agent calcium antagonist. A derivative of verapamil, D-600, was subsequently shown to block the movement of calcium through the slow channel and thereby after the plateau phase of the cardiac action potential. Verapamil do not directly antagonize the effects of calcium. Rather, it inhibit the entry of ealcium into cells or its mobilization form intracellular stores and, as such, have been termed a calcium channel blocker.
Action Potentials ; Adenosine Triphosphatases* ; Adenosine* ; Animals ; Calcium ; Calcium Channels ; Cell Size ; Gallopamil ; Ouabain ; Vasodilation ; Verapamil*

No abstract available.
Coronary Vasospasm* ; Heart Arrest* ; Verapamil*

Verapamil is highly effective in terminating paroxysmal supraventricular tachycardia(PSVT) by its depressive action on the AV node. In other countries it is already the drug of choice if vagal manevers fail for conversion of PSVT. We evaluated therapeutic efficacy of intravenous verapamil in 30 patients with PSVT who visited Severance Hospital from november 1978 to November 1984. Twenty six of 30 patients(86.7%) had a restoration of normal sinus rhythm by intravenous verapamil without significant side effects. Thus intravenous verapamil is safe and extremely effective in terminating most PSVT.
Atrioventricular Node ; Humans ; Tachycardia, Supraventricular* ; Verapamil*

No abstract available.
Allopurinol* ; Animals ; Liver* ; Rats* ; Reperfusion Injury* ; Verapamil*

No abstract available.
Animals ; Macrophages, Alveolar* ; Rats* ; Superoxides* ; Verapamil*

BACKGROUND: Among the various physiochemical stimuli, hypoxia has been known to cause coronary vasodilation. In contrast to this, endothelial dependent contracting factor(EDCF) was shown to be secreted by hypoxia and overall physiological roles of these apparently contradicting two phenomena are not clear. Although coronary vasodilation is dominant in epicardial coronary artery by hypoxia, collateral circulation may show different response from epicardial coronary artery to the same stimulus and effect of hypoxia on the vasomotor tone of collateral vessels has not been established. METHODS: Left circumflex coronary artery was chronically occluded using Ameriod occluder in the canine model and myocardial blood flow through collateral circulation was measured using microsphere during induced regional hypoxia. RESULTS: 1) Myocardial blood flow measurements during oxygenated and hypoxic solution infusion were 1.11+/-0.11 mg/min/g and 1.12+/-0.10 ml/min/g respectively in normal perfused zone(LAD territory), but in the collateral dependent zone(LCX territory) blood flow decreased significantly during hypoxic solution infusion(0.55+/-0.17 ml/min/g vs 0.43+/-0.21 ml/min/g)(p<0.05). Also myocardial blood flow ratio(LCX/LAD territory) decreased significantly during hypoxic solution infusion(0.49+/-0.16 vs 0.39+/-0.02)(p<0.05). 2) In collateral dependent zone, endocardial and epicardial blood flow ratio showed significant redistribution during hypoxic solution infusion. 3) After verapamil administration, myocardial blood flow in collateral dependent zone increased from 0.43+/-0.21ml/mg/g to 0.56+/-0.23 ml/mg/g(p<0.05). Also myocardial blood flow ratio(LCX/LAD territory) increased from 0.39+/-0.20 to 0.50+/-0.20 to 0.50+/-0.21 after verapamil administration. CONCLUSION: Hypoxia seems to cause vasoconstriction in collateral vessels and redistribution of blood flow in collateral dependent zone and these effects can be reversed by verapamil.
Anoxia* ; Collateral Circulation* ; Coronary Vessels ; Microspheres ; Oxygen ; Vasoconstriction ; Vasodilation ; Verapamil

BACKGROUND: The stomach can be generally classified anatomically into three parts; fundus, corpus, and antrum. It has not been well demonstrated how the three regions contribute to specified gastric motility. In the present study, the regional differences on contractile response and intracellular Ca2+ levels ([Ca2+]i) were investigated in a mouse gastric muscle. METHODS: An isometrical contraction was measured with a computerized physiograph, and [Ca2+]i was measured with fura-PE3/AM, a fluorescent Ca2+ indicator in gastric smooth muscle from mice. RESULTS: Carbachol (CCh), a potent muscarinic receptor agonist, generated rhythmic contractions in a dose dependent manner, superimposed on tonic components in the antral muscle. Whereas similar contractile responses to CCh was obtained in the antrum, CCh evoked tonic components predominantly. CCh increased [Ca2+]i in a dose dependent manner in both the antral and fundic smooth muscle. However, the increment of [Ca2+]i in the fundus was greater than that of the antrum. Verapamil (10nM), a l-type Ca2+ channel blocker, inhibited completely the contraction and [Ca2+]i induced by CCh in the antral strips, whereas the responses in the fundus showed a resistance to verapamil. CONCLUSIONS: These results suggest that muscarinic stimulation has a regional difference on muscle contractility and [Ca2+]i, which is mediated by differences of Ca2+ movement in mouse gastric muscle.
Animals ; Carbachol ; Mice ; Muscle, Smooth* ; Receptors, Muscarinic ; Stomach ; Verapamil

Isometric tension was recorded in uterine arterial ring preparation contracted by potassium (60 mM) and norepinephrine(1.8 X 10(-7) M). With pretreatment of various concentrations of nifedipine(2.9 x 10(-9) ~2.9 X10(-7) M) and verapamil(2.2 X 10(-7) -2.2 X 10(-5) M), the relaxation was dose-dependent and inhibitory effects of both agents were more marked on the potassium than norepinephrine-evoked contraction. After immersion of the arterial preparation in calcium-free solution, the potassium-evoked contraction was decreased to 21+/-4.1%(mean+/-SEM) of the response in normal Krebs solution and norepinephrine-evoked contraction to 26+/-3.8%. The responses to both agents were completely restored when the calcium concentration was increased to 4.0 mM. Pretreated nifedipine(2.9 x 10(-7) M) in calcium-free solution depressed the potassium-evoked contraction to 7.3+/-1.6% and norepinephrine-evoked contraction to 12+/-3.7%. In addition of calcium(0-4.0mM), the potassium-evoked contraction increased to 30+/-4.6% and that by norepinephrine to 45+/-5.4%. Pretreated verapamil(2.2 X 10(-5) M) in calcium-free solution depressed the potassium-evoked contraction to 14+/-3.6% and norepinephrine-evoked contraction to 18+/-3.3%. In addition of calcium(0-4.0mM), the potassium-evoked contraction increased to 41+/-4.2% and that by norepinephrine to 57+/-4.7%. It was concluded that nifedipine and verapamil relaxed KC1 contracted ring in the presence of external calcium and relaxed norepinephrine contracted ring in both the presence and absence of external calcium. These findings suggest that calcium antagonists interfere with the release of calcium from intracellular sites as well as with the slow inward current of calcium.
Calcium ; Humans* ; Immersion ; Nifedipine* ; Norepinephrine ; Potassium ; Relaxation ; Uterine Artery* ; Verapamil*

The effects of diltiazem and verapamil on the electrically-evoked twitch response, train-of- four and tetanic stimulation were studied in the isolated rat hemidiaphragm preparation. Diltiazem(3-150 pM) and verapamil(3-100 pM) increased the electrically-evoked(nerve stimulation, 0.1 Hz, 0.5 ms, 10 V) twitch responses in a dose-related fashion and diltiazem was more potent than verapamil. But, the large doses of diltiazem(150-300 uM) and verapamil(100-300 uM) decreased the twich responses. And the effects of diltiazem and verapamil were not effected by reducing the extracellular calcium from 2.5 to 1.25 mM. Diltiazem and verapamil decreased the train-of-four and tetanus ratio as well as the d-tubocurarine in a dose-related fashion. d-Tubocurarine, a specific nicotinic antagonist, decreased twitch response, and the potentiating twitch response of diltiazem was significantly inhibited by pretreatment of d-tubocura- rine. Furthermore, it is noteworth that the inhibitory effects of d-tubocurararine were markedly potentiated by diltiazem. In cases of the direct(muscle, 0.1 Hz, 5 ms, 10 V) stimulation, diltiazem and verapamil decreaaed the electrically-evoked twitch response with dose dependently. These results indicate that diltiazem and verapamil elicited two distinctive types of twitch response in the rat phrenic-hemidiaphragm preparation. The potentiating effect of twitch response is mediated by the acetylcholine release from the prejunctional nerve terminal and the inhibiting effect may be due to blcking influx of calcium and/or release of acetylcholine from presynaptic nerve terminals.
Acetylcholine ; Animals ; Calcium ; Diltiazem* ; Rats* ; Tetanus ; Tubocurarine ; Verapamil*