Journal of cardiovascular pharmacology
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J. Cardiovasc. Pharmacol. · Jan 1987
Clinical Trial Controlled Clinical TrialCentral hemodynamic changes of calcium antagonists at rest and during exercise in essential hypertension.
Since the cardinal hemodynamic disorder in essential hypertension is an increased total peripheral resistance, drugs that can lower resistance without reducing blood flow would be particularly useful. The calcium antagonists seem to fulfill this criterion. The purpose of this work was to study the hemodynamic effects at rest and during exercise of three calcium channel blockers, verapamil, nifedipine, and nisoldipine, in patients with mild to moderate essential hypertension. ⋯ In contrast, heart rate was reduced on verapamil treatment, particularly during exercise (about 10% of patients), but this was compensated for by an increase in the stroke volume. The hemodynamic profiles of the three calcium channel blockers were slightly different, especially with respect to the heart rate response. Total peripheral resistance was reduced, acutely as well as chronically, and no depression in cardiac pump function was seen, either at rest or during exercise.
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J. Cardiovasc. Pharmacol. · Mar 1986
Effects of intravenous diltiazem on cardiocirculatory dynamics and cardiac output distribution in conscious spontaneously hypertensive rats.
The effects of the calcium channel blocker, diltiazem hydrochloride (DZ), on conscious, resting spontaneously hypertensive rats (SHR) were evaluated and compared with results from parallel studies on Wistar-Kyoto (WKY) controls. DZ was administered as a continuous, cumulative infusion at rates equal to 0.40, 2.00, and 10.00 mg/kg/h (each dose was administered for 15 min). Parallel volume infusion (saline) controls were simultaneously conducted using volume infusion rates identical to those used in DZ studies (0.015, 0.100, and 0.500 ml/min). ⋯ DZ increased flow and reduced resistance in the coronary and skeletal muscle circulations of SHR to a greater extent than in WKY. DZ also normalized vascular resistance in previously elevated regions. These results suggest that acute intravenous infusion of DZ at doses ranging between 2 and 5 mg/kg is capable of normalizing cardiovascular hemodynamics and regional blood flow distribution in SHR.
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J. Cardiovasc. Pharmacol. · Jan 1986
Respiratory tolerance of bisoprolol and metoprolol in asthmatic patients.
The respiratory tolerance of the beta 1-adrenoceptor-selective blockers bisoprolol and metoprolol was investigated in eight male asthmatic patients. The interaction with the bronchodilatory effect of the beta 2-adrenoceptor-selective agonist terbutaline was studied to compare the beta 1-adrenoceptor selectivity of 10 and 20 mg bisoprolol and 100 mg metoprolol. The three beta-blocker doses caused a significant decrease in heart rate at rest. ⋯ Only 10 mg bisoprolol caused a significant decrease in vital capacity (VC) and forced expiratory volume in 1 s (FEV1). Bronchoconstriction was rapidly reversed by inhalation of terbutaline in all patients. There were no differences between the responses of FEV1, VC, and PEFR to terbutaline with any of the beta-blockers, indicating a good degree of beta 1-adrenoceptor selectivity of 10 and 20 mg bisoprolol and 100 mg metoprolol in humans.
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J. Cardiovasc. Pharmacol. · Sep 1985
Antagonism of vasopressin-induced coronary artery constriction by the vasopressin antagonist d(CH2)5Tyr(Me)-AVP.
d(CH2)5Tyr(Me)-AVP is a potent inhibitor of the systemic vasoconstrictor action of vasopressin (AVP). In order to examine the effectiveness of this agent in blocking AVP-induced coronary vasoconstriction, 11 pentobarbital-anesthetized mongrel dogs were instrumented for the measurement of left circumflex (LCX) coronary blood flow, systemic arterial blood pressure, heart rate, lead II electrocardiogram, left ventricular end-diastolic pressure, left ventricular developed pressure, and left ventricular +/- dP/dt. Direct injection of AVP (0.01-1 microgram) into the LCX produced a dose-dependent decrease in coronary artery blood flow (maximum reduction: 60.5 +/- 8.1% after 1 microgram), - dP/dt (maximum reduction: 41.8 +/- 5.3% after 1 microgram), and +dP/dt (maximum reduction: 14.6 +/- 5.3%), whereas a dose-dependent increase in left ventricular end-diastolic pressure was observed (maximum increase: 62.6 +/- 20.2%). ⋯ Intravenous administration of d(CH2)5Tyr(Me)-AVP reduced (1 microgram/kg) or abolished (5 micrograms/kg) the effects of AVP on coronary blood flow +/-dP/dt and left ventricular end-diastolic pressure. In addition, doses of 1,2, and 5 micrograms/kg of d(CH2)5Tyr(Me)-AVP alone produced increases of LCX blood flow of 5.1 +/- 1.5, 2.0 +/- 0.7, and 6.8 +/- 1.7 ml/min, respectively (p less than 0.05). We conclude that d(CH2)5Tyr(Me)-AVP is effective in preventing the coronary artery constriction and hemodynamic sequelae of intracoronary administered AVP.