Vasodilator Drugs in the Treatment of Hypertension

Koch‐Weser, Jan

doi:10.1001/archinte.1974.00320180135012

Cited by 242 publications

(58 citation statements)

References 93 publications

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“…We found that timolol and propranolol caused a similar decrease in cardiac index (20% decrease for each drug). The reduction in cardiac index is a major factor contributing to the antihypertensive action of propranolol'-4 9, 22 and timolol. The significant decrease in cardiac index in both groups of patients reflected the significant decrease in heart rate as neither timolol nor propranolol caused a significant change in stroke index.…”

Section: Discussionmentioning

confidence: 99%

Effect of timolol versus propranolol on hypertension and hemodynamics.

Aronow¹,

Ferlinz²,

Vicario³

et al. 1976

Circulation

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SUMMARY The effect of timolol versus propranolol on hypertension, hemodynamics, and plasma renin activity was evaluated in 20 men. After two weeks of placebo, 11 men received timolol 30 to 60 mg daily, and nine men received propranolol, 240 to 480 mg daily, for five weeks in a double-blind randomized study. The 20 men then received placebo again for two weeks. Right heart catheterization was performed in all 20 patients after two weeks of the first placebo and after five weeks of timolol or propranolol. Equipotent doses of timolol and PROPRANOLOL has been found to be effective as an antihypertensive agent as a single drug and especially in combination with other drugs such as diuretics or vasodilators."'18 Timolol is a new beta-adrenergic blocking drug with no membrane stabilizing effect and with no intrinsic sympathomimetic activity which has also been found effective as an antihypertensive agent.8 10, 13,19 Franciosa and associates8 reported that equipotent doses of propranolol and timolol which caused a similar degree of inhibition of amyl nitrite induced tachycardia had similar effects on lowering blood pressure and heart rate. However, after five weeks of treatment, the mean cardiac output rose slightly in six patients receiving timolol, whereas the mean cardiac output decreased significantly in 11 patients receiving propranolol. Franciosa and Freis'7 also reported in another study that timolol administered for five weeks to 11 patients caused a significant decrease in mean supine systolic and diastolic blood pressure, a significant decrease in mean heart rate, and no significant change in cardiac output.Therefore, we performed a double-blind randomized study to evaluate the effect of timolol versus propranolol on blood pressure, heart rate, stroke index, cardiac index, systemic vascular resistance, and other hemodynamic variables. This paper presents the data in the 20 patients who completed this study. Materials and MethodsTwenty patients with diastolic hypertension were to complete this study. Twenty-three men received either timolol or propranolol. The mean age of the 20 men who completed this study was 52.7 ± 10.8 years. None of the patients had coronary heart disease, valvular heart disease, a history of cerebrovascular disease, a history of congestive heart failure, poor myocardial contractility, sinus bradycardia, bundle branch block, atrioventricular block, chronic obstructive lung disease, a history of bronchial asthma, allergic rhinitis, or peripheral vascular disease. Informed consent was obtained from all participants.propranolol were equally effective in significantly lowering supine and upright systolic and diastolic blood pressure and heart rate recorded on an outpatient basis. Equipotent doses of timolol and propranolol caused similar hemodynamic effects including similar significant depression of cardiac index. Equipotent doses of timolol and propranolol caused similar marked depression of plasma renin activity. The hypotensive action of timolol and of propranolol was unrelated to their ef...

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Section: Discussionmentioning

confidence: 99%

Effect of timolol versus propranolol on hypertension and hemodynamics.

Aronow¹,

Ferlinz²,

Vicario³

et al. 1976

Circulation

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“…A logical approach to therapy would use drugs that reduce this increased resistance, although it is still not known if this has a favourable effect on the prognosis. Some vasodilators tend to cause reflex tachycardia, salt and water retention, tachyphylaxis, and postural hypotension (Koch-Weser, 1974).…”

Section: Introductionmentioning

confidence: 99%

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Asplund¹

1985

Brit J Clinical Pharma

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Fifty patients with mild essential (primary) hypertension entered a double‐blind, parallel‐group study with either nicardipine 30 mg three times daily or placebo, randomly assigned as monotherapy for 6 weeks. At the end of 6 weeks, the nicardipine‐treated group had a statistically significant reduction in mean supine systolic/diastolic pressure of 21.2/15.0 mm Hg (P less than 0.001) compared with the nonsignificant reduction of 0.7/2.9 mm Hg in the placebo‐treated group. The difference in mean response between the nicardipine‐ and placebo‐ treated groups was significant (P less than 0.001). In the nicardipine‐ treated group, the reduction in mean standing systolic/diastolic blood pressure, 17.9/13.8 mm Hg, was significant (P less than 0.001), whereas in the placebo‐treated group the change was +3.0/‐1.5 mm Hg. The difference between the two treatment groups was significant (P less than 0.001). In both treatment groups, changes in pulse rate were minor, and there was no evidence of tachyphylaxis occurring with nicardipine. Adverse experiences were minor in all cases except for one patient with muscle pain during treatment with nicardipine. Patients who received nicardipine showed a mean increase of 52% in plasma renin activity (PRA) after 6 weeks (P less than 0.01). Initial basal or stimulated PRA did not correlate with blood pressure reduction on nicardipine. Nicardipine 30 mg three times daily is a well‐tolerated and effective antihypertensive agent.

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“…42 The blood pressure-lowering effect of verapamil has been attributed to relaxation of vascular smooth muscle.43 " Such vasodilation, however, activates compensatory mechanisms in order to maintain pressure level.45 Thus, calcium-entry blockers (nifedipine, nitrendipine) when given over the short term are prone to provoke reflexive cardiac stimulation. 45 We found that intravenous verapamil also caused reflex tachycardia. This effect is most likely secondary to decreased baroreceptor-mediated vagal activity and/or augmented sympathetic activity.41 48 49 The net activation of the sympathetic-adrenergic system led to a rise in plasma epinephrine and norepinephrine levels, as well as to peripheral venoconstriction, as indicated by centripetal redistribution of the intravascular volume.…”

Section: Discussionmentioning

confidence: 73%

Cardiovascular effects of verapamil in patients with essential hypertension.

Schmieder¹,

Messerli²,

Garavaglia³

et al. 1987

Circulation

113

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The cardiovascular effects of intravenous verapamil and 3 months of oral administration of a slow-release form of verapamil (verapamil-SR) were studied in 10 patients with mild-tomoderate essential hypertension. Intravenous verapamil reduced arterial pressure by 15% (p < .01) through a fall in total peripheral resistance of 29% (p < .01); provoked a reflexive rise in heart rate (by 19%, p < .02), cardiac output (by 74%, p < .01), and plasma catecholamines; and shifted intravascular volume toward the cardiopulmonary circulation indicating peripheral venoconstriction. Quite in contrast to the immediate effects of the intravenous drug, oral therapy with verapamil-SR for 2 to 3 months lowered arterial pressure effectively (by 15%, p < .01) by inducing vasodilation of 15% (p < .02), but without causing reflex tachycardia, activation of the sympathetic-adrenergic or renin-angiotensin systems, or volume expansion. Oral therapy with verapamil-SR preserved systemic and renal blood flow and slightly reduced cardiac mass (by 6%, p < .05) and renal vascular resistance (by 25%, p < .05). Whereas intravenous verapamil tended to depress myocardial contractility, oral verapamil-SR did not at all affect myocardial contractility or left ventricular function. These cardiovascular effects make verapamil-SR an excellent agent for long-term antihypertensive therapy.

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Vasodilator Drugs in the Treatment of Hypertension

Cited by 242 publications

References 93 publications

Effect of timolol versus propranolol on hypertension and hemodynamics.

Effect of timolol versus propranolol on hypertension and hemodynamics.

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Cardiovascular effects of verapamil in patients with essential hypertension.

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