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Cardiovascular effects of verapamil in essential hypertension
P Städler1, L Leonardi, W Riesen
1Ospedale Italiano, Viganello, Switzerland.
Insights
Verapamil, a calcium antagonist, effectively lowers blood pressure in hypertensive patients. It reduces cardiovascular responsiveness to norepinephrine without altering sodium balance, hormonal activity, or lipid profiles.
Area of Science:
- Cardiovascular Pharmacology
- Hypertension Management
Background:
- Calcium antagonists are known to influence sodium regulation and adrenergic mechanisms.
- Essential hypertension involves complex interactions of sodium balance, the sympathetic nervous system, and the renin-angiotensin-aldosterone axis.
Purpose of the Study:
- To investigate the effects of verapamil on body sodium, fluid volume, and adrenergic responsiveness in patients with essential hypertension.
- To determine if verapamil impacts lipid metabolism and hormonal activity (renin, aldosterone) during antihypertensive treatment.
Main Methods:
- 15 patients with essential hypertension received verapamil (348 +/- 68 mg/day) for 8 weeks.
- Measurements included exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, and pressor/chronotropic responses.
- Lipid metabolism parameters were also assessed.
Main Results:
- Verapamil significantly reduced supine blood pressure (153/103 to 140/95 mm Hg).
- No significant changes were observed in exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, or lipid profiles.
- A significant rightward shift in the blood pressure dose-response curve to norepinephrine was noted, indicating decreased pressor responsiveness.
Conclusions:
- The antihypertensive effect of verapamil is linked to reduced cardiovascular pressor responsiveness to norepinephrine.
- Verapamil does not appear to alter endogenous noradrenergic activity, sodium/fluid volume status, renin-angiotensin-aldosterone axis activity, or lipid metabolism in hypertensive patients.
Abstract:
Calcium antagonists may affect the regulation of body sodium and adrenergic-dependent mechanisms. Exchangeable sodium, blood volume, plasma norepinephrine, renin, aldosterone, pressor responsiveness to norepinephrine, heart rate responses to isoproterenol, and lipid metabolism were studied in 15 patients with essential hypertension after 8 weeks of treatment with verapamil (348 +/- 68 (SD) mg/day). Supine blood pressure decreased from 153/103 +/- 19/12 mm Hg to 140/95 +/- 14/12 mm Hg (P less than 0.01). Exchangeable sodium, blood volume, plasma norepinephrine, renin and aldosterone, serum total cholesterol, the lipoprotein fractions, and apoprotein levels were unchanged. The norepinephrine pressor and the isoproterenol chronotropic doses tended to increase, whereas the dose-response curve of blood pressure related to plasma norepinephrine was significantly displaced to the right (F = 5.34; P less than 0.05). The antihypertensive effect of verapamil is associated with a decreased cardiovascular pressor responsiveness to norepinephrine without changes in endogenous noradrenergic activity. Moreover, verapamil does not modify the sodium/fluid volume state, the activity of the renin-angiotensin aldosterone axis, or lipid metabolism.