Acute and chronic sympathetic reflex activation and antihypertensive response to nifedipine.

The importance of counterregulatory mechanisms triggered by arterial vasodilation for the antihypertensive response to the calcium entry blocking agent nifedipine was investigated in 13 men with mild to moderate essential hypertension. Blood pressure and systemic vascular resistance were significantly reduced 30 minutes after sublingual administration of 10 mg of nifedipine while heart rate, cardiac index and plasma norepinephrine concentrations increased (all p less than 0.01). Also, changes in mean blood pressure correlated inversely with arterial baroreflex sensitivity (r = -0.74, p less than 0.01), suggesting that arterial baroreflex mechanisms by means of sympathetic activation tend to limit the acute antihypertensive response. Blood pressure, but not systemic vascular resistance, decreased further (p less than 0.01) after 6 weeks of therapy with nifedipine 20 mg three times daily, while average heart rate, cardiac index and plasma norepinephrine concentrations had returned toward pretreatment values. Thus, a reduction of acutely increased sympathetic activity toward pretreatment values during long-term nifedipine therapy was associated with further decreases in blood pressure. The importance of sympathetic activity was also stressed by the finding of an inverse relation between chronic changes in heart rate and blood pressure (percent of control, r = -0.76, p less than 0.01). Blood volume did not change during long-term nifedipine therapy. The results suggest that the degree of sympathetic reflex activation in part determines the antihypertensive response to nifedipine monotherapy.