Comparison of acute effects of nifedipine in normotensive and hypertensive man.

TLDR: The results suggest that the contrasting BP response is caused mainly by a decreased sensitivity of the baroreceptor mechanism in arterial hypertension.

Abstract: Acute sublingual administration of nifedipine, 10 or 20 mg, caused a rapid dose-related decrease in blood pressure (BP) in hypertensive subjects (n = 17), whereas no significant reduction of blood pressure was observed in a group of normotensive subjects (n = 12). Forearm vascular resistance (CVR) decreased significantly in both groups (31.1 and 17.2%, respectively; inter-group difference nonsignificant). The vasodilatating effect of nifedipine tended to be stronger in hypertensives than in normotensives, as reflected by a higher CVR (%)/log plasma concentration of nifedipine index. A significant negative correlation was found between the change in CVR and the change in heart rate (HR) in normotensive subjects (r = −0.72, p < 0.05), whereas no such relationship was present in hypertensive patients. There was no significant correlation between the change in BP and the change in HR in any of the groups. The rise in plasma noradrenaline and resting HR did not differ significantly in hypertensive patients and in normotensive subjects receiving nifedipine 20 mg. The results suggest that the contrasting BP response is caused mainly by a decreased sensitivity of the baroreceptor mechanism in arterial hypertension. A larger decrease in CVR in hypertensive patients than in normotensive subjects could be due at least partly to morphological changes of the resistance vessels. However, a more marked relaxing effect of the calcium antagonist in hypertensive vessels than in normotensive vessels may have contributed to the observed difference in effect.