Plasma Nifedipine Concentration Research Articles

Effect of nifedipine on plasma renin, aldosterone and catecholamines in arterial hypertension.

Acute sublingual administration of nifedipine 10--20 mg to 13 hypertensive patients caused a rapid decrease in blood pressure (BP) and a concomitant increase in heart rate (HR), plasma noradrenaline (NA) and plasma renin activity (PRA); there was no significant change in plasma adrenaline (A) or aldosterone (ALDO). Basal PRA was the major determinant of the rise in PRA, as a close correlation was present between the basal value and the increase caused by nifedipine (r = 0.92), p less than 0.001). The rise in PRA was also correlated with the plasma concentration of nifedipine after 60 min (r = 0.80, p less than 0.01), but it was not correlated with the decrease in BP, the rise in HR or the increase in NA. Nifedipine 30--60 mg daily for 6 weeks caused a reduction in mean BP from 133 to 113 mmHg (p less than 0.001). Body weight and serum potassium decreased but no consistent change was noted in NA, PRA, ALDO or 24 h-excretion of catecholamines. A significant correlation was present between the change in NA and that in PRA (r = 0.74, p less than 0.01). The alterations in the various parameters in the acute and chronic studies were not correlated. The findings indicate that different regulatory mechanisms are activated during acute and chronic administration of nifedipine. It is suggested that an initial rise in sympathetic activity gradually decreases during prolonged therapy, but it still remains a determinant of PRA.

Acute and chronic effects of nifedipine in arterial hypertension.

Sublingual administration of nifedipine 10 mg to 11 patients and 20 mg to 6 patients with arterial hypertension caused a rapid and significant decrease in blood pressure in both groups. The average maximal reductions in the two groups were 21/16 mm Hg and 27/21 mm Hg. A concomitant rise in heart rate was found. Forearm blood flow showed a significant increase and the calculated vascular resistance a significant decrease 15–60 min after administration of both the 10 mg and the 20 mg doses. There was a negative correlation between basal vascular resistance and the maximal change of this parameter (r=−0.72, p<0.01). Plasma concentrations of nifedipine showed considerable individual variation, with slow absorption in some patients, which indicated failure of sublingual absorption in them. The difference between the mean plasma concentration in the two dose groups was statistically significant after 45 min. A negative correlation was present between the plasma concentration of nifedipine and the observed change in calculated vascular resistance (r=−0.74 at t=30 min). Treatment of 10 hypertensive patients with nifedipine 30–60 mg daily for 6 weeks reduced mean blood pressure from 175/115 mm Hg to 151/96 mm Hg (p<0.001). Heart rate and forearm blood flow rose, whereas the forearm vascular resistance showed a significant decrease. Side effects of a sensation of heat and reddening of face were noted in some patients. It is suggested that nifedipine may be useful both in the acute and chronic treatment of arterial hypertension.