Influence of nicardipine on blood pressure, renal function and plasma aldosterone in normotensive volunteers.

Abstract

1 The influence of the calcium antagonist nicardipine on intrarenal sodium handling and angiotensin II induced secretion of aldosterone was investigated in 18 normotensive volunteers after the first dose and after 1 week of treatment (20 mg three times daily). 2 A short-lasting natriuresis was observed, which was caused by a decreased reabsorption of sodium localised in both proximal and distal tubules. 3 Log plasma renin activity (PRA) fell significantly on each day during angiotensin II infusion, while log plasma aldosterone (PA) rose significantly. 4 The log PRA/log PA ratio was increased during nicardipine treatment. The secretion of aldosterone, induced by angiotensin II, was not influenced by nicardipine treatment. No effect of the drug on adrenal responsiveness to angiotensin II was found.

The effects of nicardipine in hypertensive subjects with impaired renal function

“…Studies of Van Schaik and coworkers suggest that in hypertensive subjects, the natriuresis is mediated by altered renal haemodynamics (Van Schaik et al, 1984). However, other observations, including changes in solute free water excretion and osmolar clearance, implicate a direct effect of nicardipine on proximal tubular function (Young et al, 1985;Van Schaik et al, 1985). Studies with nitrendipine, a related calcium channel blocker, have demonstrated a phosphaturic effect and an increased solute free water excretion, independent of changes in glomerular filtration (Wallia et al, 1985).…”

Nicardipine vs propranolol in the treatment of essential hypertension: effect on total body elemental composition

“…Neither drug caused significant changes in the total body composition of sodium, potassium, chlorine, calcium, phosphorus or nitrogen at 12 weeks of treatment. Thus the early natriuresis which has been reported with nicardipine use (Van Schaik et al, 1985;Young et al, 1985) is not followed by a significant long-term sodium deficit. This is in contrast to other antihypertensive agents such as angiotensin converting enzyme inhibitors, which also promote an early natriuresis, but in addition may sustain a modest deficit of body sodium content with continued therapy (Hodsman et al, 1983;Sanchez et al, 1985).…”

“…Several types of antihypertensive agent, notably a-methyldopa (Birkenhager et al, 1978) and various vasodilators (Hansson, 1983), cause sodium and water retention, and this can limit their antihypertensive effect (so-called 'false tolerance ';Birkenhiiger et al, 1978). By contrast, an early modest natriuresis and diuresis has been reported with some calcium antagonists including nicardipine (Leonetti et al, 1982;Thananopavarn et al, 1984;Van Schaik et al, 1985;Young et al, 1985), and this might enhance the ability of these agents to lower blood pressure. An important aim of the present trial was to examine the extent to which a sodium deficit might be sustained during 3 months' treatment with nicardipine.…”

Metabolic and endocrine consequences of calcium channel blockade

“…In two small studies in hypertensive patients it was reported that nicardipine (Takabatake et al, 1982) and nifedipine (Murphy et al, 1983) produced a reduction in serum potassium of approximately 0.1 and 0.3 mmol P`respectively. This may possibly be attributed to an effect of these agents on renal vasculature giving rise to increased urinary sodium and potassium excretion (Van Schaik et al, 1985, Young et al, 1985. However, the majority of studies to date and the large scale experience with both nicardipine (Syntex, 1986) and nifedipine (Sorkin et al, 1985) have not shown any consistent fall in serum potassium and significant hypokalaemia has not to date been reported.…”