THE RELATIONSHIP OF RENIN-ANGIOTENSIN-ALD OSTERONE SYSTEM AND AURICULAR NATRIURETIC FACTOR IN ITS RESPONSE TO THE ACTION OF THIAZIDIC DIURETICS AND TO NIFEDIPINE, A CALCIUM-ANTAGONIST OF SUSTAINED-RELEASE

BACKGROUND: Blood pressure (BP) response to diuretics may be considere d as an index of salt-sensitivity. Salt-sensitive patients may have an enhanced response to calcium channel blockers. In this study we corre late the basal values of two of the hormonal systems involved in the c ontrol of Na balance comparing them with the antihypertensive effects of a calcium channel blocker and a diuretic, to assess if BP response depends of a particular hormonal pattern by which we could define salt -sensitive patients. METHODS: We studied 21 essential hypertensive pat ients in a lineal sequence in an open protocol, first treated with slo w release nifedipine (Nif-30), 30 mg daily, as a single dose, for 30 d ays, followed by amiloride + hidrochorothiazide (HCT+Am), 50 mg and 5 mg, daily, for another month. Plasma renin activity (PRA), plasma aldo sterone (PAld) and 24 hours urinary aldosterone (UAld) and atrial natr iuretic factor (ANF), were measured at the start and end of the study. The hormonal values on each group were compared and correlated with c hanges observed in BP at the end of each period of treatment. RESULTS: HCT+Am decreased median arterial pressure (MAP) from 121.4 +/- 11 to 110.4 +/- 8 mmHg and Nif-30 to 108.7 +/- 12.4 mmHg, both p < 0.0004. T here were 76 % controlling MAP with Nif-30 whereas 48 % did so with HC T+Am, p < 0.01, HCT + Am also increased PRA, PAld and decreased ANF, C a urinary excretion and plasma PTH. Nif-30 did not alter the renin-ang iotensin-aldosterone system, nor ANF. PTH remained unchanged. The MAP decrement caused by HCT+Am depended on baseline BP, r = -0.69, p < 0.0 005, whereas Nif-30 decreased MAP independent from its baseline values , r = -0.02, NS. PAld showed a reverse correlation with ANF after trea tment, r = -0.43, p < 0.05. The decrease of MAP holds a reverse relati onship with ANF, both with HCT+Am, r = -0.47, p < 0.02, and with Nif-3 0, r = -0.45, p < 0.04. CONCLUSIONS: Treatment with Nif-30 was superio r to HCT+Am in number of patients controlled, but the decrease in MAP is similar. Since the antihypertensive response to diuretic therapy an d to calcium channel-blockers is related to law levels of ANF this fac t could indicate some sort of defect of ANF secretion.