[Relationship of the renin-angiotensin-aldosterone system with auricular natriuretic factor in its response to the action of thiazide diuretics and to nifedipine, a sustained-release calcium antagonist].
BACKGROUND
Blood pressure (BP) response to diuretics may be considered as an index of salt-sensitivity. Salt-sensitive patients may have an enhanced response to calcium channel blockers. In this study we correlate the basal values of two of the hormonal systems involved in the control 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 patients in a lineal sequence in an open protocol, first treated with slow release nifedipine (Nif-30), 30 mg daily, as a single dose, for 30 days, followed by amiloride+hydrochlorothiazide (HCT+Am), 50 mg and 5 mg, daily, for another month. Plasma renin activity (PRA), plasma aldosterone (PAld) and 24 hours urinary aldosterone (UAld) and atrial natriuretic factor (ANF), were measured at the start and end of the study. The hormonal values on each group were compared and correlated with changes 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. There were 76% controlling MAP with Nif-30 whereas 48% did so with HCT+Am, p < 0.01, HCT+Am also increased PRA, PAld and decreased ANF, Ca urinary excretion and plasma PTH. Nif-30 did not alter the renin-angiotensin-aldosterone system, nor ANF. PTH remained unchanged. The MAP decrement caused by HCT+Am depended on baseline BP, r = -0.69, p < 0.0005, whereas Nif-30 decreased MAP independent from its baseline values, r = -0.02, NS. PAld showed a reverse correlation with ANF after treatment, r = -0.43, p < 0.05. The decrease of MAP holds a reverse relationship with ANF, both with HCT+Am, r = -0.47, p < 0.02, and with Nif-30, r = -0.45, p < 0.04.


CONCLUSIONS
Treatment with Nif-30 was superior to HCT+Am in number of patients controlled, but the decrease in MAP is similar. Since the antihypertensive response to diuretic therapy and to calcium channel-blockers is related to low levels of ANF this fact could indicate some sort of defect of ANF secretion.
Ocón
J
J
Unidad de Hipertensión Arterial, Fundación Puigvert, Barcelona.
Mora-Macià
J
J
Castellet
R
R
del Río
G
G
D000450:Aldosterone / Q000097:blood; D000584:Amiloride / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D001000:Ants / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D003692:Delayed-Action Preparations; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006852:Hydrochlorothiazide / Q000494:pharmacology* / Q000627:therapeutic use; D006973:Hypertension / Q000097:blood / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000494:pharmacology* / Q000627:therapeutic use; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology
D003692:Delayed-Action Preparations; D006852:Hydrochlorothiazide; D000450:Aldosterone; D000584:Amiloride; D012083:Renin; D009543:Nifedipine
Relaciones del sistema renina-angiotensina-aldosterona con el factor natriurético auricular en su respuesta a la acción de diuréticos-tiacídicos y al antagonista del calcio nifedipino de liberación sostenida.