Role of sympathetic nervous system activity in the blood pressure response to long-term captopril therapy in severely hypertensive patients.
Twenty severely hypertensive subjects who did not achieve blood pressure control with combination therapy with a vasodilator, a beta-adrenergic blocking agent and a diuretic received the angiotensin-converting enzyme inhibitor captopril. Marked decreases in blood pressure were observed immediately. Achievement of sustained reductions in blood pressure into the normal range for up to 3 years of follow-up required the addition of a diuretic in all patients and of a beta-adrenergic blocking agent in half. As expected, significant increases in plasma renin activity and decreases in plasma aldosterone were seen initially and sustained throughout the study. Plasma and urinary norepinephrine levels, which were markedly increased before captopril treatment, decreased significantly and remained low for the duration of study. These observations suggest a link between the renal pressor and sympathetic systems which may be involved in the pathophysiology of severe, treatment-resistant hypertension, and suggest that part of the antihypertensive action of captopril may be related to a decrease in sympathetic activity secondary to its interference with the generation of angiotensin II.
D000450:Aldosterone / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects*; D002216:Captopril / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy*; D009638:Norepinephrine / Q000652:urine; D011188:Potassium / Q000097:blood; D011392:Proline / Q000031:analogs & derivatives*; D011433:Propranolol / Q000627:therapeutic use; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000187:drug effects*
D006852:Hydrochlorothiazide; D000450:Aldosterone; D011392:Proline; D002216:Captopril; D011433:Propranolol; D012083:Renin; D011188:Potassium; D009638:Norepinephrine