Endocrine and Cardiovascular Influences of Converting Enzyme Inhibition with SQ 14225 in Hypertensive Patients in the Supine Position and during Head-Up Tilt before and after Sodium Depletion*

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Abstract
In this study we examined the effects of the orally active angiotensin-converting enzyme inhibitor SQ 14225 (Captopril) on blood pressure, heart rate, plasma norepinephrine and epinephrine, PRA, aldosterone, cortisol, and serum potassium in 15 sodium-repleted hypertensive patients in the supine position and during 30 min of head-up tilt; in 3 patients the same investigations were repeated after sodium deprivation. On normal sodium intake, a short term treatment with SQ 14225, at average doses of 480 ± 60 mg⁄day, reduced mean supine blood pressure by 19 ± 3 mm Hg (P < 0.001); this change was associated with an increase in PRA of 12.2 ± 3.2 ng⁄ml.h (P < 0.001), a fall in plasma aldosterone of 4.8 ± 1.9 ng⁄100 ml (P < 0.01), and a concurrent rise in serum potassium of 0.26 ±0.1 meq⁄liter (P ⁄ 0.05). Supine heart rate and plasma norepinephrine, epinephrine and cortisol were unchanged. Although in control tilt studies the mean blood pressure was unchanged in all patients, during converting enzyme inhibition (CEI) 3 of them fainted between 15–30 min of tilt. In the remaining 12 patients mean blood pressure was maintained during tilt on CEI; however, while heart rate and epinephrine increased as in control studies, the 30 min norepinephrine response was significantly higher (476 ± 61 us. 306 ± 34 pg⁄ml; P < 0.05). Both before and during CEI, the posturally induced responses of PRA and aldosterone were parallel and correlated to each other, while plasma cortisol and potassium had minimal increments. In all 3 patients in whom SQ 14225 treatment was then combined with sodium depletion, tilt caused hypotension in spite of greater increases in plasma norepinephrine than those seen during CEI treatment on normal salt intake. It appears that, in the supine position, the fall of blood pressure produced by CEI occurs without an accompanying rise in sympathetic nervous activity; thus, the concurrent increase in PRA is related only to the interruption of the angiotensin feed back mechanism. The rise in renin and aldosterone in response to tilt during CEI suggests that the enzymatic blockade can be partially overriden. However, while on normal sodium intake CEI does not prevent, in the majority of patients, the maintenance of blood pressure during tilt because of a compensatory, more intense response of the sympathetic nervous system, when combined with sodium depletion it may lead to significant impairment of orthostasis.

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