ATTENUATION BY CAPTOPRIL OF PRESSOR RESPONSES TO SYMPATHETIC STIMULI: EFFECTS OF PROCEDURES REDUCING ACTIVITY OF THE RENIN‐ANGIOTENSIN SYSTEM

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Abstract
Low doses (0.1-1.0 mg/kg) of the converting enzyme inhibitor captopril given i.v. to pithed rats were followed by long lasting falls in systolic and diastolic arterial blood pressures. Pressor responses were reduced to either electrical stimulation of the thoraco-lumbar sympathetic outflow or i.v. injection of the ganglion stimulant McNeil-A-343 [[4-(m-chlorophenylcarbamoyloxy)-2-butynyl]trimethylammonium chloride]. Positive chronotropic responses of the heart to cardiac nerve stimulation were unchanged after relatively large (3.0 mg/kg) doses of the drug. The reductions in arterial blood pressure and pressor responses to McNeil-A-343 caused by captopril persisted following .beta.-adrenoreceptor blockade with propranolol, renal sympathectomy or unilateral nephrectomy, but did not occur after acute bilateral nephrectomy nor during Na and H2O retention due to unilateral nephrectomy plus subacute administration of deoxycorticosterone and saline. Pressor responses to noradrenaline [norepinephrine, NE] were reduced after 1.0 mg/kg captopril i.v.; those to methoxamine or vasopressin were unaltered after 5.0 mg/kg. Evidently in the rat, after elimination of sympathetic tone by pithing, the level of the arterial blood pressure and the magnitude of pressor responses to peripheral sympathetic nerve activation depend on the basal activity of the renin-angiotensin system. This maintains sufficient angiotensin II production to ensure retention of some tone in resistance vessels together with presynaptic augmentation of NE output at a sympathetic postganglionic nerve endings. The latter effects are abolished after converting enzyme inhibition with captopril, consequent to reduced tissue levels of angiotensin II and perhaps potentiation of the actions of bradykinin.

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