SUMMARYThe present experiments investigate whether the absence of tachycardia during lowering of blood pressure (BP) with an angiotensin-converting enzyme Inhibitor (CO) in salt-depleted dogs Is due to an alteration in the activity of the baroreflex. Baroreflex activity was measured after pharmacological manipulation of BP using intravenous nitroglycerine or phenylephrine, and the heart period (R-R interval) relative to the arterial pressure pulse was recorded. The slope of the relationship between BP and R-R interval is a measure of the sensitivity of the baroreceptor reflex and displacement of the line indicates a change in the setpoint of BP. On normal sodium diet, the sensitivity and setpoint of the baroreflex were unaltered by the nonapeptide CEI given both intravenously and into a lateral cerebral ventricle. During salt depletion, however, intravenously but not centrally administered CEI altered the setpoint of the baroreflex without modifying the sensitivity. (BP) is maintained by the autonomic nervous system and by angiotensin, and it has been shown in isolated preparations that the two systems interact.

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The effects of captopril and angiotensin II on adrenergic neurotransmission have been studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In a pithed rat preparation, vasoconstrictor responses evoked by spinal stimulation were greater in SHR than WKY (p < 0.01). Captopril reduced responses to electrical stimulation and this reduction was greater in the SHR (p < 0.001). Bilateral nephrectomy reduced the vasoconstrictor responses to nerve stimulation in both strains of rat and abolished the effects of captopril. In an isolated perfused mesenteric artery preparation, responses to nerve stimulation in the absence of angiotensin II were greater in SHR than WKY (p < 0.05). Angiotensin II potentiated responses from both strains of rat, however the amplitude of the potentiation was greater in preparations from the SHR than those from WKY (p < 0.002). Captopril (30 mg/kg by mouth) reduced blood pressure in conscious SHR over a 5-day dosing period. In WKY rats, no hypotensive action of captopril was observed. However, in another normotensive strain, the Alderley Park Wistar rat (APW), captopril lowered blood pressure. Plasma renin activity was not significantly different among these three strains of rat. The APW have previously been shown to be very sensitive to the adrenergic potentiating actions of angiotensin II. Captopril thus lowers blood pressure in SHR and APW, and both these strains are sensitive to the adrenergic potentiating actions of angiotensin II. It does not lower blood pressure in WKY, which is relatively insensitive to these actions of the octapeptide. Therefore, the hypotensive action of captopril in the rat may be due to its interference with the adrenergic potentiating effect of angiotensin II. (Hypertension 4: 764-772, 1982) KEY WORDS • angiotensin • converting enzyme inhibition • pithed rat perfused rat mesenteric artery • sympathetic nervous system * adrenergic vasoconstriction • plasma renin activity • blood pressure • captopril T HE mechanism of action of captopril in lowering blood pressure is unclear. In both humans and animals, a fall in blood pressure is seen in those with elevated, normal, and low levels of circulating renin. 1 "* This could suggest that the inhibition of angiotensin II formation is not an important factor in the hypotensive action of captopril. However, recent studies suggest that the level of angiotensin II that participates in the control of blood pressure is closer to the normal range than previously realized. 7 ' 8 In addition , a functional interaction of the octapeptide with the sympathetic nervous system has been largely over

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