The reflex responses of heart rate (HR) to bolus injection and infusion of
phenylephrine and nitroglycerine were studied in rats with one-kidney, one
clip (1-K, 1C)
hypertension and
hypertension produced by aortic
ligation. Rats with mild 1-K, 1C
hypertension (147 +/- 4 mmHg) and a normal renin-angiotensin system (RAS) activity had normal bradycardic and tachycardic responses, whereas rats with severe
hypertension (208 +/- 3 mmHg) and over-active RAS showed impairment (70-80%) of the responses. After 12 days of aortic
ligation rats with mild (146 +/- 2 mmHg) and severe (175 +/- 3 mmHg)
hypertension exhibited overactivity of the RAS and marked impairment of the baroreflex control of HR. Normalization of RAS activity in rats with mild
hypertension 60 days after aortic
ligation, coincided with normalization of the bradycardic responses, whereas the abnormality persisted in those rats with severe
hypertension in which hyperactivity of RAS also persisted. The response to 20-s carotid occlusion and the HR responses to electrical stimulation of the vagus nerve were normal in rats with
renal hypertension, 12 days after aortic
ligation. An
ether inhalation test produced a marked reduction of 60% in the HR of control awake rats accompanied by a 46 +/- 5 mmHg increase in blood pressure. Reflex pathways other than those through the baroreceptors were largely responsible for the
bradycardia since responses remained unchanged in rats with sino-aortic
denervation (SAD) or when the pressure increase was prevented by
phenoxybenzamine administration.(ABSTRACT TRUNCATED AT 250 WORDS)