Abstract

The influence of the carotid sinus on centrally mediated peripheral hypertensive effects of angiotensin II was studied utilizing an in situ isolated perfused brain preparation. A low concentration (0.5 µg/mi) of the polypeptide was perfused through the brains of two groups of cats. The first group possesses intact carotid sinuses and other afferent pressoceptor innervation. In the second group, cranial nerves IX, X, XI and XII were sectioned cephalad to the nodose ganglion. The data obtained from the first group indicate that in the presence of the baroreceptor afferents there was no evidence of a centrally induced peripheral hypertensive effect due to the angiotensin II. In the second group, however, there was clear evidence of a centrally induced peripheral hypertension resulting from perfusion of angiotensin II, but there was no relation between the increased cerebral perfusion pressure and the peripheral hypertension. These data permit the conclusion that in intact animals a centrally mediated peripheral hypertensive response produced by angiotensin II may be reflexly inhibited by carotid sinus baroreceptor activation secondary to increased cerebral perfusion pressure.