Regulation of arterial pressure lability in rats with chronic sinoaortic deafferentation.
After chronic (2-6 wk) sinoaortic deafferentation (SAD), rats exhibit slight increases in mean arterial pressure (MAP) and heart rate and marked increases in arterial pressure lability. Neither antagonists of humoral vasoconstrictors angiotensin and vasopressin nor acute hypophysectomy altered MAP or lability after chronic SAD. Ganglionic blockade produced hypotension and significantly reduced lability in SAD rats but decreased MAP and increased lability in normal rats. Although chlorisondamine reduced lability in rats with SAD to levels observed in similarly treated sham-operated rats, lability was significantly greater in both groups than in saline-treated sham-operated rats. When intact or SAD rats were administered chlorisondamine plus either captopril or a vasopressin antagonist, pressure lability was returned to levels seen in intact untreated animals. Selective antagonism of alpha 1- or alpha 2-adrenergic receptors did not markedly alter lability in SAD rats. Combined alpha-adrenergic blockade reduced lability in SAD rats and increased lability in intact rats, similar to chlorisondamine treatment. These data suggest that chronic SAD establishes arterial pressure variability that is maintained or generated in large part by the sympathetic nervous system through mechanisms dependent on higher central structures or descending efferent sympathetic nerves. The data further suggest that peripheral mechanisms may also be involved in arterial pressure regulation in baroreceptor-deficient rats.
D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D001794:Blood Pressure; D002346:Carotid Sinus / Q000502:physiology*; D003714:Denervation; D007016:Hypophysectomy; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013564:Sympathetic Nervous System / Q000502:physiology