Visceral afferents and the fastigial nucleus in vascular and plasma renin adjustments to head-up tilting.

A two min orthostatic stress of 30 degrees head-up tilting in alpha-chloralose anesthetized and paralyzed cats results in compensatory changes in cardiovascular parameters (systemic blood pressure, renal perfusion pressure) and renin release. The dynamics of the response leads to shifts in systemic arterial pressure characterized by 3 phases. The initial phase, a fall in systemic pressure, is followed by a rapid compensatory phase with a period that does not exceed 50 s. The near steady-state adjustment in blood pressure and renal vascular resistance represents the third phase, has a longer time constant and is adequately accounted for by both arterial and cardiopulmonary baroreflex mechanisms. Indeed, fixing carotid sinus pressure in the vagotomized cat at high or low levels alters only the magnitude of the steady-state pressure obtained with tilt and not the early rapid compensation of the second phase. By contrast, bilateral lesions of the fastigial nucleus of the cerebellum abates the rapid phase of systemic compensation to tilting. Renin secretion significantly increased (greater than 2 1/2) with tilt and this increase was abolished by vagotomy. By fixing carotid sinus pressure at high or low levels in the vagotomized cat, tilt resulted in only a modest rise in renin secretion. Following fastigial lesions such as upwards trend was abated. Three neural components (cerebellar fastigial pressor, arterial baroreflex and cardiopulmonary baroreflex) appear necessary for the integrated response in cardiovascular adjustment to head-up tilt. The adjustments to orthostatic stress comprise both rapid neural as well as long-term humoral responses.