Studies on neural and humoral contributions to arterial pressure lability.

The mechanisms of arterial pressure lability in rats following sinoaortic deafferentation (SAD) remain unknown. In this paper, we review several studies that have investigated the potential mechanisms of this lability. Combined ganglionic and alpha-adrenergic receptor blockade reduced lability but not to control levels, indicating that the sympathetic nervous system plays a major role but is not the only mechanism involved in the generation of lability. When ganglionic blockade was combined with blockade of an endogenous humoral vasoconstrictor (vasopressin or angiotensin), lability was returned to control levels in SAD rats; however, humoral blockade alone did not alter lability. Infusion of phenylephrine or endogenous vasoconstrictors in the presence of combined neural and humoral blockade increased arterial pressure lability to levels similar to those found in rats with SAD. The neurogenic contribution to lability was further investigated by recording renal sympathetic nerve activity in conscious freely moving intact rats and rats with SAD. These studies demonstrated that one day after SAD, there was little direct correlation between transient changes in renal sympathetic nerve activity and arterial pressure lability. Thus, the evidence presented in this paper is consistent with the hypothesis that arterial pressure lability is not the direct result of unbuffered variations in sympathetic discharge but rather is produced by an interaction between neural and humoral components.