Renal sympathetic and cardiac changes associated with anaphylactic hypotension

Severe anaphylactic reactions can result in life-threatening hypotension, but little is known about the autonomic changes that accompany the hypotensive response. The aim of this study was to determine the renal sympathetic and cardiac responses to anaphylactic hypotension, and to evaluate the contribution of sinoaortic and vagal afferent inputs in producing these responses. Rats were sensitized with bovine serum albumin (BSA) and, after 10-14 days, were anaesthesized with sodium pentobarbitone and arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded. In about two thirds of the rats, injection of BSA evoked a severe and sustained hypotension, while in the remainder, there was either a more transient hypotension or else no significant change in arterial pressure. In control unsensitized rats, BSA injection had no significant effect on arterial pressure, heart rate, or RSNA. The BSA-induced hypotension in sensitized rats was associated with increases in HR and RSNA, the magnitudes of which were correlated with the magnitude of the hypotension. There were two components to the cardiac and renal sympathoexcitatory response: (1) an initial increase in HR and RSNA, which immediately followed the onset of hypotension and which was abolished by sinoaortic denervation and vagotomy, and (2) a delayed and gradual increase in HR and RSNA, which continued even while the arterial pressure was recovering and was reduced but not abolished by sinoaortic denervation and vagotomy. Thus, BSA-induced anaphylactic hypotension causes prolonged tachycardia and renal sympathoexcitation, which is only partly due to reflex effects arising from sinoaortic baroreceptors and cardiopulmonary receptors.