| Receptor endings have been identified in the kidney that are activated by mechanical stimuli, such as, changes in intrarenal pressure and chemical stimuli such as renal ischemia or concentrated urine in the renal pelvis. Although no specific functional role for the renal receptors has been demonstrated, available evidence suggests a role in body fluid and electrolyte homeostasis or a role in the etiology of experimental renal hypertension.;Cardiovascular responses to RANS were abolished by spinal cord transection at T(,6), indicating supraspinal integration of the reflex. Ablation of the nucleus tractus solitarius (NTS), a cardiovascular integrative site in the medulla, abolished the cardiovascular responses produced by RANS.;The integrity of the lateral parabrachial nucleus in the dorsolateral pons was also shown to be essential for the hemodynamic responses to RANS. In contrast, the paraventricular nucleus of the hypothalamus appeared to provide inhibitory modulation of the cardiovascular reflex pathway since responses were exaggerated after lesion of this nucleus.;The reflex responses depend in part on structures in the rostral diencephalon. Hindquarter vasodilation appeared to require integrity of the ventral nucleus medianus and surrounding tissue, whereas the organum vasculosum of the lamina terminalis was postulated to be necessary for the mesenteric vasoconstriction produced by RANS. The diencephalon, therefore, provides inhibitory as well as excitatory integration of the cardiovascular responses evoked by RANS. These findings, which functionally identify neural projections from kidney to diencephalon via the NTS and parabrachial nucleus, serve as a framework for future studies on the role of the renal afferent system in physiological and pathophysiological states.;Electrical stimulation of afferent renal nerves (RANS) evokes a neurally mediated change in arterial pressure. The central nervous system connections necessary for the blood pressure response are not known. The present investigation examined; (1) the cardiovascular consequences of RANS in the rat and (2) the central nervous system pathways necessary for hemodynamic alterations. In the anesthetized rat, RANS elicited a depressor response with no change in heart rate. With continuous monitoring of regional flows, vascular resistance was increased in the superior mesenteric artery, whereas hindquarter and renal vascular resistance decreased during RANS. |
