Enhanced bradycardia but not renal sympathoinhibition during hemorrhage in rats with area postrema lesions

• Published in: The American journal of physiology Vol. 267; no. 2 Pt 2; pp. H569 - H573
• Main Authors: Edwards, G L, Johnson, A K, Peuler, J D
• Format: Journal Article
• Language: English
• Published: United States 01-08-1994
• Subjects: Animals; Arginine Vasopressin - pharmacology; Cerebral Ventricles - physiopathology; Denervation; Female; Heart Rate - drug effects; Heart Rate - physiology; Hemorrhage - physiopathology; Injections, Intravenous; Kidney - innervation; Rats; Rats, Sprague-Dawley; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiopathology
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1994.267.2.H569

Hypotensive hemorrhage inhibits renal sympathetic nerve activity (SNA) and heart rate (HR) in rats. The area postrema (AP) is reported to modulate autonomic responses to arginine vasopressin (AVP) and may be a site where circulating AVP influences SNA and HR during hypotensive hemorrhage. We found a similar renal sympathoinhibition in AP-lesioned (APX) and sham-lesioned (Sham) rats during hypotensive hemorrhage and a greater bradycardia in APX compared with Sham rats. Further inhibition of renal SNA with AVP infusion was not observed in APX rats, although the bradycardic action of AVP infusion was comparable to that in Sham rats. Thus the AP attenuates bradycardia but not renal sympathoinhibition during hypotensive hemorrhage in normal rats. Nonetheless, an intact AP permits further reduction in renal SNA during infusion of AVP. If AVP contributes to hypotensive hemorrhage-induced renal sympathoinhibition, its action may occur at sites other than the AP or at the AP where such action is counterbalanced by sympathoexcitatory factor(s) also activated during hypotensive hemorrhage. Finally, enhanced bradycardia during hypotensive hemorrhage in APX rats suggests it may not be the site of action for AVP-induced bradycardia in intact rats.