ENHANCED BRADYCARDIA BUT NOT RENAL SYMPATHOINHIBITION DURING HEMORRHAGE IN RATS WITH AREA POSTREMA LESIONS

Citation
Gl. Edwards et al., ENHANCED BRADYCARDIA BUT NOT RENAL SYMPATHOINHIBITION DURING HEMORRHAGE IN RATS WITH AREA POSTREMA LESIONS, The American journal of physiology, 267(2), 1994, pp. 80000569-80000573
Citations number
14
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
267
Issue
2
Year of publication
1994
Part
2
Pages
80000569 - 80000573
Database
ISI
SICI code
0002-9513(1994)267:2<80000569:EBBNRS>2.0.ZU;2-5
Abstract
Hypotensive hemorrhage inhibits renal sympathetic nerve activity (SNA) and heart rate (HR) in rats. The area postrema (AP) is reported to mo dulate autonomic responses to arginine vasopressin (AVP) and may be a site where circulating AVP influences SNA and HR during hypotensive he morrhage. 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 inhibitio n of renal SNA with AVP infusion was not observed in APX rats, althoug h the bradycardic action of AVP infusion was comparable to that in Sha m rats. Thus the AP attenuates bradycardia but not renal sympathoinhib ition during hypotensive hemorrhage in normal rats. Nonetheless, an in tact AP permits further reduction in renal SNA during infusion of AVP. If AVP contributes to hypotensive hemorrhage-induced renal sympathoin hibition, 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 bradyc ardia during hypotensive hemorrhage in APX rats suggests it may not be the site of action for AVP-induced bradycardia in intact rats.