MODULATION OF AUTONOMIC NERVOUS-SYSTEM ADJUSTMENTS TO HEAT-STRESS BY CENTRAL ANG-II RECEPTOR ANTAGONISM

Citation
Kc. Kregel et al., MODULATION OF AUTONOMIC NERVOUS-SYSTEM ADJUSTMENTS TO HEAT-STRESS BY CENTRAL ANG-II RECEPTOR ANTAGONISM, The American journal of physiology, 266(6), 1994, pp. 180001985-180001991
Citations number
35
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
266
Issue
6
Year of publication
1994
Part
2
Pages
180001985 - 180001991
Database
ISI
SICI code
0002-9513(1994)266:6<180001985:MOANAT>2.0.ZU;2-R
Abstract
The purpose of this study was to determine whether central angiotensin II (ANG II) participates in mediating selected sympathetic nervous sy stem and neuroendocrine adjustments to heat stress in conscious freely moving rats. Mean arterial pressure (MAP), heart rate (HR), splanchni c sympathetic nerve activity (SpNA), plasma arginine vasopressin (AVP) concentration, and colonic temperature were measured before and durin g whole body heating (42 degrees C ambient temperature). Heating was s topped when a colonic temperature of 41 degrees C was attained. On con secutive days, rats received an intracerebroventricular (icv) injectio n of saline (0.9%) or 25 mu g of the ANG II AT(1)-selective receptor a ntagonist losartan 20 min before the start of heating. Neither treatme nt influenced control levels of any parameter. The increase above base line for MAP at the end of heating was attenuated by > 50% in the losa rtan, compared with the saline trial (P < 0.05), while HR remained unc hanged from control values for both trials. Pretreatment with losartan icv eliminated the increase in SpNA observed during the heating perio d in the saline trial. Furthermore, the magnitude of change in plasma AVP during heating was significantly elevated in rats after icv admini stration of saline compared with losartan. These findings indicate tha t central ANG II receptor antagonism significantly attenuates the heat ing-induced elevations in MAP, sympathetic neural activity to visceral regions, and plasma AVP and suggest that the central nervous system a ctions of endogenous ANG II are required for full expression of the sy mpathoexcitatory, presser, and neuroendocrine responses associated wit h nonexertional heat stress in the conscious rat.