Open AccessOVLT lesion decreases basal arterial pressure and the chronic hypertensive response to Ang II in rats on a high‐salt diet
Author(s) -
Collister John P.,
Olson Marin K.,
Nahey David B.,
Vieira Alexandre A.,
Osborn John W.
Publication year - 2013
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.1002/phy2.128
Subject(s) - lamina terminalis , medicine , endocrinology , basal (medicine) , angiotensin ii , lesion , blood pressure , renin–angiotensin system , mean arterial pressure , central nervous system , heart rate , surgery , insulin
We have reported that lesion of the organum vasculosum of the lamina terminalis ( OVLT ) has no effect on basal levels of mean arterial pressure ( MAP ) but abolishes the hypertensive effects of angiotensin II (Ang II ) in rats consuming a normal‐salt diet. These results suggest that the OVLT does not contribute to regulation of MAP under conditions of normal salt intake, but it is an important brain site for the hypertensive actions of Ang II . The OVLT has been proposed as a major sodium sensor in the brain and the hypertensive effects of Ang II are exacerbated by high‐salt intake. Therefore, the objective of this study was to investigate the role of the OVLT during Ang II ‐induced hypertension in rats fed a high‐salt diet. Male Sprague‐Dawley rats underwent sham (Sham; n = 9) or OVLT lesion ( OVLT x; n = 8) surgery and were placed on a high‐salt (2% NaCl) diet. MAP was measured by radio telemetry during three control days, 10 days of Ang II infusion (10 ng/kg/min, i.v.), and a 3‐day recovery period. MAP was significantly lower in OVLT x (97 ± 2 mmHg) compared to Sham (106 ± 1 mmHg) rats during the control period ( P < 0.05). Moreover, the chronic pressor response to Ang II was markedly attenuated in OVLT x rats. MAP increased 58 ± 3 mmHg in Sham rats by Day 10 of Ang II compared to a 40 ± 7 mmHg increase in OVLT x rats ( P < 0.05). We conclude that (1) the OVLT regulates the basal levels of MAP in rats consuming a high‐salt and (2) the OVLT is an important brain site of action for the pathogenesis of Ang II ‐salt hypertension in the rat. Supported by HL 076312.