Key result
OVLT lesion attenuated the chronic pressor response to AngII in rats on a high-salt diet, with MAP increasing by 40 ± 7 mmHg compared to 58 ± 3 mmHg in sham rats.
Why the study?
Does OVLT lesion reduce AngII-induced hypertension in rats on a high-salt diet?
Does OVLT lesion reduce AngII-induced hypertension in rats on a high-salt diet?
Lesion of the OVLT attenuates basal arterial pressure and the chronic hypertensive response to AngII in rats on a high-salt diet, highlighting its role in AngII-salt hypertension pathogenesis.
Answers are grounded in this paper and cite their sources.
OVLT lesion attenuates AngII-salt hypertension in rats; leaves open translational relevance to human hypertension.
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 (AngII) 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 AngII. The OVLT has been proposed as a major sodium sensor in the brain and the hypertensive effects of AngII are exacerbated by high-salt intake. Therefore, the objective of this study was to investigate the role of the OVLT during AngII-induced hypertension in rats fed a high-salt diet. Male Sprague-Dawley rats underwent sham (Sham; n = 9) or OVLT lesion (OVLTx; 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 AngII infusion (10 ng/kg/min, i.v.), and a 3-day recovery period. MAP was significantly lower in OVLTx (97 ± 2 mmHg) compared to Sham (106 ± 1 mmHg) rats during the control period (P < 0.05). Moreover, the chronic pressor response to AngII was markedly attenuated in OVLTx rats. MAP increased 58 ± 3 mmHg in Sham rats by Day 10 of AngII compared to a 40 ± 7 mmHg increase in OVLTx 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 AngII-salt hypertension in the rat. Supported by HL076312.
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Collister et al. (2013) studied AngII-induced hypertension on a high-salt diet (n=17). OVLT lesion vs. Sham surgery was evaluated on Increase in mean arterial pressure (MAP) by Day 10 of AngII infusion (p=< 0.05). OVLT lesion attenuated the chronic pressor response to AngII in rats on a high-salt diet, with MAP increasing by 40 ± 7 mmHg compared to 58 ± 3 mmHg in sham rats.
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