OVLT lesion decreases basal arterial pressure and the chronic hypertensive response to AngII in rats on a high-salt diet

Abstract

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.

Chemoreflex control of the cardiovascular system remains altered after recovery from low protein diet early in life

“…Among the possible outcomes, removal of peripheral chemoreflex may result in blood pressure increase, similar to previous results in malnourished rats (Penitente et al, 2007) or that increased pressor response could result from latent alterations corroborating with other factors to increase blood pressure levels late in life. Side studies, supporting the last hypothesis, showed that increased NaCl (2%) in the diet does not increase blood pressure by itself, but increase rostral ventrolateral medulla (RVLM) neurons excitability and lead to hypertension when combined with angiotensin II infusion (King et al, 2007;Stocker et al, 2010;Collister et al, 2013). Therefore, further studies are required to clarify the outcome of chemoreflex removal and interaction with baroreflex.…”

NaCl and osmolarity produce different responses in organum vasculosum of the lamina terminalis neurons, sympathetic nerve activity and blood pressure

“…Limited data are available regarding the specific contribution of OVLT neurons (Collister et al . ). In regard to an Na + versus NaCl‐specific mechanism, Na + supplementation with non‐Cl − anions does not raise BP in these models (Kotchen et al .…”

Organum Vasculosum of the Lamina Terminalis Detects NaCl to Elevate Sympathetic Nerve Activity and Blood Pressure

“…The contribution of OVLT neurons to salt-sensitive hypertension is limited with the exception of one investigation in which OVLT lesion attenuated angiotensin II plus high salt hypertension. 32 …”