Antihypertensive effects of central ablations in spontaneously hypertensive rats

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Moreira, Thiago S.
Takakura, Ana C. [UNIFESP]
Colombari, Eduardo [UNIFESP]
Menani, Jose V.
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Moreira TS, Takakura AC, Colombari E, Menani JV. Antihypertensive effects of central ablations in spontaneously hypertensive rats. Am J Physiol Regul Integr Comp Physiol 296: R1797-R1806, 2009. First published April 1, 2009; doi:10.1152/ajpregu.90730.2008.-Commissural nucleus of the solitary tract (commNTS) lesions transitorily (first 5 days) reduce mean arterial pressure (MAP) in spontaneously hypertensive rats (SHR), and lesions of the tissue surrounding the anteroventral third ventricle (AV3V region) chronically reduce MAP in other models of hypertension. in the present study, we investigated the effects of combined AV3V+commNTS electrolytic lesions on MAP and heart rate (HR) in conscious SHR. Baseline MAP and HR were recorded in male SHR before and for the next 40 days after sham or AV3V lesions combined with sham or commNTS lesions. the AV3V lesions produced no change in MAP in SHR, while commNTS lesions reduced MAP acutely (121 +/- 2 to 127 +/- 3 mmHg in the 1st and 5th days, respectively, vs. prelesion: 192 4 mmHg) but not chronically (from 10 to 40 days). However, combined AV3V+commNTS lesions reduced MAP of SHR chronically (119 +/- 2 to 161 +/- 4 mmHg, in the 1st and 40th day, respectively, vs. prelesion levels: 186 +/- 4 mmHg) or sham-lesioned SHR (187 +/- 4 to 191 +/- 6 mmHg). Sympathetic and angiotensinergic blockade produced less reduction in MAP in SHR with AV3V+commNTS-lesions, and there was no relationship between changes on water and food intake, body weight, or urinary excretion produced by AV3V+commNTS lesions with the changes in MAP. the present findings suggest that in the absence of the commNTS, the AV3V region contributes to the hypertension observed in SHR by mechanisms that appear to involve enhanced angiotensinergic and sympathetic activity.
American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 296, n. 6, p. R1797-R1806, 2009.