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Hypertension, Vol 19, 355-361, Copyright © 1992 by American Heart Association

ARTICLES

Angiotensin II receptors in the solitary-vagal area of hypertensive rats

DP Healy and N Zhang
Department of Pharmacology, Mount Sinai School of Medicine, City University of New York, NY 10029.

Angiotensin II (Ang II) has been proposed to be an endogenous neuromodulator of the baroreceptor reflex at the level of the brain stem solitary-vagal area. Elevated activity of the brain Ang II system has been implicated in the development and maintenance of hypertension in spontaneously hypertensive rats and deoxycorticosterone acetate-salt hypertensive rats. In the present study, we sought to determine if Ang II receptors in the solitary-vagal area exhibited altered binding kinetics in spontaneously hypertensive rats or deoxycorticosterone-salt hypertensive rats. Ang II receptors were examined by quantitative autoradiographic analysis of iodine-125-labeled [Sar1,Ile8]Ang II binding in the solitary-vagal area in six groups of animals: 1) spontaneously hypertensive rats, 2) normotensive Wistar-Kyoto rats, 3) uninephrectomized rats, 4) uninephrectomized rats with a 1% solution of saline for drinking water, 5) uninephrectomized and deoxycorticosterone- treated rats, and 6) uninephrectomized and deoxycorticosterone-treated rats given a 1% solution of saline for drinking water. Blood pressure was significantly elevated in the spontaneously hypertensive rats and deoxycorticosterone-salt rats relative to control animals. There was a significant decrease in the binding affinity (increased KD) for 125I- [Sar1,Ile8]Ang II and a significant increase in the maximum binding density for 125I-[Sar1,Ile8]Ang II in the solitary-vagal area of spontaneously hypertensive rats relative to Wistar-Kyoto rats. Deoxycorticosterone-salt rats also exhibited significantly higher KD and maximum binding density values compared with controls. These results indicate that Ang II receptor binding is altered in the solitary-vagal area of two different models of experimental hypertension and suggest that these changes could contribute to the expression of the hypertensive state.

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