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

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Abstract
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.