Increased vascular sensitivity to angiotensin ii in psychosocial hypertensive mice.

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Abstract
CBA mice develop hypertension when placed in complex population cages that facilitate social interactions and competition for territory. After 1 month, these mice have normal plasma renin levels, but blockade of converting enzyme lowers blood pressure to normal. To test the possibility that this normal-renin hypertension is caused by enhanced pressor responsiveness to angiotensin II (AII), we examined the effects of AII on hindquarter and renal vasculatures from 13 hypertensive and 13 normotensive mice. Both vascular beds were pump-perfused at a constant flow with plasma substitute. Optimal perfusion flows and basal pressures were similar in hindquarter (8 ml/100 g/min; 60 mm Hg) and renal vasculatures (130 ml/100 g/min; 50 mm Hg) from normotensive and hypertensive mice. Threshold constrictor responses to AII were elicited at a significantly lower dose in both vasculatures of hypertensive mice than in those of normotensive mice. Maximal pressor responses to AII were greater in the hindquarters of hypertensive mice than in those of normotensive mice, but were not different in the renal vasculatures of the two groups. Vasoconstrictor sensitivity to norepinephrine was also increased in the hindquarters of hypertensive mice; however, the changes in threshold and maximal pressor response were less than for AII. Responsiveness to norepinephrine in the renal vasculatures of hypertensive mice was not different from that in the kidneys of normotensive mice. We conclude that the hyperresponsiveness to AII in the resistance vessels plays an important role in maintaining elevated blood pressure in this psychosocial model of hypertension.