Captopril, blood pressure, and vascular reactivity in psychosocial hypertensive mice

Sustained hypertension can be induced in CBA mice by exposure to social stress in a complex population cage. At 1 week the hypertension is not altered by short-term administration of captopril, but after 1 month the mice have increased vascular sensitivity to angiotensin II, and shortterm administration of captopril rapidly abolishes the hypertension. The present study was performed to determine whether captopril treatment (oral dosage via drinking water, 4 mg/kg body weight) started 10 days before social stress and continued for 2 months could prevent the hypertension and altered vascular responsiveness. One week after being placed in the cages, the captopril-treated mice showed the usual rise in blood pressure (20 mm Hg) but then became nearly normotensive after 2 months. At this time the hindquarter vascular bed was pump perfused at a constant flow with plasma substitute. Threshold constrictor responses to angiotensin II were elicited at a significantly lower dose in the hindquarters of hypertensive mice than in those of both groups of normotensive control mice (untreated and captopril treated), indicating increased vascular sensitivity. Threshold responses to angiotensin II in captopril-treated caged mice were shifted to the right compared with hypertensive mice and did not differ significantly from normotensive control values. Maximal pressor responses to angiotensin II were greater in the hindquarters of hypertensive mice than in those of normotensive control mice and captopril treated caged mice. We concluded that captopril treatment prevented the sustained hypertension and vascular hyperresponsiveness to angiotensin II in this psychosocial model of hypertension.