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Hypertension, Vol 3, 544-550, Copyright © 1981 by American Heart Association

ARTICLES

Effects of bromocriptine on responses to stress in spontaneously hypertensive rats

JR Sowers

Treatment of 2-month-old spontaneously hypertensive rats (SHR) and age- matched Wistar-Kyoto (WKY) normotensive controls with the dopamine agonist, bromocriptine, for 7 days significantly affected hormonal responses to immobilization stress in both groups. However, basal blood pressures and pressor responses to immobilization stress were significantly reduced only in SHR. Basal levels of catecholamines were similar in the two groups of rats, but catecholamine responses to immobilization stress following saline (vehicle) treatment were marked greater in SHR; following bromocriptine treatment for 7 days, catecholamine responses were similar in the two groups. Basal serum prolactin levels and prolactin responses to immobilization were greater in SHR after saline treatment; after bromocriptine, they were similar in the two groups. Basal plasma renin activity (PRA)and PRA responses to immobilization were significantly less in SHR following saline treatment; after bromocriptine treatment these responses were paradoxically greater in SHR without being significantly changed in WKY. Basal levels of plasma aldosterone and corticosterone following saline were significantly greater, but responses to immobilization less, in SHR. Bromocriptine treatment decreased aldosterone and corticosterone responses to stress in WKY but paradoxically increased these responses in SHR. These results suggest that increased pressor responses to stress are dependent on heightened sympathetic nerve activity, perhaps secondary to decreased central dopaminergic activity. Increased basal prolactin levels and stress-mediated prolactin responses may be related to decreased central dopaminergic activity. Paradoxical PRA, plasma aldosterone, and corticosterone responses to stress following bromocriptine suggest altered dopaminergic modulation of these hormones in the SHR.