Chronic activation of dorsal hindbrain corticosteroid receptors augments the arterial pressure response to acute stress.
Augmented cardiovascular responses to acute stress can predict cardiovascular disease in humans. Chronic systemic increases in glucocorticoids produce enhanced cardiovascular responses to psychological stress; however, the site of action is unknown. Recent evidence indicates that glucocorticoids can act within the dorsal hindbrain to modulate cardiovascular function. Therefore, we tested the hypothesis that the endogenous glucocorticoid corticosterone can act in the dorsal hindbrain to enhance cardiovascular responses to restraint stress in conscious rats. Adrenal-intact animals with indwelling arterial catheters were treated for 4 or 6 days with 3- to 4-mg pellets of corticosterone or silastic (sham pellets) implanted on the dorsal hindbrain surface. Corticosterone pellets were also implanted either on the surface of the dura or subcutaneously to control for the systemic effects of corticosterone (systemic corticosterone). The integrated increase in arterial pressure during 1 hour of restraint stress was significantly (P<0.05) greater in dorsal hindbrain corticosterone (912+/-98 mm Hg per 60 minutes) relative to dorsal hindbrain sham (589+/-57 mm Hg per 60 minutes) or systemic corticosterone (592+/-122 mm Hg per 60 minutes) rats. The plasma glucose response after 10 minutes of stress was also significantly higher in dorsal hindbrain corticosterone-treated rats relative to both other groups. There were no significant between-group differences in the heart rate or corticosterone responses to stress. There were no differences in baseline values for any measured parameters. We conclude that corticosterone can act selectively in the dorsal hindbrain in rats with normal plasma corticosterone levels to augment the arterial pressure response to restraint stress.
Scheuer
Deborah A
DA
School of Medicine, University of Florida, Gainesville 32610-0274, USA. scheuerd@ufl.edu
Bechtold
Andrea G
AG
Vernon
Kathy A
KA
D000311:Adrenal Glands / Q000503:physiopathology; D000315:Adrenalectomy; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002319:Cardiovascular System / Q000503:physiopathology; D003345:Corticosterone / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D011987:Receptors, Steroid / Q000378:metabolism*; D012149:Restraint, Physical; D012249:Rhombencephalon / Q000187:drug effects / Q000378:metabolism*; D013312:Stress, Physiological / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D013997:Time Factors
D001786:Blood Glucose; D011987:Receptors, Steroid; D003345:Corticosterone