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Effects of chronic dorsal hindbrain glucocorticoid receptor blockade on cardiovascular responses to acute stress
Author(s) -
Bechtold Andrea G,
Ver Kathy,
Scheuer Deborah A
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a771-a
Subject(s) - medicine , corticosterone , glucocorticoid , mean arterial pressure , endocrinology , antiglucocorticoid , heart rate , blockade , mifepristone , chronic stress , glucocorticoid receptor , blood pressure , anesthesia , receptor , hormone , biology , pregnancy , genetics
We previously reported that corticosterone can act in the dorsal hindbrain (DHB) to enhance the arterial pressure response to acute restraint stress. The current study was designed to determine the contribution of DHB glucocorticoid receptors (GRs) to the cardiovascular response to restraint stress. Rats were treated with small pellets of the GR antagonist Mifepristone (Mif) or sham (silastic) pellets implanted on the DHB of adult male Wistar‐Kyoto (WKY) or borderline hypertensive (BHR) rats. Arterial pressure and heart rate (HR) responses to acute restraint stress were measured via indwelling arterial catheters in conscious rats 14–17 days later. Baseline arterial pressure and the HR response to restraint stress were enhanced in BHR vs WKY rats (P<0.01). DHB Mif treatment decreased baseline mean arterial pressure (P<0.01) in BHR (DHB sham=127 ± 3 and DHB Mif=116 ± 3 mmHg), but not WKY rats (DHB sham=102 ± 3 and DHB Mif=103 ± 3 mmHg). However, the increase in arterial pressure in response to restraint was not significantly affected by DHB Mif treatment. Baseline heart rate was decreased in DHB Mif‐treated rats in both strains relative to DHB sham‐treated rats (P=0.028). In response to restraint stress HR increased to similar levels in DHB sham vs DHB Mif rats. Consequently, DHB Mif enhanced the increase in HR in response to acute restraint (P<0.01) in both rat strains. We conclude that blockade of the GR in the DHB reduces baseline arterial pressure in BHRs and reduces baseline HR in both BHR and WKYs, while enhancing the increase in HR in response to restraint. Supported by NIH Grant HL‐076807