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Estrogen, progesterone, and testosterone: gonadal hormones modulate the autonomic and myogenic responses to treadmill locomotion in rats
Author(s) -
Rogers Jennifer,
Sheriff Don
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.20.5.a1401-c
The purpose of this study was to determine the effects of various sex factors, being male vs. female and plasma estradiol (E 2 ), progesterone (P), and testosterone (T), upon autonomic and myogenic components of cardiovascular regulation, with specific emphasis on P. Mean arterial pressure (MAP), terminal aortic blood flow (TAQ, ultrasonic flow probe), vascular conductance (VC, equals TAQ/MAP), and heart rate (HR) were determined in M, F, ovariectomized, and P‐supplemented ovariectomized Sprague‐Dawley rats ( n =7 per group) during treadmill locomotion (0, 7.5, and 15 m/min). Blood samples were analyzed for E 2 , P, and T (immunoassay). Regression analysis revealed that sex did not influence MAP, TAQ, VC, or HR but E 2 and P were each independently associated with lower MAP across the data set. E 2 was also associated with greater VC, TAQ, and HR. T was associated with decreased VC and TAQ. Autonomic inhibition (hexamethonium; 10 mg/kg BW, ia) increased the strength of the estrogenic effects to lower MAP and raise VC and TAQ, and eliminated the progestagenic lowering of MAP. L‐type Ca +2 channel activity inhibition (nifedipine; 10 mg/kg BW, ip) eliminated the remaining E 2 ‐dependent effects. Gonadal hormones may modulate the autonomic (E 2 , P) and myogenic (E 2 ) components of cardiovascular regulation in rats at rest and during treadmill locomotion, with the greatest hemodynamic effects exerted by E 2 . Supported by HL‐46314.