TY - JOUR T1 - Effects of estrogen on cardiovascular responses of premenopausal monkeys. JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 671 LP - 676 VL - 271 IS - 2 AU - J K Williams AU - Y D Kim AU - M R Adams AU - M F Chen AU - A K Myers AU - P W Ramwell Y1 - 1994/11/01 UR - http://jpet.aspetjournals.org/content/271/2/671.abstract N2 - Exogenous estrogen administration has been shown to reduce the risk of coronary heart disease in women. However, there are limited data in regard to the effects of estrogen on cardiovascular function and hemodynamics. This experiment sought to determine the effect of exogenous estrogen administration on systemic hemodynamic variables and cardiovascular responses to adrenergic and vasodilator agonists in premenopausal cynomolgus monkeys. Adult female monkeys were given weekly i.m. injections of 1) saline (control, n = 6), 2) estradiol cypionate (100 micrograms/kg, n = 6) or 3) estradiol cypionate (700 micrograms/kg, n = 5) for 6 weeks. A Swan-Ganz thermodilution catheter and arterial catheters were used to measure cardiovascular hemodynamic parameters in anesthetized monkeys before and during i.v. infusion of 1, 2, 4 and 8 micrograms kg-1 min-1 of isoproterenol, phenylephrine and nitroprusside. The high-dose estradiol group had a higher cardiac output index (0.6 +/- 0.1 versus 0.25 +/- 0.1 liter min-1 kg-1, mean +/- S.E.M.) and lower systemic vascular resistance index (628 +/- 160 versus 2630 +/- 872 dyne x cm-5 x sec-2 kg-1) than the control group at base line before infusion of agonists (P < .05). High-dose estradiol administration attenuated the mean arterial blood pressure, cardiac output and systemic vascular resistance changes in response to infusions of phenylephrine, isoproterenol and nitroprusside (P < .05 versus control). It was concluded that the administration of high-dose estradiol resulted in systemic arterial dilation, although changes in hemodynamic variables (systemic vascular resistance and cardiac output) were attenuated during adrenergic stimulation and vasodilation. ER -