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  • Title: Progesterone stimulates cardiac muscle protein synthesis via receptor-dependent pathway.
    Author: Goldstein J, Sites CK, Toth MJ.
    Journal: Fertil Steril; 2004 Aug; 82(2):430-6. PubMed ID: 15302294.
    Abstract:
    OBJECTIVE: To examine the effect of ovarian hormones on the regulation of cardiac growth. DESIGN: Ovariectomized rat model with replacement of 17beta-estradiol (E(2)) and progesterone (P). SETTING: University research laboratory. PATIENT(S): Female Sprague-Dawley rats (7-8 weeks old). INTERVENTION(S): Rats were separated into five groups: [1] sham-operated (S; n = 6), [2] ovariectomized plus placebo (OVX; n = 8), [3] OVX plus 17beta-E(2) (OVX+E(2); n = 8), [4] OVX plus P (OVX+P; n = 8), and [5] OVX+E(2)+P (n = 7). MAIN OUTCOME MEASURE(S): Cardiac muscle protein synthesis rates, steroid hormone receptor protein expression, and plasma volume. RESULT(S): Cardiac protein synthesis was greater in OVX+P (mean +/- SE; 11.4 +/- 1.5% per day) rats compared with S (5.9 +/- 0.6%/day), OVX (6.9 +/- 0.5%/day), OVX+E(2) (5.2 +/- 0.4%/day), and OVX+E(2)+P (6.8 +/- 0.3%/day) groups. Treatment of OVX+P rats with the P receptor antagonist RU 486 (n = 9) reduced protein synthesis rates to control levels (7.5 +/- 0.5% per day), indicating that P regulates cardiac protein metabolism through a receptor-dependent pathway. Both P and estrogen receptors were found in cardiac tissue homogenates, suggesting the possibility of direct effects of ovarian hormones on the heart. Progesterone replacement had an additional effect of increasing plasma volume. Rats in the OVX+P group had a 20% greater plasma volume compared with animals in the S group (5.24 +/- 0.22 vs. 4.19 +/- 0.26 mL/100 g). This effect of P replacement to increase plasma volume was not blocked by RU 486 (5.01 +/- 0.24 mL/100 g), suggesting that volume expansion was not solely responsible for the effects of P on cardiac protein synthesis. CONCLUSION(S): Our findings indicate a role for ovarian hormones in the regulation of cardiac growth in female rats.
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