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Experiments were performed to investigate the effects of estrogen on the responses to stress of the adrenocorticotropic hormone (ACTH), cortisol, epinephrine (Epi) and norepinephrine (NE) in ovariectomized ewes. In particular, the responses to the audiovisual and hypoglycemic stress in the follicular and luteal phases of the estrous cycle were described. The findings suggest that the administration of estrogen attenuated the glucocorticoid reaction to audiovisual and hypoglycemic stress, while the responses of ACTH, Epi and NE were heightened during the luteal phase.

The effects of adenosine 3',5'-cyclic monophosphate (cAMP) on glucocorticoid action and glucocorticoid receptor (GR) function were investigated in neonatal rat cardiomyocytes. DNA and protein levels were monitored and used as a function of cardiomyocyte growth. The results revealed that glucocorticoids inhibit the growth of cardiomyocytes. The effect of glucocorticoids was mediated by cAMP, suggesting that cAMP downregulates GR in cardiomyocytes.

Objective: Increased cardiac collagen is seen in uninephrectomised rats made hypertensive by aldosterone infusion and high salt, with the possibility of a direct effect of aldosterone at the level of the cardiac fibroblast. The aim of this study was to examine the effects of aldosterone, glucocorticoids, and angiotensin II on collagen production in a series of rat cardiac fibroblast cultures. Methods: Cardiac fibroblast cultures were established from neonatal and adult rats of Sprague-Dawley, WKY, and SHR strains, with collagen synthesis measured by incorporation of [3H]proline into collagen. Cells were grown alone or co-cultured with cardiomyocytes, and exposed to aldosterone, glucocorticoids, or angiotensin II for 24-28 h before determination of [3H]proline incorporation. Results: Aldosterone did not affect production of collagen; in contrast, angiotensin II increased, and the glucocorticoid agonist RU28362 suppressed, collagen production in cultured cardiac fibroblasts in the various rat strains. Conclusions: Aldosterone does not exert a direct effect on collagen synthesis in rat cardiac fibroblasts grown in culture. The increased cardiac collagen observed in vivo in aldosterone treated, salt loaded rats may thus represent secondary effects of aldosterone in this model.Cardiovascular Research 1994;28:1863-1867 [ABSTRACT FROM PUBLISHER]

This paper addresses whether the enhanced left ventricular (LV) contractility and heart rate, seen in transgenic mice overexpressing beta -adrenergic receptor in the heart, might raise the incidence of LV rupture after myocardial infarct. Transgenic and wild-type mice underwent left coronary artery occlusion. Postinfarct deaths that occurred 1-7 days after surgery were analyzed. Hemodynamics, morphologic parameters, and collagen content in the LV were determined. A significantly lower incidence of LV rupture was observed in transgenic than in wild-type mice 3-5 days after myocardial infarct (2.5 versus 19.7%, p < 0.05), despite a similar infarct size between the two groups and better hemodynamic function in transgenic mouse hearts. Morphologic analysis showed a more severe infarct expansion in wild-type versus transgenic mice or in mice dying of rupture versus those that died of acute heart failure. Collagen content was higher in the LV of sham-operated transgenic than wild-type mice (p < 0.01) with both type I and type III collagen elevated. Such difference in collagen content between transgenic and wild-type mice was maintained in noninfarcted and infarcted LV. In conclusion, transgenic mice overexpressing beta -adrenergic receptor had a lower risk of cardiac rupture during the acute phase after infarction despite the markedly enhanced LV contractility and heart rate. As a hyperdynamic function due to beta-adrenergic activation would likely increase the risk of cardiac rupture and infarct expansion, the lack of rupture in this transgenic mouse model suggests that the interstitial collagen level is a more important factor than functional status in the pathogenesis of rupture and infarct expansion.