coronary vasospasm/progesterone

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Coronary artery spasm: a hypothesis on prevention by progesterone.

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The mechanism of coronary artery spasm has been hypothesized as follows: the dormant gene of the smooth muscle of the human coronary artery is identical or similar to the active gene of the smooth muscle of ductus arteriosus, but can be activated by estrogen. The activation could be preventable by

The mechanism of coronary artery spasm: roles of oxygen, prostaglandins, sex hormones and smoking.

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A reduced oxygen supply to the heart causes coronary vasodilatation in the first instance. But if the hypoxia is severe or prolonged, the dilatation passes off and coronary vasospasm develops leading to a vicious circle with a further reduction of myocardial oxygenation. The spasm is associated with

Medroxyprogesterone interferes with ovarian steroid protection against coronary vasospasm.

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Cardiovascular disease, the major cause of death in post-menopausal women, can be reduced by replacement of ovarian steroid hormones. To compare medroxyprogesterone with progesterone as the progestin in hormone replacement therapy from the standpoint of coronary artery vasospasm, we treated

Ca2+ release mechanism of primate drug-induced coronary vasospasm.

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Cellular mechanisms of protection against drug-stimulated coronary vasospasm were studied by multiweek estrogen plus progesterone (P) vs. medroxy-progesterone acetate (MPA) treatments by measuring intracellular Ca2+ and protein kinase C (PKC) signals. Ovariectomized monkeys (OVX) were treated by

In vitro modulation of primate coronary vascular muscle cell reactivity by ovarian steroid hormones.

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Susceptibility to drug-induced coronary vasospasm in rhesus monkeys increases after removal of the ovaries and can be normalized by adding back physiological levels of estradiol-17ss (E2) and/or natural progesterone (P) in vivo as reported recently by our group. Furthermore, the reactivity status

Nomegestrol acetate and vascular reactivity: nonhuman primate experiments.

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Prevention of coronary artery disease has been recognized as a major benefit of estrogen replacement therapy (ERT) in postmenopausal women. However, endometrial hyperplasia induced by unopposed ERT has raised important safety concerns. Progesterone or synthetic progestins have been used in combined

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