Progesterone induces endothelium-independent relaxation of rabbit coronary artery in vitro

Jiang, Canwen; Sarrel, Philip M.; Lindsay, David; Poole‐Wilson, Philip A.; Collins, Peter

doi:10.1016/0014-2999(92)90524-8

Cited by 125 publications

(83 citation statements)

References 17 publications

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“…Regarding the porcine coronary arteries, progesterone has been shown to relax pre-contracted coronary segments or isolated smooth muscles (Crews & Khalil, 1999;Murphy & Khalil, 1999;Teoh & Man, 1999). A similar relaxing effect of progesterone has been demonstrated in pre-contracted coronary artery segments obtained from the dog and the rabbit (Jiang et al 1992;Lamping & Nuno, 1996). Another new finding of the present investigation was the demonstration that progesterone infusion did not significantly affect left ventricular dPÏdtmax, which in the absence of changes in heart rate, arterial blood pressure and filling pressures of the heart indicated no change in ventricular contractility (Furnival et al 1970).…”

Section: Discussionmentioning

confidence: 70%

“…In contrast, there has been little information on the acute effect of progesterone on coronary blood flow. For instance, progesterone was found to induce a coronary vasoconstriction in the isolated rabbit heart (Raddino et al 1989), but to relax pre-contracted rabbit coronary artery preparations (Jiang et al 1992). Progesterone has also been found to relax precontracted pig coronary artery strips (Crews & Khalil, 1999) or rings (Teoh & Man, 1999) and pig coronary smooth muscles (Murphy & Khalil, 1999).…”

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confidence: 99%

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The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Molinari

Battaglia

Grossini

et al. 2001

Experimental Physiology

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The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h−1 of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h−1. The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of Nω‐nitro‐L‐arginine methyl ester (L‐NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L‐NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide.

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Section: Discussionmentioning

confidence: 70%

mentioning

confidence: 99%

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Molinari

Battaglia

Grossini

et al. 2001

Experimental Physiology

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“…13 Other studies, however, have shown that progesterone induces endothelium-independent relaxation of rabbit coronary artery. 28 The cause of the difference between the results is not clear but may be related to differences in experimental animal species. There have also been inconsistent reports on the effects of testosterone on vascular reactivity.…”

Section: Discussionmentioning

confidence: 98%

Antagonistic Effects of 17β-Estradiol, Progesterone, and Testosterone on Ca ²⁺ Entry Mechanisms of Coronary Vasoconstriction

Crews

Khalil

1999

ATVB

152

185

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Abstract-The clinical observation that coronary artery disease is more common in men and postmenopausal women than in premenopausal women has suggested cardioprotective effects of female sex hormones including hormone-mediated coronary vasodilation. The purpose of this study was to investigate whether the sex hormone-induced coronary relaxation is caused by inhibition of Ca 2ϩ mobilization into coronary smooth muscle. Key Words: sex hormones Ⅲ calcium Ⅲ coronary Ⅲ contraction C oronary artery disease is one of the most common and costly diseases. Coronary vasospasm and subsequent occlusion are frequently associated with increased cardiovascular risk and may lead to myocardial infraction and death. 1 Clinical data suggest that the incidence of coronary heart disease is greater in men and postmenopausal women compared with premenopausal women. This is believed to be because of putative cardioprotective effects of the female sex hormone estrogen. The cardioprotective effects of estrogen have been explained by several mechanisms, including modification of lipid and carbohydrate metabolism, 2 modification of the composition of circulating lipoproteins, 3-5 and changes in blood coagulation, 6 as well as direct cardiovascular protective effects on hemodynamics. 7 Estrogens are vasodilators. For example, it has been reported that subcutaneous administration of ␤-estradiol in female guinea pigs reversibly and significantly lowers both the resting systolic blood pressure and the peak systolic blood pressure induced by a pressor challenge of norepinephrine. 8 Also intravenous infusion of estrogen in ovariectomized nonpregnant sheep has been shown to cause a significant increase in cardiac output and a decrease in systemic vascular resistance whereas local application of estrogen to the uterine artery only causes uterine vasodilation and increased uterine blood flow. 9 The vasodilator effects of estrogen have also been observed in normal coronary arteries. 10 The vascular endothelium has been suggested to play a role in mediating the estrogen-induced vasodilation. However, indomethacin does not affect the 17␤-estradiol-induced relaxation in endothelium-intact coronary arteries, 10 indicating that the release of vasodilator prostanoids is not involved in the 17␤-estradiol-induced coronary relaxation in vitro. Furthermore, estrogen causes vasodilation in deendothelialized rabbit coronary artery precontracted by endothelin-1, prostaglandin F 2␣ (PGF 2␣ ), and high-potassium depolarizing solution 10 suggesting that the estrogen-induced inhibition of vascular tone has an endothelium-independent component that involves direct action on vascular smooth muscle. 5,11,12

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“…On the other hand, sex hormones are among the endogenous compounds with vasodilator properties. The female sex hormones estradiol and progesterone, as well as the androgenic hormone testosterone, have shown vasodilator activity (3,8,9,17,26). Some of the vascular effects of estrogen are of nongenomic origin and are mediated by estrogen receptors localized into caveolae in endothelial cells (24).…”

mentioning

confidence: 99%

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta

Castillo

Ceballos²,

Rodríguez³

et al. 2006

American Journal of Physiology-Cell Physiology

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Progesterone induces endothelium-independent relaxation of rabbit coronary artery in vitro

Cited by 125 publications

References 17 publications

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Antagonistic Effects of 17β-Estradiol, Progesterone, and Testosterone on Ca ²⁺ Entry Mechanisms of Coronary Vasoconstriction

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta

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Progesterone induces endothelium-independent relaxation of rabbit coronary artery in vitro

Cited by 125 publications

References 17 publications

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

The Effect of Progesterone on Coronary Blood Flow in Anaesthetized Pigs

Antagonistic Effects of 17β-Estradiol, Progesterone, and Testosterone on Ca 2+ Entry Mechanisms of Coronary Vasoconstriction

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta

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Antagonistic Effects of 17β-Estradiol, Progesterone, and Testosterone on Ca ²⁺ Entry Mechanisms of Coronary Vasoconstriction