Sex Differences in Susceptibility to Epinephrine-Induced Arrhythmias

Teplitz, Linda; Igić, Rajko; Berbaum, Michael L.; Schwertz, Dorie W.

doi:10.1097/01.fjc.0000179435.26373.81

Cited by 15 publications

(6 citation statements)

References 39 publications

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“…Interestingly, OVX has been shown to promote the spontaneous release of SR Ca 2+ [39]. This may explain previous observations that OVX increases arrhythmias in myocardial ischemia and during adrenergic stimulation [24, 107] and could, in part, explain the increase in risk for arrhythmias in post-menopausal women [82]. Taken together, these results suggest that oestrogen suppresses SR Ca 2+ release, limits SR Ca 2+ content and inhibits the spontaneous release of SR Ca 2+ .…”

Section: The Impact Of Sex Steroid Hormones On Cardiac Ec Coupling Mementioning

confidence: 73%

Sex differences in mechanisms of cardiac excitation–contraction coupling

Parks

Howlett

2013

Pflugers Arch - Eur J Physiol

116

109

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The incidence and expression of cardiovascular diseases differs between the sexes. This is not surprising, as cardiac physiology differs between men and women. Clinical and basic science investigations have shown important sex differences in cardiac structure and function. The pervasiveness of sex differences suggests that such differences must be fundamental, likely operating at a cellular level. Indeed, studies have shown that isolated ventricular myocytes from female animals have smaller and slower contractions and underlying calcium transients compared to males. Recent evidence suggests that this arises from sex differences in components of the cardiac excitation–contraction coupling pathway, the sequence of events linking myocyte depolarization to calcium release from the sarcoplasmic reticulum and subsequent contraction. The concept that sex hormones may regulate intracellular calcium at the level of the cardiomyocyte is important, as levels of these hormones decline in both men and women as the incidence of cardiovascular disease rises. This review focuses on the impact of sex on cardiac contraction, in particular at the cellular level, and highlights specific components of the excitation–contraction coupling pathway that differ between the sexes. Understanding sex hormone regulation of calcium homeostasis in the heart may reveal new avenues for therapeutic strategies to treat cardiac dysfunction and cardiovascular diseases.

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Section: The Impact Of Sex Steroid Hormones On Cardiac Ec Coupling Mementioning

confidence: 73%

Sex differences in mechanisms of cardiac excitation–contraction coupling

Parks

Howlett

2013

Pflugers Arch - Eur J Physiol

116

109

View full text Add to dashboard Cite

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“…Females were also found to have lower sympathetic activation in nonischemic CHF compared to males, whereas males demonstrated greater decline in the inotropic and chronotropic responses to β‐adrenergic stimulation with age in comparison to females (Turner et al, 1999). The susceptibility of animals to catecholamine‐induced arrhythmias was also dependent upon sex (Teplitz et al, 2005). Thus, it appears that responses of heart function to β‐AR stimulation under some conditions may be sex‐dependent, but the mechanisms underlying such differences in male and females are poorly understood.…”

mentioning

confidence: 99%

Gender related alterations of β‐adrenoceptor mechanisms in heart failure due to arteriovenous fistula

Dent

Tappia

Dhalla

2012

Journal Cellular Physiology

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This study was undertaken to determine gender related changes in different components of β-adrenoceptor (β-AR) system in response to arteriovenous fistula (AV-shunt), which is known to produce heart failure due to volume overload. AV-shunt was induced in male and female rats for 16 weeks by the needle technique; ovariectomized (OVX) rats treated with or without estrogen were also used. Although AV-shunt for 16 weeks produced cardiac hypertrophy in both sexes, male animals showed cardiac dysfunction whereas cardiac performance was maintained in females. Both β(1) -AR and β(2) -AR protein content and mRNA levels were decreased in male and increased in female hearts post-AV-shunt. The basal adenylyl cyclase (AC) activity was lower in the female heart; however, AC protein content and the increase in epinephrine (EPi)-stimulated AC activity were greater in the female AV-shunt group as compared to males. While AC V/VI and β-arrestin 2 mRNA levels were decreased in males, mRNA level for GRK2 was increased in females post-AV-shunt. In contrast to intact females, AV-shunt OVX animals showed depressed cardiac function, decreased β(1) -AR, β(2) -AR, and AC protein content, as well as reduced EPi-stimulated AC activity. Treatment of OVX rats with 17-β estradiol attenuated the AV-shunt induced changes in β-AR and AC protein content as well as cardiac dysfunction. These results reveal that β-AR signal transduction system in response to AV-shunt is downregulated in males and upregulated in females. Furthermore, estrogen appears to play an important role in the upregulation of β-AR mechanisms and the maintenance of cardiac function in AV-shunt females.

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“…For example, Du and colleagues (14), in the in situ perfused rat heart model with chronic infarction and failure, documented that ventricular arrhythmias, triggered by sympathetic activation, were less frequent in female than in male rats. Similarly, Teplitz and colleagues (46), in the pentobarbital sodium-anesthetized rat, reported that male rat hearts are more susceptible than female hearts to epinephrine-induced arrhythmias and more than twice as many male rats died following epinephrine treatment compared with females. Furthermore, ovariectomy increased the susceptibility to epinephrine-induced arrhythmias, whereas castration had a minimal effect in males.…”

mentioning

confidence: 88%

Sex differences to myocardial ischemia and β-adrenergic receptor blockade in conscious rats

Lujan

DiCarlo²

2008

American Journal of Physiology-Heart and Circulatory Physiology

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Lujan HL, DiCarlo SE. Sex differences to myocardial ischemia and ␤-adrenergic receptor blockade in conscious rats. Am J Physiol Heart Circ Physiol 294: H1523-H1529, 2008. First published February 8, 2008 doi:10.1152/ajpheart.01241.2007.-We recently documented sex differences in the susceptibility to reperfusion-induced sustained ventricular tachycardia and ␤-adrenergic receptor blockade in conscious rats. However, the effect of sex on ischemia-induced ventricular arrhythmias and ␤-adrenergic receptor blockade is underinvestigated. Therefore, we tested the hypothesis that gonadal hormones influence the ventricular arrhythmia threshold (VAT) induced by coronary artery occlusion as well as the response to ␤-adrenergic receptor blockade. The VAT was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Male and female intact and gonadectomized (GnX) rats were instrumented with a radiotelemetry device for recording arterial pressure, temperature, and ECG, as well as a Doppler ultrasonic flow probe to measure cardiac output and a snare around the left main coronary artery. The VAT was determined in conscious rats by pulling on the snare. The VAT was significantly longer in intact females (5.56 Ϯ 0.19) vs. intact males (4.31 Ϯ 0.14 min). This sex difference was abolished by GnX. Specifically, GnX decreased the VAT in females (4.55 Ϯ 0.22) and increased the VAT in males (5.14 Ϯ 0.30 min). Thus male sex hormones increase and female sex hormones decrease the susceptibility to ischemia-induced sustained ventricular tachycardia. ␤-Adrenergic receptor blockade increased the VAT in intact males and GnX females only. Thus gonadal hormones influence the response to ␤-adrenergic receptor blockade. Uncovering major differences between males and females in the pathophysiology of the cardiovascular system may result in sex-specific optimization of patient treatments. cardiovascular risks; arrhythmia ISCHEMIA-INDUCED TACHYARRHYTHMIAS that culminate in ventricular fibrillation (19) are the leading cause of death in industrially developed countries (36). Despite the clinical relevance of ischemia-induced arrhythmias, very little experimental data are available regarding sex-specific responses. Specifically, Humphreys and colleagues (20), in the pentobarbital sodium-anesthetized rat as well as isolated rat heart, reported that females experienced fewer arrhythmias than males during myocardial ischemia.Other investigators using different mechanisms to induce arrhythmias also reported a sex difference. For example, Du and colleagues (14), in the in situ perfused rat heart model with chronic infarction and failure, documented that ventricular arrhythmias, triggered by sympathetic activation, were less frequent in female than in male rats. Similarly, Teplitz and colleagues (46), in the pentobarbital sodium-anesthetized rat, reported that male rat hearts are more susceptible than female hearts to epinephrine-induced arrhythmias and more than twice as many male rats di...

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Sex Differences in Susceptibility to Epinephrine-Induced Arrhythmias

Cited by 15 publications

References 39 publications

Sex differences in mechanisms of cardiac excitation–contraction coupling

Sex differences in mechanisms of cardiac excitation–contraction coupling

Gender related alterations of β‐adrenoceptor mechanisms in heart failure due to arteriovenous fistula

Sex differences to myocardial ischemia and β-adrenergic receptor blockade in conscious rats

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