Estrogen Reduces Cardiac Injury and Expression of β<sub>1</sub>-Adrenoceptor upon Ischemic Insult in the Rat Heart

Kam, Kenneth Wan Lung; Qi, Jian Song; Chen, Mai; Wong, Tak Ming

doi:10.1124/jpet.103.058339

Cited by 92 publications

(62 citation statements)

References 33 publications

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“…It has been shown that the estrogen administration could suppress the expression of ␤-adrenoceptor in rat cardiomyocytes (Kam et al, 2004). Our results indicated that the heart vtgAo1 expression could be regulated by both E2 and adrenergic agonist treatments.…”

Section: Figsupporting

confidence: 52%

Effects of adrenergic agonists on the extrahepatic expression of vitellogenin Ao1 in heart and brain of the Chinese rare minnow (Gobiocypris rarus)

Wang

et al. 2009

Aquatic Toxicology

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Section: Figsupporting

confidence: 52%

Effects of adrenergic agonists on the extrahepatic expression of vitellogenin Ao1 in heart and brain of the Chinese rare minnow (Gobiocypris rarus)

Wang

et al. 2009

Aquatic Toxicology

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“…In addition, the pattern of LV remodeling in female rats differs with a smaller increase in hypertrophy of the viable portions of the LV, but comparable LV cavity enlargement and systolic dysfunction. Despite similar infarct size, females have less abnormal LV diastolic filling compared with males (21). However, there are no reports to date of sex-related deterioration of cardiac function in post-MI mice.…”

mentioning

confidence: 89%

“…On the other hand, women are known to benefit from the cardioprotective actions of sex hormones which discontinue with the onset of menopause (21,24). Estrogen indirectly affects cardiac function by increasing elastin and decreasing collagen accumulation in blood vessels.…”

mentioning

confidence: 99%

Sex-related changes in cardiac function following myocardial infarction in mice

Shioura¹,

Geenen²,

Goldspink³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Shioura KM, Geenen DL, Goldspink PH. Sex-related changes in cardiac function following myocardial infarction in mice. Am J Physiol Regul Integr Comp Physiol 295: R528 -R534, 2008. First published June 11, 2008 doi:10.1152/ajpregu.90342.2008.-Recent awareness of cardiovascular diseases as a number one killer of the middle-aged women has prompted interest in sex differences leading to heart failure (HF). Therefore, we evaluated cardiac function in female and male mice following myocardial infarction (MI) using the Millar pressure-volume (P-V) conductance system in vivo, at time points corresponding to early (2 wk), late compensatory hypertrophy (4 wk), and decompensation (10 wk) to HF. A significant deterioration of the load dependent and independent hemodynamic measurements occurred in both female and male mice during the early phase of hypertrophy. Later, compensatory hypertrophy was marked by a normalization of volumes to control levels in females compared with males. The most notable differences between sexes occurred in the measurements of cardiac contractility during the decompensation to HF. In females, there was a significant improvement in contractility compared with males, which was apparent in the load-independent measurements of preload recruitable stroke work (10 wk post-MI, female ϭ 48.7 Ϯ 8.0 vs. male ϭ 25.2 Ϯ 1.8 mmHg, P Ͻ 0.05) and maximum dP/dt vs. maximum end-diastolic volume (10 wk post-MI, femaleϭ359 Ϯ 58 vs. maleϭ149 Ϯ 28 mmHg ⅐ s Ϫ1 ⅐ l Ϫ1 , P Ͻ 0.05). Despite these differences, there were no differences in the heart weight to body weight ratio and infarct size between the sexes. These data demonstrate that compensatory hypertrophy is associated with an improvement in contractility and a delayed decompensation to HF in females. However, compensatory hypertrophy in males appears to be undermined by a steady decline in contractility associated with decompensation to HF. contractility; pressure-volume loops DAMAGE TO THE MYOCARDIUM FOLLOWING myocardial infarction (MI) is associated with compensatory responses such as left ventricular (LV) hypertrophy and activation of the sympathetic nervous system to maintain cardiac output. Eventually, these changes are inadequate and contractile dysfunction along with subsequent chamber dilation underlie the transition to heart failure (HF) (11, 32).There are known sex-related responses to ischemia following myocardial infarction (MI) ranging from symptoms, diagnoses, preventions, courses of disease and outcomes of existing therapies. Women have more diverse symptoms than men, which are the major causes for delayed diagnoses and treatments (18,29,37). Also, women have poorer outcomes for a number of clinical complications such as a non-Q wave MI and invasive percutaneous transluminal coronary angioplasty (16,25). Despite these sex differences in incidence, manifestation and outcome, clinical data on cardiac function changes following MI are obscured by numerous baseline differences such as age, risk factors, symptoms, and the presence of coexisting disease...

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“…Several studies demonstrate that myocardial βAR-mediated positive inotropic responses are greater in male hearts than matched female hearts, and these differences are mediated by a lower level of β1AR-signalling. The reduced myocardial β1AR-signalling in ovulating females appears protective from myocardial insults including high catecholamines from stress stimuli as well as ischaemia-reperfusion injury 29,89 . Oophrectomy removes this protective effect in preclinical models, and is associated with an increase in β1AR-signalling and inotropy.…”

Section: Post-menopausal Hormonal Status and Catecholaminergic Responsesmentioning

confidence: 99%

Epidemiology and pathophysiology of Takotsubo syndrome

2015

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Takotsubo syndrome is an acute cardiac syndrome first described in 1990 and characterized by transient left ventricular dysfunction affecting more than one coronary artery territory, and often in a circumferential apical, mid-ventricular or basal distribution. A number of pathophysiological explanations for this syndrome with its intriguing appearance have been proposed, and there is a growing awareness that these are not mutually exclusive, and that the reversible apical myocardial dysfunction observed could result from more than one pathophysiological phenomenon. The pathophysiology of takotsubo syndrome is complex, with integration of both neuroendocrine physiology involving the cognitive centres of the brain and hypothalamic-pituitary-adrenal axis, and the cardiovascular responses to the sudden sympathetic activation and surge in circulating catecholamines. The latter have been explored in detail, starting with the histological findings at biopsy, with the multiple morphological changes seen in the myocardium matching those seen after established catecholamine cardiotoxic effects. Clinically, both the acute prognosis and recurrence rate are unfortunately worse than previously reported. It is clear that the modern cardiology community has much still to learn regarding the epidemiology and the underlying pathophysiology of this fascinating condition in order to improve diagnostic and treatment pathways. 3 Key points Approximately 2% of all patients presenting to the hospitals with suspected acute coronary syndrome are usually identified with takotsubo syndrome. There is a predominance in post-menopausal women compared to men or younger women. Both the acute and long-term mortality are higher than previously recognized.The cumulative incidence of recurrence increased from 1.2% at first 6 months to nearly 5% at 6 years, and there is no current evidence to support treatment with any specific to prevent recurrence. Systemic surges in catecholamines may cause vascular effects including acute coronary vasospasm and severe acute hypertension due to acute peripheral vasospasm followed by later peripheral vasodilation and hypotension. In the clinical setting, profound hypotension and cardiogenic shock is a common complication, however, it is not solely related to the extent of impairment of left ventricular (LV) systolic function, and thus probably relates in part to inappropriate peripheral vasodilation. Biopsies during acute takotsubo syndrome are characterized by multiple morphological changes that are similar to those after catecholamine cardiotoxic effects supporting a direct effect in addition to the vascular influences. The apical myocardium of the left ventricle has the highest density of β-adrenergic receptors (βAR), and is therefore most sensitive to circulating catecholamines.

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Estrogen Reduces Cardiac Injury and Expression of β₁-Adrenoceptor upon Ischemic Insult in the Rat Heart

Cited by 92 publications

References 33 publications

Effects of adrenergic agonists on the extrahepatic expression of vitellogenin Ao1 in heart and brain of the Chinese rare minnow (Gobiocypris rarus)

Effects of adrenergic agonists on the extrahepatic expression of vitellogenin Ao1 in heart and brain of the Chinese rare minnow (Gobiocypris rarus)

Sex-related changes in cardiac function following myocardial infarction in mice

Epidemiology and pathophysiology of Takotsubo syndrome

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Estrogen Reduces Cardiac Injury and Expression of β1-Adrenoceptor upon Ischemic Insult in the Rat Heart

Cited by 92 publications

References 33 publications

Effects of adrenergic agonists on the extrahepatic expression of vitellogenin Ao1 in heart and brain of the Chinese rare minnow (Gobiocypris rarus)

Effects of adrenergic agonists on the extrahepatic expression of vitellogenin Ao1 in heart and brain of the Chinese rare minnow (Gobiocypris rarus)

Sex-related changes in cardiac function following myocardial infarction in mice

Epidemiology and pathophysiology of Takotsubo syndrome

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Estrogen Reduces Cardiac Injury and Expression of β₁-Adrenoceptor upon Ischemic Insult in the Rat Heart