Single acute stress-induced progesterone and ovariectomy alter cardiomyocyte contractile function in female rats

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Abstract

Aim

To assess how ovarian-derived sex hormones (in particular progesterone) modify the effects of single acute stress on the mechanical and biochemical properties of left ventricular cardiomyocytes in the rat.

Methods

Non-ovariectomized (control, n = 8) and ovariectomized (OVX, n = 8) female rats were kept under normal conditions or were exposed to stress (control-S, n = 8 and OVX-S, n = 8). Serum progesterone levels were measured using a chemiluminescent immunoassay. Left ventricular myocardial samples were used for isometric force measurements and protein analysis. Ca ²⁺-dependent active force (F _active), Ca ²⁺-independent passive force (F _passive), and Ca ²⁺-sensitivity of force production were determined in single, mechanically isolated, permeabilized cardiomyocytes. Stress- and ovariectomy-induced alterations in myofilament proteins (myosin-binding protein C [MyBP-C], troponin I [TnI], and titin) were analyzed by sodium dodecyl sulfate gel electrophoresis using protein and phosphoprotein stainings.

Results

Serum progesterone levels were significantly increased in stressed rats (control-S, 35.6 ± 4.8 ng/mL and OVX-S, 21.9 ± 4.0 ng/mL) compared to control (10 ± 2.9 ng/mL) and OVX (2.8 ± 0.5 ng/mL) groups. F _active was higher in the OVX groups (OVX, 25.9 ± 3.4 kN/m ² and OVX-S, 26.3 ± 3.0 kN/m ²) than in control groups (control, 16.4 ± 1.2 kN/m ² and control-S, 14.4 ± 0.9 kN/m ²). Regarding the potential molecular mechanisms, F _active correlated with MyBP-C phosphorylation, while myofilament Ca ²⁺-sensitivity inversely correlated with serum progesterone levels when the mean values were plotted for all animal groups. F _passive was unaffected by any treatment.

C onclusion Stress increases ovary-independent synthesis and release of progesterone, which may regulate Ca ²⁺-sensitivity of force production in left ventricular cardiomyocytes. Stress and female hormones differently alter Ca ²⁺-dependent cardiomyocyte contractile force production, which may have pathophysiological importance during stress conditions affecting postmenopausal women.

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Most cited references 57

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Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Alan Rozanski, James Blumenthal, Jay A. Kaplan (1999)

Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

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Restraint stress in biobehavioral research: Recent developments.

Tatyana Buynitsky, David I Mostofsky (2009)

In the 15 years since the publication of two previous reviews on restraint stress much advancement has been made in the field. However, while previous reviews have focused mainly on drug effects, recent research has focused on broader implications in the health fields. This research has placed an increased emphasis on stress effects in physiological, immunological, endocrine and developmental processes as well as the impact of stress on numerous disorders. A major problem with our review was the inability to identify a large number of articles focusing on restraint and immobilization, since those keywords were often omitted from the title or not referred to within the body of the article. It seems likely that additional reviews with extended literature research of this field are required.

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Relaxation in rabbit and rat cardiac cells: species-dependent differences in cellular mechanisms.

J W Bassani, A Bassani, J W Bassani (1994)

The roles of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase and Na(+)-Ca2+ exchange in Ca2+ removal from cytosol were compared in isolated rabbit and rat ventricular myocytes during caffeine contractures and electrically stimulated twitches. Cell shortening and intracellular calcium concentration ([Ca2+]i) were measured in indo-1-loaded cells. Na(+)-Ca2+ exchange was inhibited by replacement of external Na+ by Li+. To avoid net changes in cell or SR Ca2+ load during a twitch in 0 Na+ solution, intracellular Na+ (Na+i) was depleted using a long pre-perfusion with 0 Na+, 0 Ca2+ solution. SR Ca2+ accumulation was inhibited by caffeine or thapsigargin (TG). Relaxation of steady-state twitches was 2-fold faster in rat than in rabbit (before and after Na+i depletion). In contrast, caffeine contractures (where SR Ca2+ accumulation is inhibited), relaxed faster in rabbit cells. Removal of external Na+ increased the half-time for relaxation of caffeine contractures 15- and 5-fold in rabbit and rat myocytes respectively (and increased contracture amplitude in rabbit cells only). The time course of relaxation in 0 Na+, 0 Ca2+ solution was similar in the two species. Inhibition of the Na(+)-Ca2+ exchange during a twitch increased the [Ca2+]i transient amplitude (delta[Ca2+]i) by 50% and the time constant of [Ca2+]i decline (tau) by 45% in rabbit myocytes. A smaller increase in tau (20%) and no change in delta[Ca2+]i were observed in rat cells in 0 Na+ solution. [Ca2+]i transients remained more rapid in rat cells. Inhibition of the SR Ca(2+)-ATPase during a twitch enhanced delta[Ca2+]i by 25% in both species. The increase in tau after TG exposure was greater in rat (9-fold) than in rabbit myocytes (2-fold), which caused [Ca2+]i decline to be 70% slower in rat compared with rabbit cells. The time course of [Ca2+]i decline during twitch in TG-treated cells was similar to that during caffeine application in control cells. Combined inhibition of these Ca2+ transport systems markedly slowed the time course of [Ca2+]i decline, so that tau was virtually the same in both species and comparable to that during caffeine application in 0 Na+, 0 Ca2+ solution. Thus, the combined participation of slow Ca2+ transport mechanisms (mitochondrial Ca2+ uptake and sarcolemmal Ca(2+)-ATPase) is similar in these species. We conclude that during the decline of the [Ca2+]i transient, the Na(+)-Ca2+ exchange is about 2- to 3-fold faster in rabbit than in rat, whereas the SR Ca(2+)-ATPase is 2- to 3-fold faster in the rat.(ABSTRACT TRUNCATED AT 400 WORDS)

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Author and article information

Journal

Journal ID (nlm-ta): Croat Med J

Journal ID (iso-abbrev): Croat. Med. J

Journal ID (publisher-id): CMJ

Title: Croatian Medical Journal

Publisher: Croatian Medical Schools

ISSN (Print): 0353-9504

ISSN (Electronic): 1332-8166

Publication date (Print): June 2014

Volume: 55

Issue: 3

Pages: 239-249

Affiliations

[1 ]University of Debrecen, Faculty of Medicine, Institute of Cardiology, Division of Clinical Physiology, Debrecen, Hungary

[2 ]University of Debrecen, Faculty of Medicine, Department of Laboratory Medicine, Debrecen, Hungary

[3 ]Cedars-Sinai Medical Center, International Research and Innovation Management Program, Los Angeles, CA, USA

[4 ]J. J. Strossmayer University of Osijek, School of Medicine, Department of Medical Biology, Osijek, Croatia

Author notes

Correspondence to:  Attila Borbély  University of Debrecen, Institute of Cardiology Division of Clinical Physiology Móricz Zsigmond krt. 22 H-4032 Debrecen, Hungary  borbelya@ 123456med.unideb.hu

Article

Publisher ID: CroatMedJ_55_0239

DOI: 10.3325/cmj.2014.55.239

PMC ID: 4049214

PubMed ID: 24891282

SO-VID: 014001bb-600a-4b27-a0d1-7bd3e73ea83b

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Single acute stress-induced progesterone and ovariectomy alter cardiomyocyte contractile function in female rats

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Abstract

Aim

Methods

Results

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Measurement of Glucocorticoid Receptor Signaling in Major Depression

Most cited references 57

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Restraint stress in biobehavioral research: Recent developments.

Relaxation in rabbit and rat cardiac cells: species-dependent differences in cellular mechanisms.

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