Affiliation:
1. Departments of 1Pathophysiology and
2. Physiology, National Key Discipline of Cell Biology, and
3. Department of Cardiac Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China
Abstract
Modulation of intracellular calcium ([Ca2+]i) transient in response to β-adrenoceptor stimulation in the hearts of hindlimb unweighted (HLU) rats during simulated weightlessness has not been reported. In the present study, we adopted the rat tail suspension for 4 wk to simulate weightlessness. Effects of simulated microgravity on β-adrenoceptor responsiveness were then studied. Mean arterial blood pressure, left ventricular pressure (LVP), systolic function [maximum positive change in pressure over time (+dP/d tmax)], and diastolic function [maximum negative change in pressure over time (−dP/d tmax)] were monitored during the in vivo experiment. β-Adrenoceptor density was quantitated by radioactive ligand binding. Single rat ventricular myocyte was obtained by enzymatic dissociation method. ±dP/d tmax, myocyte contraction, intracellular [Ca2+]itransient, and L-type calcium current in response to β-adrenoceptor stimulation with isoproterenol were measured. Compared with the control group, no significant changes were found in heart weight, body weight, and mean arterial blood pressure, whereas LVP and ±dP/d tmaxwere significantly reduced. LVP and ±dP/d tmaxwere significantly attenuated in the HLU group in response to isoproterenol administration. In the in vitro study, the β-adrenoceptor density was unchanged. Effects of isoproterenol on electrically induced single-cell contraction and [Ca2+]itransient in myocytes of ventricles in HLU rats were significantly attenuated. The enhanced L-type Ca2+current elicited by isoproterenol in cardiomyocytes was significantly decreased in the HLU group. The above results indicate that impaired function of L-type Ca2+current and decreased [Ca2+]itransient cause the depressed responsiveness of the β-adrenoceptor stimulation, which may be partially responsible for the depression of cardiac function.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
13 articles.
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