Cui Y.,Xian Jiaotong University |
Zhang S.-M.,National Key Discipline of Cell Biology |
Zhang Q.-Y.,National Key Discipline of Cell Biology |
Fan R.,National Key Discipline of Cell Biology |
And 11 more authors.
Journal of Applied Physiology
Modulation of intracellular calcium ([Ca- ],) transient in response to ß-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. ß-adrenoceptor responsiveness were then studied. Mean arterial blood pressure, left ventricular pressure (LVP), systolic function [maximum positive change in pressure over time (+dP/dt max)], and diastolic function [maximum negative change in pressure over time (-dP/dtmax.,)] 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/dtmax, myocyte contraction, intracellular [Ca 2+], transient, and L-type calcium current in response to ß-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/dt max were significantly reduced. LVP and ±dP/dtmax were significantly attenuated in the HLU group in response to isoproterenol administration. In the in vitro study, the ß-adrenoceptor density was unchanged. Effects of isoproterenol on electrically induced single-cell contraction and [Ca2-]i transient 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 Ca 2+ current and decreased [Ca2+]i transient cause the depressed responsiveness of the ß-adrenoceptor stimulation, which may be partially responsible for the depression of cardiac function. Copyright © 2010 the American Physiological Society. Source