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Differential regulation of L-type Ca²⁺ channels in cerebral and mesenteric arteries after simulated microgravity in rats and its intervention by standing

Department of Aerospace Physiology, Fourth Military Medical University, Xi'an, China

Submitted 8 November 2006 ; accepted in final form 19 February 2007

This study was designed to clarify whether simulated microgravity can induce differential changes in the current and protein expression of the L-type Ca²⁺ channel (Ca_L) in cerebral and mesenteric arteries and whether these changes can be prevented by daily short-duration –G_x exposure. Tail suspension [hindlimb unloading (HU)] for 3 and 28 days was used to simulate short- and medium-term microgravity-induced deconditioning effects. Standing (STD) for 1 h/day was used to provide –G_x as a countermeasure. Whole cell patch-clamp experiments revealed an increase in current density of Ca_L of vascular smooth muscle cells (VSMCs) isolated from cerebral arteries of rats subjected to HU and a decrease in VSMCs from mesenteric arteries. Western blot analysis revealed a significant increase and decrease of Ca_L channel protein expression in cerebral and small mesenteric arterial VSMCs, respectively, only after 28 days of HU. STD for 1 h/day did not prevent the increase of Ca_L current density in cerebral arterial VSMCs, but it prevented completely (within 3 days) and partially (28 days) the decrease of Ca_L current density in small mesenteric arterial VSMCs. Consistent with the changes in Ca_L current, STD for 1 h/day did not prevent the increase of Ca_L expression in cerebrovascular myocytes but did prevent the reduction of Ca_L expression in mesenteric arterial VSMCs subjected to 28 days of HU. These data indicate that simulated microgravity up- and downregulates the current and expression of Ca_L in cerebral and hindquarter VSMCs, respectively. STD for 1 h/day differentially counteracted the changes of Ca_L function and expression in cerebral and hindquarter arterial VSMCs of HU rats, suggesting the complexity of the underlying mechanisms in the effectiveness of intermittent artificial gravity for prevention of postflight cardiovascular deconditioning, which needs further clarification.

postflight cardiovascular deconditioning; hindlimb unloading; vascular smooth muscle cells; calcium channels; countermeasure; intermittent artificial gravity