ABSTRACT
The aim of the present study was to examine the changes in the function of voltage-dependent calcium channels (VDC) of vascular smooth muscle cells (VSMCs) isolated from small mesenteric arteries of rats subjected to 1-week or 4-week simulated weightlessness. The whole-cell recording mode was used to record current densities and Ba(2+) was used as charge carrier. Curves and fitting parameters describing steady-state activation and inactivation characteristics of VDC were thus obtained. The inward currents recorded from the VSMCs of small mesenteric arteries were mainly the Ba(2+) currents through the long-lasting type VDC (L-VDC). Compared with that of the control rats, the L-VDC current density of VSMCs from small mesenteric arteries showed a trend toward a decrease in the rats after 1-week , while a significant decrease was observed in the rats after 4-week simulated weightlessness. However, there were no significant differences in the opening and closing rates of L-VDCs, the position of steady-state activation and inactivation curves, and in the parameters, V(0.5) and k, between either of the two groups and its respective control group. The membrane capacitance and the reversal potential of the VSMCs from the small mesenteric arteries of rats after simulated weightlessness also showed no significant changes. These findings suggest that the decreased function of the L-VDC in hindquarter VSMCs might be one of the electrophysiological mechanisms that mediate the depressed vasoreactivity and atrophic change in hindquarter arteries during adaptation to simulated weightlessness in rats.
Subject(s)
Animals , Male , Rats , Calcium Channels , Physiology , Hindlimb Suspension , Membrane Potentials , Physiology , Mesenteric Arteries , Cell Biology , Physiology , Muscle, Smooth, Vascular , Cell Biology , Metabolism , Physiology , Patch-Clamp Techniques , Rats, Sprague-Dawley , Weightlessness Simulation , MethodsABSTRACT
The aim of the present study was to investigate the changes in single-channel currents of large conductance calcium-activated potassium channels (BK(Ca) channels) in cerebral vascular smooth muscle cells (VSMCs) of rats after 1-week simulated microgravity. Sprague-Dawley rats were subjected to tail-suspension (SUS) to simulate cardiovascular deconditioning due to microgravity. Cytosolic calcium ([Ca(2+)](i)) was examined by laser-scanning confocal microscopy with calcium-sensitive-dye Fluo-3/AM as fluorescent probe. Single-channel currents of BK(Ca) channels were measured with cell-attached membrane patches bathed in symmetrical high potassium solution. The [Ca(2+)](i)i level was significantly higher in cerebrovascular myocytes of SUS than that of control (CON) rats. The probability of open (Po) and the mean open time (To) of BK(Ca) channels in cerebral VSMCs significantly increased in SUS as compared with CON. However, there were no significant differences in the unitary conductance and mean close time (Tc) between the two groups. The results obtained suggest that both the elevated [Ca(2+)](i) and enhanced single-channel activities of BK(Ca) channels in cerebral VSMCs might be among the electrophysiological mechanisms that mediate the increased vasoreactivity and hypertrophic change in cerebral arteries during adaptation to simulated microgravity in rats.
ABSTRACT
The changes in potassium currents of vascular smooth muscle cells (VSMCs) isolated from saphenous arteries and the 2nd-6th order branches of the mesenteric arteries of 4-week tail-suspended rats (SUS) were examined using whole cell patch clamp technique. The resting potential (RP) of the VSMCs from SUS group was more negative compared with that of the control group (CON).The whole cell potassium current densities of VSMCs isolated from the saphenous arteries and small mesenteric arteries in SUS group were significantly larger than those of the CON group.The BK(Ca) and K(V) current densities of VSMCs from saphenous arteries and small mesenteric arteries from SUS group were also significantly larger than those from the CON group.It is speculated that the hyperpolarization of VSMCs and decreased calcium influx through voltage-dependent calcium channels might be one of the electrophysiological mechanisms involved in the depressed vasoreactivity of hindquarter arteries induced by simulated weightlessness.