ObjectiveTo explore the distribution of sodium pump α-subunit isoforms at both mRNA and protein level in normal Sprague-Dawley(SD) rats. MethodsWith RT-PCR (reverse transcription-polymerase chain reaction) and immunohistochemical assay, sodium pump α1-, α2-, andα3-subunit isoforms were detected at mRNA level and protein level in the myocardium, liver, kidney, adrenal gland, aortic smooth muscle, pituitary and hypothalarnus in normal rats. ResultsSodium pump α1-, α2-, and α3-subunit isoforms distribute in a tissue-specific fashion in normal SD rats. α1 and α2 are the main isoforms and α3 is much less in myocardium. α1 is more than α2 or α3 isoform at mRNA level in liver, while all of α1-,α2-, and α3-isoform are less expressed at protein level. α1-isoform is abundantly but α2 and α3 are less expressed both at mRNA and protein levels in kidney. α2isoform is just more than α1 and α3 isoforms in aortic smooth muscle. All of three isoforms are expressed abundantly in pituitary. α2 and α3 are more and α1 is less expressed in hypothalamus. ConclusionThe results of this study have revealed the distribution of sodium pump α-subunit isoforms at both mRNA and protein level in normal SD rats, which might be helpful for the further studying the physiologic and pathologic roles of sodium pump.

Objective:To test the effects of propofol on intracellular calcium free concentration ([Ca~(2+)]i) and inositol 1,4,5-triphosphate (IP_3) biological synthesis induced by norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in aortic smooth muscle cells (ASMC)of rats for the mechanism of relaxtion of propofol on vascular smooth muscle.Method: Using the flurospectrophotometry and Fura-2/AM loading method,the changes of [Ca~(2+)]i levels in primary culture ASMC were measured,and using the specific, IP_3 assay system and isotope radioactive protein binding experiment IP_3 production levels in aortic smooth muscle were measured. Result:The baselines of [Ca~(2+)]i was decreased when primary culture ASMC was pretreated with propofol in 72 hours. Propofol inhibited [Ca~(2+)]i increase induced by NE and 5-HT in dose-dependent way. With extracellular calcium free or calcium channel blocker(Verapamil),inhibition of propofol on NE and 5-HT increasing [Ca~(2+)]i levels were decreased,but could not be cancelled. Propofol depressed IP_3 biological synthesis induced by NE and 5-HT in dose-dependent way. Conclusion:Relaxation of propofol on aortic smooth muscle is closely related to inhibiting IP_3- induced calcium release to decrease intracellular calcium concentration.