摘要
本实验研究了皮下注射６—羟多巴胺（６—ＯＨＤＡ）施行交感神经损毁术对成年自发性高血压大鼠（ＳＨＲ）血压和红细胞Ｎａ＋外流动力学的影响。结果表明，在幼年期施行交感神经损毁术的ＳＨＲ血压显著低于未损毁组，同时红细胞Ｎａ泵驱动的的Ｎａ＋外流最大速率显著下降、Ｎａ＋－Ｋ＋外向协同转运系统的单位活性升高。三者均接近ＷＫＹ大鼠的测定值。相反，损毁成年ＳＨＲ交感神经不影响上述两个动力学参数，血压也未见明显改变。此外，不论幼年或成年期注射６—ＯＨＤＡ均可降低Ｎａ＋—Ｌｉ＋对向转运系统驱动的Ｎａ＋外流最大速率。上述结果提示，在ＳＨＲ早期发育过程中，交感神经营养因子可能降低Ｎａ＋—Ｋ＋外向协同转运活性，继而刺激Ｎａ泵代偿功能增强。这种现象可能同时存在于ＳＨＲ动脉平滑肌，因而是高血压产生的一个原因。关于交感神经损毁术后ＳＨＲ红细胞Ｎａ＋—Ｌｉ＋对向转运最大速率下降的机制尚不清楚，但与交感神经早期营养作用的消除无关。
Sodium efflux kinetics in erythrocytes of adult spontaneously hypertensive rat(SHR)wasstudied after chemical sympathectomy by sc injection of 6-hydroxydopamine. It was found thatneonatal sympathectomized SHRs(N-Sx) showed decreased blood pressure,erythrocyticmaximal Na+pump rate and increased unit activity of outward Na+-K+cotransport as com-pared with those in age-matched untreated SHRs,while these values approximated those inWKY. However,sympathectomy performed in adult SHRs(A-Sx)did not influence the abovetwo kinetic parameters and only slightly lowered the blood pressure. In addition,both neonataland adult sympathectomy decreased maximal Na+efflux rate of Na+-Li+countertransport.It ap-pears that in the early stage of development of SHR, the sympathetic nerve may have a trophic ef-fect on erythrocytic Na+transport by lowering outward Na+-K+cotransport which can in turnstimulate the Na+pump function.This might also be the case in arterial muscle,and hence be re-lated to the pathogenesis of hypertension in SHRs. The decrease in maximalNa+-Li+countertransport seems not to be related to the early elimination of sympathetic trophiceffect.
出处
《中国应用生理学杂志》
CSCD
1994年第2期159-163,共5页
Chinese Journal of Applied Physiology
基金
国家自然科学基金
关键词
高血压
红细胞
血压
钠转运动学
spontaneously hypertensive rat
erythrocyte
sodium transport
sympathetic nerve
