心钠素对卒中易感型自发性高血压大鼠血浆和脑组织加压素的影响

EFFECTS OF HUMAN ATRIAL NATRIURETIC FACTOR-(99-126) ON PLASMA AND BRAIN VASOPRESSIN IN STROKE--PRONE SPONTANEOUSLY HYPERTENSIVE RATS

为研究心钠素(ANF)和精氨酸加压素(AVP)的相互作用在原发性高血压发病中的意义,对卒中易感型自发性高血压大鼠(SHRsp)和对照大鼠(WKY)侧脑室(icv)或静脉(iv)注射人ANF-(99-126)观察其对血浆、下丘脑和垂体AVP含量以及平均动脉压(MAP)和尿量(UV)、尿钠(U_(Na)V)排泌的影响。静脉注射ANF后10min,SHRsp和WKY大鼠的MAP分别下降9.4％和12.2％(P<0.05),UV分别增加9和20倍(P<0.01),U_(Na)V增加16和29倍(P<0.01)。侧脑室注射ANF对两种大鼠的MAP、UV和U_(Na)V排泌均无明显作用。静脉或侧脑室注射ANF均使两种大鼠的血浆AVP水平明显下降,其中SHRsp的血浆AVP浓度下降程度(iv,-58％;icv,-31％)弱于WKY大鼠(iv,-80％;icv,-65％),下丘脑AVP含量在两种大鼠中都明显增加,而垂体AVP含量无明显变化。 结果表明,人ANF-(99-126)有明显的抑制AVP释放和降压、利尿、利纳作用,而SHRsp对这些作用的敏感性都降低,提示SHRsp对ABF的反应减弱可能在自发性高血压大鼠的发病中具有一定的意义。

In order to investigate the interction between atrial natriuretic factor(ANF)and arginine vasopressin(AVP)in the pathogenesis of essential hypertension,theeffects of intravenous(iv)or intracerebroventricular(icv)injection of human ANF-(99-126)on plasma and brain AVP,as well as mean arterial pressure(MAP),urinary volume(UV) sodium(U_(Na)V)excretion in stroke-prone spontaneouslyhypertensive rats(SHRsp)and age-matched no rmotensive Wistar-Kyoto rats(WKY)were stodied.The results showed that ten minutes after iv injection of ANF,MAP decreased by 9.4％ and 12.2％(P<0.05),UV increased about 9 and 20folds(P<0.01),U_(Na)V increased about 16 and 29 folds(P<0.01)in SHRsp andWKY rats,respectively.No such significant changes in these parameters were foundin the icv group.Although iv and icv injection of ANF caused significant decreaseof plasma AVP in both strains,the decrease was less marked in SHRsp than inWKY rats,While the maximum decreases were 58％(iv)and 31％(icv)in SHRsp,the corresponding values were 80％(iv)and 65％(icv)in WKY.Intravenous andintracerebroventricular injection of ANF also induced significant increase of hypo-thalamic AVP in both SHRsp and WKY rats,but no significant change could befound in hypophyseal AVP content. The results suggest that decreased sensitivity of AVP inhibition as well as lessmarked hypotensive,diuretic and natriur etic effects to ANF in SHRsp might play a role in the pathogenesis of their hypertension.