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第三节肾脏泌尿功能的调节Regulationofurineformationofthekidney中山大学基础医学院生理学教研室王庭槐尿生成的调节regulationofurineformation肾血流量的调节神经—体液调节regulationofrenalbloodflownervousandhumonalcontrol(对滤过的调节)(对重吸收和分泌)自身神经体液调节调节调节ADH醛固酮甲状旁腺素Aldosteroneparathyroidhormone一、抗利尿激素antidiuretichormone,ADH合成部位：视上核(supraopticnucleus)、室旁核(paraventricularnucleus)合成ADH运输：丘脑—垂体束贮存释放：神经垂体（贮存于膨大神经末梢中）前激素ADH九肽蛋白水解酶靶器官：远曲小管集合管ThehypothalamuscontainstwotypesofneuronsthatsynthesizeADHinthesupraopticnucleusandparaventricularnucleus.onceADHissynthesized,itistransporteddowntheaxonsoftheneuronstotheirtips,terminatingintheposteriorpituitarygland.作用：1.提高远曲小管和集合管上皮细胞对水的通透性，促进水的重吸收尿液浓缩、尿量减少（抗利尿）[主要作用]。ThemostimportantrenalactionofADHistoincreasethewaterpermeabilityofthedistaltubule,collectingtubule.Thiseffecthelpsthebodytoconservewaterincircumstancessuchasdehydration.2.增加内髓部集合管对尿素的通透性并减少肾髓质的血流量。ADHincreasestheureapermeabilityofcollectingtubuleininnerzoneanddecreasesthebloodflowinmedulla.3.促进髓绊升支粗段对NaCl的重吸收，使直小血管收缩。ADHincreasesthereabsorptionofNaClinthicksegmentofascendinglimbandsoleadstoconstrictionofvasarecta.（一）、作用机理：ADH与远曲小管、集合管上皮细胞管周膜上受体结合激活膜内的腺苷酸环化酶上皮细胞中cAMP管腔膜中蛋白激酶激活膜蛋白磷酸化膜构型改变水通道开放管腔膜对水通透性。ADH，水通道小泡内移，对水通透性。ADHcombineswiththereceptorinbasolateralmembraneandactivatedtheadenylatecyclase,itproducescyclicadenosinemonophosphate,whichleadstoactivationofproteinkinaseinbasolateralmembrane,thenthemembraneproteinisphosphorylated,sotheconfigurationofmembranechanges,thisprocessincreasesthepermeabilitytowaterbytheopenofwaterchannel.（二）ADH分泌的调节(theregulationofADHsecretion)血浆晶体渗透压的改变(thechangeofcrystalosmoticpressure)有效刺激因素effectivestimuli循环血量的改变(thechangeofeffectivebloodvolume)1、血浆晶体渗透压的改变特点：敏感，晶体渗透压改变1～2%时即有反应。电解质(+)有效尿素无效感受器：位于视上核及其附近区域。大量出汗、腹泻、失水血浆晶体渗透压视上核及其周围区域渗透压感受器(+)神经垂体膨大神经末梢去极化释放ADH远曲小管、集合管对水通透性对水重吸收，尿液浓缩尿量减少。TheprecisewaythattheosmoticconcentrationoftheextracellularfluidscontrolsADHsecretionisnotclear.Yetsomewhereinornearthehypothalamusaremodifiedneuronreceptorscalledosmoreceptors.whentheextracellularfluidbecomestooconcentrated,fluidispulledbyosmosisoutoftheosmoreceptorcell,initiatingappropriatenervesignalsinthehypothalamustocauseadditionalADHsecretion.水利尿waterdiuresis大量饮清水尿量饮1000ml清水，隔30分钟尿量，（1小时末达高峰，2—3小时恢复）饮1000mlNS，隔30分钟变化不大2、循环血量的改变（容量感受器途径）过度输液，血量过多(+)左心房内膜下容量感受器迷走N，传入冲动中枢，间接抑制下丘脑—垂体后叶系统释放ADH远曲小管集合管对水通透性对水重吸收尿量。Whenbloodvolumeincreasesbecauseofexcesstransfuse,thevolumereceptorinendometriumofleftatriumsendsimpulsethroughVagusnervetocenterandinhibitthereleaseofADHbyHypothalami-Pituitaryposteriorlobesystem,sothewaterpermeabilityindistaltubuleandcollectingtubuledecreases,thereforethereaborptionofwaterdecreasesandtheurinevolumeincreases.3、其它因素①AP(+)颈动脉窦压力感受器窦NADH反射性释放尿量②痛刺激、情绪紧张ADH尿量③弱冷刺激ADH尿量④下丘脑病变累及视上核、室旁核ADH合成释放障碍尿崩症(diabetesinsipidus)。Whenarterialpressureincreases,pressoreceptoincarotidsinussendssignalstohypothalamicnucleithroughsinusnervethatdecreasesADHsecretion.ADHsecretioncanalsobecontrolledbyotherstimulisuchaspainandnervousmood.二、醛固酮的作用（Aldosterone）分泌部位：肾上腺皮质球状带靶器官：远曲小管集合管作用：促进对Na+的主动重吸收，同时促进K+的排出——保Na+排K+作用。Aldosterone,secretedbythezonaglomerulosecellsoftheadrenalcortex,isanimportantregulatorofsodiumreabsorptionandpotassiumsecretionbytherenaltubules.Theprimarysiteofaldosteroneactionisontheprincipalcellsofthecorticalcollectingtubule.themechanismbywhichaldosteroneincreasesodiumreabsorptionwhileatthesametimeincreasingpotassiumsecretionisstimulatingthesodium-potassiumATPasepumponthebasolateralsideofthecorticalcollectingtubulemembrane.（一）作用机制：醛固酮进入远曲小管集合管的上皮细胞后与胞浆受体结合形成激素—胞浆受体复合物通过核膜与核中受体结合激素—核受体复合物促进mRNA的合成醛固酮促进小管上皮细胞Na+泵运转诱导蛋白促进生化氧化提供ATP促进加强Na+增加管腔膜对Na+通透性的主动重吸收(保Na+)造成小管腔内负电位K+被分泌到小管液（排K+)Aldosteronediffusesreadilytotheinteriorofthetubulaarepithelialcellsandcombineswithahighlyspecificcytoplasmicreceptorprotein,thenthealdosterone-receptorcomplexdiffusesintothenucleuswhereitmayundergofurtheralterations,finallyinducingoneormorespecificportionsoftheDNAtoformoneormoretypesofmessengerRNArelatedtotheprocessofsodiumandpotassiumtransport.（心房利尿肽ANP）28个氨基酸残基集合管对Na+重吸收(-)，使出入球小动脉舒张心钠素（Cardionatrin）(-)aldosterone释放ADH肾素分泌作用：促进肾脏排钠排水Thefunctionofcardionatrinistopromotethesecretionofsodiumandwaterbykidney.thecardionatrincanreducethereleaseofaldosterone、ADHandrenin.（二）醛固酮分泌的调节：肾素—血管紧张素—醛固酮系统、血K+、血Na+浓度促肾上腺皮质激素（ACTH）对醛固酮分泌的日常调节不起重要作用Potassiumionconcentrationandtherenin-angiotensinsystemarebyfarthemostpotentinregulatingaldosteronesecretion.1.肾素—血管紧张素—醛固酮系统（renin-angiotensin-aldosteronesystem,RAAS）RAA系统的活性取决于血浆中肾素浓度，故凡能影响肾素分泌的因素均可间接影响醛固酮的分泌。肝硬化继发性醛固酮增多症水肿、腹水组织液循环血量肾素醛固酮cirrhosisofliversecondaryaldosteronismEdema、Hydroperitoniatissuefluidbloodvolumereninaldosterone2.血K+和血Na+浓度①血K+Na+直接刺激肾上腺皮质球状带醛固酮分泌保Na+排K+②血K+Na+醛固酮分泌保Na+排K+功能减弱③醛固酮的分泌对K+浓度改变较敏感，K+仅增加0.5～1.0mmol/L醛固酮（敏感度K+Na+）Increasedpotassiumionconcentrationintheextracellularfluidgreatlyincreasesaldosteronesecretion.asmallpercentageincreaseinpotassiumconcentrationcancauseaseveralfoldincreaseinaldosteronesecretion.三、甲状旁腺激素(parathyroidhormone,PTH)的作用分泌部位：甲状旁腺作用：1.促进远球小管和集合管对Ca2+的重吸收，减少尿Ca2+排出量；2.抑制近球小管对磷酸盐的重吸收，增加尿中磷酸盐的排