Plovsing Ronni R, Wamberg Christian, Sandgaard Niels C F, Simonsen Jane A, Holstein-Rathlou Niels-Henrik, Hoilund-Carlsen Poul Flemming, Bie Peter
Dept. of Physiology and Pharmacology, Institute of Medical Biology, 21 Winsloewparken, DK-5000 Odense, Denmark.
Am J Physiol Regul Integr Comp Physiol. 2003 Nov;285(5):R981-91. doi: 10.1152/ajpregu.00263.2003. Epub 2003 Jul 17.
Angiotensins different from ANG II exhibit biological activities, possibly mediated via receptors other than ANG II receptors. We studied the effects of 3-h infusions of ANG III, ANG-(1-7), and ANG IV in doses equimolar to physiological amounts of ANG II (3 pmol. kg-1. min-1), in six men on low-sodium diet (30 mmol/day). The subjects were acutely pretreated with canrenoate and captopril to inhibit aldosterone actions and ANG II synthesis, respectively. ANG II infusion increased plasma angiotensin immunoreactivity to 53 +/- 6 pg/ml (+490%), plasma aldosterone to 342 +/- 38 pg/ml (+109%), and blood pressure by 27%. Glomerular filtration rate decreased by 16%. Concomitantly, clearance of endogenous lithium fell by 66%, and fractional proximal reabsorption of sodium increased from 77 to 92%; absolute proximal reabsorption rate of sodium remained constant. ANG II decreased sodium excretion by 70%, potassium excretion by 50%, and urine flow by 80%, whereas urine osmolality increased. ANG III also increased plasma aldosterone markedly (+45%), however, without measurable changes in angiotensin immunoreactivity, glomerular filtration rate, or renal excretion rates. During vehicle infusion, plasma renin activity decreased markedly ( approximately 700 to approximately 200 mIU/l); only ANG II enhanced this decrease. ANG-(1-7) and ANG IV did not change any of the measured variables persistently. It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially.
与血管紧张素II（ANG II）不同的血管紧张素具有生物活性，其可能通过ANG II受体以外的受体介导。我们研究了在6名低钠饮食（30 mmol/天）男性中，以与生理量ANG II（3 pmol·kg⁻¹·min⁻¹）等摩尔的剂量静脉输注血管紧张素III（ANG III）、血管紧张素-(1-7)（ANG-(1-7)）和血管紧张素IV（ANG IV）3小时的效果。受试者分别预先用坎利酸钾和卡托普利进行急性预处理，以抑制醛固酮作用和ANG II合成。输注ANG II使血浆血管紧张素免疫反应性增加至53±6 pg/ml（增加490%），血浆醛固酮增加至342±38 pg/ml（增加109%），血压升高27%。肾小球滤过率下降16%。同时，内源性锂清除率下降66%，近端钠分数重吸收率从77%增加到92%；近端钠绝对重吸收率保持不变。ANG II使钠排泄减少70%，钾排泄减少50%，尿流量减少80%，而尿渗透压增加。ANG III也显著增加血浆醛固酮（增加45%），然而，血管紧张素免疫反应性、肾小球滤过率或肾排泄率无明显变化。在输注溶媒期间，血浆肾素活性显著下降（约700至约200 mIU/l）；只有ANG II增强了这种下降。ANG-(1-7)和ANG IV均未持续改变任何测量变量。结论为：1）ANG III和ANG IV从血浆中的清除速度比ANG II快得多；2）在血管升压素和心房利钠肽血浆浓度恒定的情况下，ANG II导致滤过减少、尿液浓缩以及钠和钾潴留；3）ANG III浓度的非常小的增加（常规技术无法检测到）可能会显著增加醛固酮分泌。
