Relaxin is a potent renal vasodilator in conscious rats

被引:201
作者
Danielson, LA
Sherwood, OD
Conrad, KP
机构
[1] Univ New Mexico, Sch Med, Dept Pathol, Albuquerque, NM 87131 USA
[2] Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA
[3] Univ Illinois, Coll Med, Urbana, IL 61801 USA
[4] Univ Pittsburgh, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA 15213 USA
[5] Univ Pittsburgh, Dept Cell Biol & Physiol, Pittsburgh, PA 15213 USA
[6] Magee Womens Res Inst, Pittsburgh, PA 15213 USA
关键词
D O I
10.1172/JCI5630
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The kidneys and other nonreproductive organs vasodilate during early gestation; however, the "pregnancy hormones" responsible for the profound vasodilation of the renal circulation during pregnancy are unknown. We hypothesized that the ovarian hormone relaxin (RLX) contributes. Therefore, ne tested whether the administration of RLX elicits renal vasodilation and hyperfiltration in conscious adult, intact female rats. After several days of treatment with either purified porcine RLX or recombinant human RLX 2 (rhRLX), effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) increased by 20%-40%. Comparable renal vasodilation and hyperfiltration was also observed in ovariectomized rats, suggesting that estrogen and progesterone are unnecessary for the renal response to rhRLX. The nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester completely abrogated the increase in ERPF and GFR elicited by chronic administration of purified porcine RLX. In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment. Short-term infusion of purified porcine RLX to conscious rats over several hours failed to increase ERPF and GFR Plasma osmolality was consistently reduced by the chronic administration of both RLX preparations. In conclusion, the renal and osmoregulatory effects of chronic RLX administration to conscious rats resemble the physiological changes of pregnancy in several respects: (a) marked increases in ERPF and GFR with a mediatory role for nitric oxide; (b) attenuation of the renal circulatory response to angiotensin II; and (c) reduction in plasma osmolality.
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收藏
页码:525 / 533
页数:9
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