Relaxin is a potent renal vasodilator in conscious rats

Citation
La. Danielson et al., Relaxin is a potent renal vasodilator in conscious rats, J CLIN INV, 103(4), 1999, pp. 525-533
Citations number
38
Categorie Soggetti
Medical Research General Topics
Journal title
JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00219738 → ACNP
Volume
103
Issue
4
Year of publication
1999
Pages
525 - 533
Database
ISI
SICI code
0021-9738(199902)103:4<525:RIAPRV>2.0.ZU;2-D
Abstract
The kidneys and other nonreproductive organs vasodilate during early gestat ion; however, the "pregnancy hormones" responsible for the profound vasodil ation of the renal circulation during pregnancy are unknown. We hypothesize d that the ovarian hormone relaxin (RLX) contributes. Therefore, ne tested whether the administration of RLX elicits renal vasodilation and hyperfiltr ation in conscious adult, intact female rats. After several days of treatme nt with either purified porcine RLX or recombinant human RLX 2 (rhRLX), eff ective renal plasma flow (ERPF) and glomerular filtration rate (GFR) increa sed 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 in crease in ERPF and GFR elicited by chronic administration of purified porci ne RLX. In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment. Short-term infusion of purified porcin e 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 c irculatory response to angiotensin II; and (c) reduction in plasma osmolali ty.