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Relaxin (RLX) does not reduce blood pressure or attenuate kidney damage in L‐NAME induced hypertension
Author(s) -
Sasser Jennifer M,
Molnar Miklos,
Baylis Chris
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a496-b
Subject(s) - relaxin , endocrinology , medicine , nitric oxide , blood pressure , kidney , vasodilation , nitric oxide synthase , pharmacology , chemistry , receptor
We and others have recently shown that chronic administration of RLX, the putative vasodilatory signal of normal pregnancy, preserves kidney structure and function in the renal mass reduction and angiotensin II infusion models of chronic kidney disease and during aging. However, the mechanisms underlying the beneficial effects of RLX have not been fully elucidated. Therefore, the purpose of this study was to determine if the antihypertensive and renoprotective effects of RLX are dependent upon activation of nitric oxide synthase (NOS). We examined the effect of RLX in male Sprague‐Dawley rats given the NOS inhibitor L‐NAME (1.5 mg/100g iv followed by 150 mg/L in drinking water) or vehicle (V) for 3 weeks. After 7 days of L‐NAME treatment, blood pressure (BP) was elevated compared to baseline (161±4 vs 123±3 mmHg, p<0.05). Human recombinant RLX (4 μg/h, SC by minipump) or V was then administered for the next 2 weeks. As shown in the Table, BP was increased in rats given L‐NAME (* p<0.05 vs V+RLX), and RLX treatment did not attenuate this rise. Furthermore, the number of damaged glomeruli was not decreased by RLX treatment during L‐NAME hypertension. In conclusion, RLX treatment had no effect on BP or renal injury in the L‐NAME model of hypertension. These data suggest that the antihypertensive and renoprotective effects of RLX are dependent upon a functional NOS system.