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(Hypertension. 2005;46:745.)
© 2005 American Heart Association, Inc.

Original Articles

Relaxin Increases Cardiac Output and Reduces Systemic Arterial Load in Hypertensive Rats

Dan O. Debrah; Kirk P. Conrad; Arundhathi Jeyabalan; Lee A. Danielson; Sanjeev G. Shroff

From the Department of Bioengineering (D.O.D., S.G.S.), University of Pittsburgh, Pa; Departments of Obstetrics, Gynecology, and Reproductive Sciences (K.P.C., A.J.), and Cell Biology and Physiology (K.P.C.), University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pa; and Department of Pathology (L.A.D.), University of New Mexico School of Medicine, Albuquerque.

Correspondence to Kirk P. Conrad, MD, Magee-Womens Research Institute, 204 Craft Ave, Pittsburgh, PA 15213. E-mail rsikpc{at}mwri.magee.edu

Chronic administration of recombinant human relaxin (rhRLX) to conscious, normotensive rats (male and female) increases cardiac output (CO) and global arterial compliance (AC_g) and reduces systemic vascular resistance (SVR) with no change in mean arterial pressure (MAP). Effects (magnitude and temporal pattern) of relaxin on systemic hemodynamics and arterial properties in hypertensive animal models are not known. Accordingly, the major goal of the present study was to determine the cardiovascular effects of rhRLX in hypertensive rats using 2 models: Long–Evans rats chronically administered angiotensin II (AII) and spontaneously hypertensive rats (SHR). CO and systemic arterial load, as quantified by SVR and AC_g, were obtained using methods reported previously by us. In rats with AII-induced hypertension, acute rhRLX administration (up to 6 hours) significantly increased CO and AC_g (24.9±3.9 and 34.3±12.6% above baseline, respectively) and significantly decreased SVR (17.2±3.5%) without changing MAP. In contrast, acute rhRLX administration to SHR and normotensive rats for up to 6 hours failed to produce any significant changes in CO, AC_g, SVR, or MAP. However, chronic rhRLX administration (1 to 7 days) to SHR yielded significant changes (24.0±8.1 and 22.3±6.6% increases in CO and AC_g, respectively, and a 13.3±5.3% decrease in SVR, with no change in MAP). In conclusion, rhRLX increases CO and reduces arterial load in hypertensive rats without reducing MAP. However, the time course of response to rhRLX treatment is dependent on the model of hypertension such that rats characterized by AII-mediated hypertension responded more rapidly to rhRLX administration than SHR.

Key Words: angiotensin II • hypertension, arterial • cardiac output • hormones • rats, spontaneously hypertensive • vascular resistance • vasodilation • arterial compliance

This article has been cited by other articles:

				M. C. Smith, Lee. A. Danielson, Kirk. P. Conrad, and J. M. Davison Influence of Recombinant Human Relaxin on Renal Hemodynamics in Healthy Volunteers J. Am. Soc. Nephrol., November 1, 2006; 17(11): 3192 - 3197. [Abstract] [Full Text] [PDF]