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Am J Physiol Heart Circ Physiol 287: H767-H772, 2004. First published April 1, 2004; doi:10.1152/ajpheart.00047.2004
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Cardiac structural and functional responses to salt loading in SHR

Jwari Ahn, Jasmina Varagic, Michel Slama, Dinko Susic, and Edward D. Frohlich

Hypertension Research Laboratory, Research Division, Ochsner Clinic Foundation, New Orleans, Louisiana 70121

Submitted 21 January 2004 ; accepted in final form 26 March 2004

Increased dietary salt intake induces cardiac fibrosis in the spontaneously hypertensive rat (SHR), yet little information details its effects on left ventricular (LV) function. Additionally, young normotensive rats are more sensitive to the trophic effect of dietary sodium than older rats. Thus cardiac responses to salt loading were evaluated at two ages in the SHR; LV collagen content was also examined. SHR (8 or 20 wk of age) were given an 8% salt diet; their age-matched controls received standard chow. Echocardiographic indexes, arterial pressure, and LV hydroxyproline concentration were measured at 16 and 52 wk in the younger and older SHR groups, respectively. In most SHR, salt excess increased arterial pressure, LV mass, and hydroxyproline concentration and impaired LV relaxation manifested by prolonged isovolumic relaxation time, decreased early and atrial filling velocity ratio (VE/VA), and slower propagation velocity of E wave (VP). LV systolic function remained normal. However, one-quarter of the young salt-loaded SHR developed cardiac failure with systolic and diastolic dysfunction associated with greater LV mass and ventricular fibrosis. They also had lower arterial pressure, decreased fractional shortening, and a restrictive pattern of mitral flow. Moreover, the shorter deceleration time of the E wave and increased VE/VP, an index of LV filling pressure, indicated increased LV stiffness in these rats. These findings demonstrated that sodium sensitivity in SHR is manifested not only by further pressure elevation but also by significant LV functional impairment that most likely is related to enhanced ventricular fibrosis. Moreover, the SHR are more susceptible to cardiac damage when high dietary salt is introduced earlier in life.

sodium excess; ventricular systolic and diastolic function; echocardiography; spontaneously hypertensive rats



Address for reprint requests and other correspondence: J. Varagic, Ochsner Clinic Foundation, 1516 Jefferson Highway, New Orleans, LA 70121 (E-mail: jvaragic{at}ochsner.org).




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