INFLUENCE OF SODIUM-INTAKE ON IN-VIVO LEFT-VENTRICULAR ANATOMY IN EXPERIMENTAL RENOVASCULAR HYPERTENSION

Citation
G. Desimone et al., INFLUENCE OF SODIUM-INTAKE ON IN-VIVO LEFT-VENTRICULAR ANATOMY IN EXPERIMENTAL RENOVASCULAR HYPERTENSION, The American journal of physiology, 264(6), 1993, pp. 2103-2110
Citations number
36
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
264
Issue
6
Year of publication
1993
Part
2
Pages
2103 - 2110
Database
ISI
SICI code
0002-9513(1993)264:6<2103:IOSOIL>2.0.ZU;2-I
Abstract
The effect of different dietary salt contents (0.0035, 0.4, and 4%) on in vivo left ventricular (LV) geometry was studied by necropsy-valida ted echocardiographic methods in groups of 30 two-kidney, one-clip (2K ,1C) and one-kidney, one-clip (1K,1C) male Wistar rats and two-kidney (2K) and one-kidney (1K) shams 9 wk after surgery. The salt-deficient diet was associated with lower body weight, higher plasma renin activi ty in both 2K,1C and 2K shams (P < 0.004) and higher hematocrit in 2K, 1C (P < 0.02). Blood pressure was increased by high-salt diet in expe rimental groups but not in shams (P < 0.01). Increase in dietary sodiu m content was associated with increased cross-sectional area index (CS AI) and LV mass index in 2K rats independently of renal artery stenosi s (P < 0.0007) and also in 1K shams (P < 0.01). LV end-diastolic dimen sion was greater in 1K,1C and 1K shams than in 2K,1C and 2K shams at e very level of sodium intake and was directly related to atrial natriur etic factor levels in both 1K,1C (r = 0.68) and 2K,1C (r = 0.59). LV h ypertrophy was independently predicted by blood pressure (P < 0.0006) and high-sodium diet (P < 0.05) in 1K rats (multiple r = 0.57, P < 0.0 01) and by high-sodium diet (P < 0.0001) and low hematocrit (P < 0.05) in 2K rats (multiple r = 0.76, P < 0.0001). Thus provision of normal or high sodium content in the diet was a more consistent stimulus to L V hypertrophy than the level of blood pressure. The effect of dietary sodium on myocardial growth is due at least in part to its influence o n LV chamber volumes; however, it may also reflect additional nonhemod ynamic effects.