Effects of chronic sodium depletion on function of isolated normal and hypertensive hypertrophied rat heart.
Since in vivo ejection fraction is said to be reduced in chronically sodium depleted dogs, this study was conducted to investigate the direct effects of sodium deprivation on intrinsic ventricular contractility, independent of haemodynamic or adrenergic influences. Since low sodium diet and/or diuretics are commonly used in the treatment of hypertension, we included a hypertensive group in the study. Normotensive male Sprague-Dawley rats and age matched renovascular hypertensive rats were subdivided into three groups. The first group was fed regular sodium diet (RS) for 6 weeks. The second (LS) and third (LSD) groups received low sodium diet for 6 weeks, and the LSD group also received diuretic (frusemide) treatment to achieve marked sodium depletion (last dose given 2 weeks before the cardiac study). Left ventricular (LV) contractility was investigated in the isolated isovolumetric rat heart (Langendorff preparation) paced at 180 beats-min-1. Results showed that LV +dP/dt max at zero LV end diastolic pressure was higher (p less than 0.01) in the LSD group than in the other groups in normotensive rats [2672 (SEM127) mm Hg.s-1 in LSD, 2267(96) in LS, 2174(111) in RS] and higher in LSD (p less than 0.01) and LS (p less than 0.05) groups than in the RS group in hypertensive rats [2332(110) mm Hg.s-1, 2287(93), 1781(104), respectively]. Calculated LV balloon volume at zero LV end diastolic pressure was not significantly different in any dietary group. These results suggested that after 6 weeks of in vivo sodium depletion, in vitro LV contractility was enhanced rather than depressed under these experimental conditions. This enhancement is contrary to the in vivo findings in the dog model and could not be explained by differences in myocardial flow rate, LV chamber stiffness or myocardial stiffness constant. The mechanism of this accentuated ventricular contractility under these experimental conditions remains to be determined.
Hori
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Department of Heart and Hypertension Research, Cleveland Clinic Foundation, Ohio 44195-5069.
Mirsky
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Fouad-Tarazi
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FM
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D003131:Combined Modality Therapy; D004039:Diet, Sodium-Restricted; D004548:Elasticity; D005665:Furosemide / Q000627:therapeutic use; D006352:Heart Ventricles; D006439:Hemodynamics / Q000187:drug effects*; D006978:Hypertension, Renovascular / Q000150:complications* / Q000178:diet therapy / Q000188:drug therapy; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000172:deficiency* / Q000502:physiology; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000494:pharmacology*
D012982:Sodium, Dietary; D005665:Furosemide; D012964:Sodium