HEMODYNAMIC AND METABOLIC EVIDENCE OF SALT SENSITIVITY IN SPONTANEOUSLY HYPERTENSIVE RATS

Sixteen female Wistar Kyoto (WKY) and 16 female spontaneously hypertensive rats (SHR) were studied hemodynamically and metabolically after prolonged (3 months) high sodium intake. Eight rats of each strain were given tap water to drink and served as controls, and another eight rats of each strain reveived 1% sodium chloride in tap water. Hemodynamic and metabolic evaluation disclosed that high salt intake by the WKY rats increased their cardiac index, oxygen consumption, and urinary sodium excretion; decreased body weight, total peripheral resistance index, oxygen extraction, and plasma renin activity; and had no effect upon mean arterial pressure, heart rate, fluid intake, urine volume, and potassium excretion. In contrast, high salt intake by the SHR increased their mean arterial pressure, total peripheral resistance index, fluid intake, urinary volume and sodium excretion; decreased plasma renin activity; and had no effect upon heart rate, cardiac index, and urinary potassium excretion. Salt-treated SHR rats had significantly higher fluid intake than their WKY counterparts had. The elevated arterial pressure and peripheral vascular resistance demonstrate an increased sensitivity to dietary salt in SHR but not in corresponding WKY controls. The further elevation of arterial pressure by salt in the SHR was due mainly to a further increase in vascular resistance.