EFFECT OF HIGH-SALT INTAKE ON BLOOD-PRESSURE AND VASCULAR REACTIVITY OF DIABETIC RATS

The etiopathogenesis of diabetes mellitus (DM)-associated hypertension is not known. Sodium and an increased vascular reactivity to vasopressor agents have been implicated in the pathogenesis of this disease in humans. The aim of the present study was to experimentally evaluate the possible role of salt intake and changes in vascular reactivity in the pathogenesis of DM-associated hypertension. Male Wistar rats, weighing 180 to 200 g, rendered diabetic by streptozotocin (65 mg/kg) and maintained moderately hyperglycemic with insulin were submitted to high-salt intake (tap water replaced with 1.0% NaCl) for 8 weeks (D+salt rats, N = 8). Mean arterial pressure and reactivity of the isolated aorta to norepinephrine and angiotensin II were then determined. Diabetic rats on normal-salt intake (group D+nl, N = 6) and non-diabetic rats on high- (group non-D+salt, N = 6) or normal-salt intake (group non-D+nl, N = 8) were used as controls. Mean blood pressure was significantly higher in D+salt rats (123 +/- 3 mmHg) compared with the D+nl (113 +/- 3 mmHg), non-D+salt (111 +/- 2 mmHg) and non-D+nl (105 +/- 2 mmHg) groups. Mean blood pressure was also significantly higher in diabetic rats on normal-salt intake compared with control rats on normal-salt intake. Vascular reactivity of the aorta to norepinephrine was increased only in diabetic rats on high-salt intake. No modification in reactivity was detected with regard to the reactivity to angiotensin II. We conclude that high-salt intake increases blood pressure in diabetic rats and that increased aorta vascular reactivity to norepinephrine might be involved in the blood pressure alteration.