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Summary: Chronic exposure to lead is associated with adverse effects on renal function in laboratory animals and man. There is controversy concerning the direction of change of renal function parameters following chronic lead intoxication. The renal effects of low-dose lead exposure, as opposed to acute and pharmacological doses, require further scrutiny. In order to determine the effect of prolonged lowdose lead exposure, male Sprague Dawley rats (initial weight, 150.5±17.4g; final weight, 300.5±17.4g; n=10) administered lead acetate (100 p.p.m.) in drinking water over a period of 3 months, were investigated for renal function parameters. Treated rats had elevated blood pressures (114.4±4.2 vs. 95.7±3.5 mmHg; P<0.01). There was no significant difference in renal blood flow (3.99±0.28 vs. 4.19±0.63 ml/min; P=NS). GFR was comparable in the two groups (0.77±0.05 vs. 0.88±0.06 ml/min; P=NS). No significant difference in serum creatinine was observed (57.8±7.5 vs. 49.0±2.7 μmol/l; P=NS). Renal histology showed minimal interstitial changes in the experimental group. Interestingly, significant sodium (P<0.01); potassium (P<0.05) and chloride (P<0.05) retention were observed in the lead treated rats. Elevation of blood pressure occurred at a stage when low-level lead exposure did not alter renal function parameters appreciably. These results suggest that hypertension may be a forerunner of significant renal damage following chronic exposure to low-levels of lead and further underscore fluid and electrolyte retention as a significant mechanism responsible for elevated blood pressure in the chronic stages of lead exposure.

The present study was undertaken to investigate the effect of vitamin C treatment on blood pressure and vascular reactivity in salt-induced hypertension. Male Sprague-Dawley rats were fed a normal rat diet, a high-sodium (8% NaCl) diet, a normal rat diet plus vitamin C treament (100 mg x kg(-1) x day(-1)), or a high-sodium diet plus vitamin C treatment for 6 weeks. Salt loading significantly increased blood pressure, which was attenuated by vitamin C treatment. Aortic rings from the different groups were suspended for isometric-tension recording. The contractile response to noradrenaline was significantly increased in the salt-loaded rats. Vitamin C reduced the sensitivity of aortic rings to noradrenaline in rats on normal and high-sodium diets. In noradrenaline-precontracted rings, the relaxation response to acetylcholine, which was attenuated in the salt-loaded rats, was restored by vitamin C treatment. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME) abolished the enhanced response to acetylcholine caused by vitamin C. The results suggest that the antihypertensive effect of vitamin C is associated with a reduction in vascular sensitivity to noradrenaline and enhancement of endothelium-dependent relaxation due to increased nitric oxide bioavailability.

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