Lead-induced hypertension is not associated with altered vascular reactivity in vitro.

In confirmation of a previous study (Am J Hypertens 1993;6:723), mean arterial blood pressure (MBP), as determined by tail cuff plethysmography, was found to be significantly elevated in Sprague-Dawley rats after 3 months of feeding 0.48 mmol/L (100 ppm) lead acetate/day (144 +/- 3.3 [SEM], in lead-treated [L] v 107 +/- 3.3 mm Hg in controls [C], P < .001). Thoracic aorta was excised from L and C animals (n = 6). Segments were suspended in tissue baths with Krebs' bicarbonate solution, then tested sequentially for vasoreactivity to 68 mmol/L K+, followed by graded concentrations of phenylephrine (PE), 0.01 to 0.3 micromol/L, acetylcholine (Ach), 0.001 to 3 micromol/L, nitroprusside (SNP), 0.0001 to 0.1 micromol/L, norepinephrine (NE), 0.001 to 300 micromol/L. There were no differences between L and C animals with respect to either vasoconstrictors (PE and NE) or vasodilators (Ach and SNP). The tissue levels of cGMP measured with and without phosphodiesterase inhibition, and in the absence and presence of either Ach or SNP, were comparable in the two groups. We conclude that the intrinsic vascular responsiveness is unchanged in lead-treated animals. The elevation of MBP is due to the presence of circulating factor(s) and hemodynamic changes.