Effect of mercuric chloride on the rat mesenteric vascular bed: Relevance to the mechanism of mercury toxicity

Abstract

The effects of mercuric chloride on the vasculature were studied in the perfused rat mesenteric vascular bed. Mercuric chloride inhibited the vascular response to bolus injections of norepinephrine (100 ng) and potassium chloride (2 mg) even at a low concentration (3.7 × 10 −8 m) and the inhibition increased in a dose-dependent manner. Mercuric chloride at concentrations of 3.7 × 10 −7 m or more significantly increased the baseline perfusion pressure, an effect which was rapidly reversed probably as a result of severe damage to the vascular wall. This rise of baseline was in proportion to the calcium concentration of the perfusing buffer. In calcium-free buffer, mercuric chloride, even in high concentration (3.7 × 10 −5 m), had no effect on baseline pressure but the vascular responses to both pressor agents were inhibited almost in the same manner as in the case of normal calcium buffer. Prepefusing the preparation with 10 −5 m lanthanum chloride in calcium-containing buffer and then adding mercuric chloride to this buffer, with lanthanum still present, also prevented the rise of baseline pressure by mercury. Heavy metal antagonists ( d-penicillamine, N-acetyl- dl-penicillamine, dimercaprol) were effective in the treatment of early stage damage and in its prophylaxis. These results indicate that circulatory disturbances may play an important role in mercury toxicity and that the effects are in part related to modulation of calcium movements.