Decreased pulmonary arterial endothelium- dependent relaxation in heartworm-infected dogs with pulmonary hypertension

Abstract

Objective - To investigate the contractility of pulmonary arterial smooth muscle and the relation between pulmonary hypertension and endothelium-derived relaxing factor in canine heartworm disease. Animals - 18 noninfected control and 9 heartworm- infected dogs. Procedure - Mean pulmonary arterial blood pressure was measured in vivo, and tension of pulmonary arterial strips was measured by use of the isometric tension method. Results - After phenylephrine (10-5M)-induced contraction of the pulmonary vascular smooth muscle, carbamylcholine chloride (CCh, 10-6M) caused more relaxation of the vascular smooth muscle of noninfected dogs than that of heartworm-infected dogs. Furthermore, the degree of CCh-induced relaxation was inversely correlated with mean pulmonary arterial blood pressure in the noninfected and the heartworm- infected dogs, The CCh-induced relaxation was inhibited by pretreatment with NG-nitro-L-arginine methyl ester hydrochloride (10-5M), and in reversed dose-dependent manner by L-arginine (10-4 to 3 × 10-2M). Sodium nitroprusside (10-8 to 10-5M) caused a dose- dependent relaxation in all vessels, and there was no significant difference in the relaxation responses in both groups except at 10-7M for vessels with intact endothelium from noninfected dogs. Conclusion - The depression of endothelium-dependent relaxation is correlated with the pulmonary arterial blood pressure in heartworm-infected dogs, suggesting that the decrease is one of the essential factors for the genesis of pulmonary hypertension in canine filariasis.