Aims: 

Endothelin (ET-1) is an endogenous peptide which is produced in the vascular endothelium under endothelin converting enzyme (ECE) action. In overphysiological concentration ET-1 has an evident vasoconstrictor activity but the role of ET-1 in circulation control in health is poorly understood. ET-1 plays a very important role in regulation of lung and renal functions. In this work we investigated the changes of rat pulmonary (PA) and renal (RA) arteries reactivity after ECE inhibition by substance PP-36 (consumption with drinking water in the dosage of 1.8 mg/kg per day during two weeks), that decreased plasma concentration of ET-1 by 12%.

Methods: 

Contractile activity of PA and RA (3^rd-order branches of main pulmonary and renal arteries, diameters 571.6±21.1 mm and 350.9±18.6 mm respectively) was investigated in isometric regimen.

Results: 

PP-36 consumption had no influence on systolic arterial pressure. PA constraction in response to a1-adrenoreceptor agonist phenylephrine did not change while RA sensitivity to phenylephrine significantly increased (pD2=5.32±0.68 in control and pD2=6.62±0.12 after ECE blockade). PA endothelium-independent relaxation (to sodium nitroprusside) did not change but endothelium-dependent relaxation (to acetylcholine) significantly increased which indicates higher nitric oxide production by the endothelium. RA responses to both acetylcholine and sodium nitroprusside increased which can be due to alteration of endothelial secretion and/or higher smooth muscle sensitivity to NO.

Conclusion: 

ECE inhibition may be accompanied by the enhancement of arterial constriction as well as relaxation. Probably, in health ET-1 action contributes to stabilization of vascular resistance.