The experiments performed in endothelin-denuded preparations (the strips of thoracic aorta and perfused tail arteries) showed that: 1) ET-1 exerts dose-dependent and slowly developing contractions and in subthreshold doses it potentiates vasoconstriction reactions to stimulate sympathetic nerve endings or phenylephrine exposure. 2) ion F(-), that activates G-proteins in the cell membranes, at a dose of 2 microM increased about two times the ET-1-induced vasoconstriction. 3) the aortic strip incubation with the protein kinase C inhibitor staurosporin led to a 50% decrease in the contraction amplitude. Results suggest that G proteins and protein kinase C may participate in the development of ET-1 induced vascular smooth muscle contraction.