Tertatolol, a non cardioselective beta-blocker, maintains or increases renal blood flow in animals and in man. In this work, we confirmed in vitro the renal vasodilator effect of tertatolol and we investigated its mechanism. The rat kidney was isolated and perfused at constant flox in an open circuit with a Krebs-Henseleit solution. A vascular tone was restablished by sequential bolus injections of serotonine (every 5 mn) at a dose increasing perfusion pressure by 40 mm Hg. Tertatolol and other drugs were perfused at increasing concentrations during successive periods of 15 mn. Any relaxation was expressed as percentage inhibition of the initial vaso-constriction induced by serotonine. Tertatolol (3 x 10(-7) to 3 x 10(-5) M) induced a concentration-dependent renal vasodilatation (CI50 = 4.6 +/- 0.4 x 10(-6) M, n = 5) with a maximum effect of nearly 100 p. 100 relaxation. (-) tertatolol and (+) tertatolol were respectively more and less active (CI50 = 1.7 +/- 0.3 x 10(-6) M and 10.6 +/- 2.5 x 10(-6) M, n = 5). Tertatolol metabolites (4-OH tertatolol and sulfoxytertatolol) were inactive, excluding a vascular effect of tertatolol related to its metabolism into vasoactive derivatives. Other beta-blocking drugs, (+/-) sotalol and (+/-) nadolol, were also inactive on the renal vasculature and (-) bunolol only induced renal vasodilatation at concentrations 40 fold higher than that of (-) tertatolol.(ABSTRACT TRUNCATED AT 250 WORDS)