CoenzymeA glutathione disulfide is a potent modulator of angiotensin II-induced vasoconstriction

CoenzymeA glutathione disulfide (CoASSG) has recently been isolated from bo vine adrenal glands and is assumed to play an important rule in blood press ure (BP) control. We used the isolated perfused rat kidney to investigate t he modulating effects of CoASSG on angiotensin II (AngII)induced vasoconstr iction. Permanent perfusion with CoASSG (1 mu mol/L) for 60 min induced a s ignificant (P <.05) shift to the left in the dose-response curve for AngII (about 3.1-fold), whereas the dose-response curve for norepinephrine (NE) w as unaffected. During continuous perfusion with 1 <mu>mol/L CoASSG, the rep etitive application of 10 pmol AngII significantly increased its vasoconstr iction by 170% +/- 14% (P <.05) and 235% +/- 50% (P <.05) for 60 and 120 mi n, respectively. The potentiation of AngII by permanent perfusion with CoAS SG is dose- and time-dependent and shows a plateau at 120 min. Glutathione, oxidized coenzymeA, and coenzymeA teach 1 mu mol/L) are not able to enhanc e the vasoconstriction induced by AngII. We conclude that CoASSG is able to potentiate the vasoactive properties of AngII, and that CoASSG might play an important role in BP regulation via modulating effects of AngII. Am J Hy pertens 2001;14:164-168 (C) 2001 American Journal of Hypertension, Ltd.