van der Giet M, Schmid A, Jankowski J, Schlüter H, Zidek W, Tepel M
Ruhr-Universität Bochum, Universitätsklinikum, Medizinische Klinik I, Herne, Germany.
Am J Hypertens. 2001 Feb;14(2):164-8. doi: 10.1016/s0895-7061(00)01237-1.
CoenzymeA glutathione disulfide (CoASSG) has recently been isolated from bovine adrenal glands and is assumed to play an important role in blood pressure (BP) control. We used the isolated perfused rat kidney to investigate the modulating effects of CoASSG on angiotensin II (AngII)-induced vasoconstriction. Permanent perfusion with CoASSG (1 micromol/L) for 60 min induced a significant (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) was unaffected. During continuous perfusion with 1 micromol/L CoASSG, the repetitive application of 10 pmol AngII significantly increased its vasoconstriction by 170% +/- 14% (P < .05) and 235% +/- 50% (P < .05) for 60 and 120 min, respectively. The potentiation of AngII by permanent perfusion with CoASSG is dose- and time-dependent and shows a plateau at 120 min. Glutathione, oxidized coenzymeA, and coenzymeA (each 1 micromol/L) are not able to enhance 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.
辅酶A谷胱甘肽二硫化物（CoASSG）最近已从牛肾上腺中分离出来，并被认为在血压（BP）控制中起重要作用。我们使用离体灌注大鼠肾脏来研究CoASSG对血管紧张素II（AngII）诱导的血管收缩的调节作用。用CoASSG（1微摩尔/升）持续灌注60分钟可使AngII的剂量-反应曲线显著（P<.05）向左偏移（约3.1倍），而去甲肾上腺素（NE）的剂量-反应曲线未受影响。在持续灌注1微摩尔/升CoASSG期间，重复应用10皮摩尔AngII分别在60分钟和120分钟时使其血管收缩显著增加170%±14%（P<.05）和235%±50%（P<.05）。CoASSG持续灌注对AngII的增强作用具有剂量和时间依赖性，并在120分钟时达到平台期。谷胱甘肽、氧化型辅酶A和辅酶A（各1微摩尔/升）均不能增强AngII诱导的血管收缩。我们得出结论，CoASSG能够增强AngII的血管活性特性，并且CoASSG可能通过对AngII的调节作用在血压调节中发挥重要作用。
