CoenzymeA glutathione disulfide is a potent modulator of angiotensin II-induced vasoconstriction
Standard
CoenzymeA glutathione disulfide is a potent modulator of angiotensin II-induced vasoconstriction. / van der Giet, M; Schmid, A; Jankowski, J; Schlüter, H; Zidek, W; Tepel, M.
In: AM J HYPERTENS, Vol. 14, No. 2, 02.2001, p. 164-8.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - CoenzymeA glutathione disulfide is a potent modulator of angiotensin II-induced vasoconstriction
AU - van der Giet, M
AU - Schmid, A
AU - Jankowski, J
AU - Schlüter, H
AU - Zidek, W
AU - Tepel, M
PY - 2001/2
Y1 - 2001/2
N2 - 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.
AB - 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.
KW - Angiotensin II
KW - Animals
KW - Antihypertensive Agents
KW - Coenzyme A
KW - Dose-Response Relationship, Drug
KW - Imidazoles
KW - In Vitro Techniques
KW - Losartan
KW - Male
KW - Perfusion
KW - Rats
KW - Rats, Inbred WKY
KW - Tetrazoles
KW - Time Factors
KW - Vasoconstriction
KW - Vasomotor System
KW - Journal Article
U2 - 10.1016/s0895-7061(00)01237-1
DO - 10.1016/s0895-7061(00)01237-1
M3 - SCORING: Journal article
C2 - 11243308
VL - 14
SP - 164
EP - 168
JO - AM J HYPERTENS
JF - AM J HYPERTENS
SN - 0895-7061
IS - 2
ER -
