JCI - Carbon monoxide of vascular origin attenuates the sensitivity of renal arterial vessels to vasoconstrictors

Carbon monoxide of vascular origin attenuates the sensitivity of renal arterial vessels to vasoconstrictors

Jun-Ichi Kaide, Fan Zhang, Yuan Wei, Houli Jiang, Changhua Yu, WenHui Wang, Michael Balazy, Nader G. Abraham, Alberto Nasjletti

Published in Volume 107, Issue 9

J Clin Invest. 2001; 107(9):1163–1171 doi:10.1172/JCI11218

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Figure 4

Concentration-response curve to vasopressin in rat renal interlobar artery rings maintained in organ culture for 18 hours prior to experimentation in media containing HO-2 AS-ODN (40 μg/ml) (a) or the corresponding scrambled oligodeoxynucleotides (HO-2 S-ODN, 40 μg/ml) (b). (a) HO-2 AS-ODN without CO (EC₅₀, 0.71 ± 0.15 nmol/l; R_max, 3.74 ± 0.22 mN/mm; n = 9), with 0.1 μmol/l CO (EC₅₀, 5.59 ± 2.07^A nmol/l; R_max, 3.81 ± 0.23 mN/mm; n = 9), and with 1.0 μmol/l CO (EC₅₀, 8.20 ± 2.71^A nmol/l; R_max, 4.04 ± 0.30 mN/mm; n = 9). (b) HO-2 S-ODN without CO (EC₅₀, 3.67 ± 0.70 nmol/l; R_max, 3.97 ± 0.13 mN/mm; n = 9), with 0.1 μmol/l CO (EC₅₀, 4.62 ± 1.06 nmol/l; R_max, 3.96 ± 0.11 mN/mm; n = 9), and with 1.0 μmol/l CO (EC₅₀, 3.75 ± 0.50 nmol/l; R_max, 3.88 ± 0.15 mN/mm; n = 9). The experiments were conducted with and without addition of exogenous CO to the bathing buffer. L-NAME (1 mmol/l) was included in the buffer used in contractility studies. Results are the mean ± SEM. ^AP < 0.05 relative to corresponding data in vessels not exposed to exogenous CO.