The role of eNOS on the compensatory regulation of vascular tonus by H2S in mouse carotid arteries

• Published in: Nitric oxide Vol. 69; pp. 45 - 50
• Main Authors: Ertuna, Elif, Loot, Annemarieke E., Fleming, Ingrid, Yetik-Anacak, Gunay
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 30.09.2017
• Subjects: eNOS; Hydrogen sulfide; Mouse carotid artery; Vascular relaxation; Hydrogen sulfide; AOAA; eNOS; CSE; CBS; PE; WTxeNOS; eNOS−/−xeNOS; Mouse carotid artery; Vascular relaxation
• ISSN: 1089-8603; 1089-8611
• DOI: 10.1016/j.niox.2017.04.007

The gasotransmitter nitric oxide (NO) has an important role in vascular function and a decrease in its bioavailability is accepted as a main pathological mechanism for cardiovascular diseases. However, other gasotransmitters such as hydrogen sulfide (H2S) are also generated by the endothelium and can also affect vascular tone and a crosstalk may exist between H2S and NO. We therefore investigated the consequences of deficiency, replacement or overexpression of endothelial nitric oxide synthase (eNOS) on H2S-induced vascular responses in murine carotid arteries. In pre-contracted carotid arteries from wild-type (WT) mice, l-cysteine elicited relaxation that was inhibited by the H2S synthesis inhibitor amino-oxyacetic acid (AOAA). Genetic deletion of eNOS increased l-cysteine-induced relaxation compared to WT, but the replacement of eNOS by adenoviral transfection or H2S synthesis inhibition by AOAA reversed it. Furthermore, eNOS deletion did not alter NaHS-induced relaxation in carotid arteries while eNOS overexpression/replacement increased NaHS-induced relaxation responses in carotid arteries from WT or eNOS−/−. We suggest that, endogenously produced H2S can compensate for impaired vasodilatory responses in the absence of NO to maintain vascular patency; while, eNOS abundance can limit endogenous H2S-induced vascular responses in mice carotid arteries. Our result suggests that endogenous vs. exogenous H2S-induced relaxation are reciprocally regulated by NO in mice carotid arteries. [Display omitted] •Lack of eNOS increases endogenous H2S-induced vasodilatation to maintain relaxation.•eNOS overexpression abolishes endogenous H2S-induced vasodilatation.•Endogenous vs. exogenous H2S-induced relaxations are reciprocally regulated by NO.