Aims: Hydrogen sulfide (HS) is shown in ocular tissues and suggested to involve in the regulation of retinal circulation. However, the mechanism of HS-induced relaxation on retinal artery is not clarified yet. Herein, we aimed to evaluate the role of several calcium (Ca) signaling and Ca sensitization mechanisms in the relaxing effect of HS donor, NaHS, on retinal arteries.
Materials And Methods: Relaxing effects of NaHS (10-3 × 10M) were determined on precontracted retinal arteries in Ca free medium as well as in the presence of the inhibitors of Ca signaling and Ca sensitization mechanisms. Additively, Ca sensitivity of the contractile apparatus were evaluated by CaCl-induced contractions in the presence of NaHS (3 × 10M). Functional experiments were furtherly assessed by protein and/or mRNA expressions, as appropriate.
Key Findings: The relaxations to NaHS were preserved in Ca free medium while NaHS pretreatment decreased the responsiveness to CaCl. The inhibitors of plasmalemmal Ca-ATPase, sarcoplasmic-endoplasmic reticulum Ca-ATPase, Na-Ca ion-exchanger and myosin light chain kinase (MLCK) unchanged the relaxations to NaHS. Likewise, Ca sensitization mechanisms including, rho kinase, protein kinase C and tyrosine kinase were unlikely to mediate the relaxation to NaHS in retinal artery. Whereas, a marked reduction was determined in NaHS-induced relaxations in the presence of MLCP inhibitor, calyculin A. Supportively, NaHS pretreatment significantly reduced phosphorylation of MYPT1-subunit of MLCP.
Significance: The relaxing effect of NaHS in retinal artery is likely to be related to the activation of MLCP and partly, to decrement in Ca sensitivity of contractile apparatus.
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| http://dx.doi.org/10.1016/j.lfs.2020.117834 | DOI Listing |
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