Abstract
To assess the underlying mechanism of diabetes mellitus (DM)‐induced vascular hypercontractility, we evaluated the participation of the sarcoendoplasmic reticulum calcium ATPase (SERCA), the protein kinase C (PKC) and prostaglandins during the contraction induced by phenylephrine (PE) of aorta rings from a 10 weeks streptozotocin (STZ)‐induced DM rat model.PE produced a stronger contraction of DM aorta rings with endothelium vs control (CTRL), (Emax: DM .69 ± .06 vs CTRL .38 ± .07 g. p<0.02). This vascular hypercontractility was eliminated by: a) indomethacin (10μM) pretreatment (Emax: DM .64 ± .07 vs CTRL .55 ± .11 g. ns), and b) endothelium removal (Emax: DM 1 ± .07 vs CTRL .93 ± .04 g., ns). On the other hand, Gö6976 (1μM), a PKC inhibitor, decreased the contractile response in CTRL more than in DM (Emax: DM .55 ± .06 vs CTRL .28 ± .04 g., p<0.01). Also, 1μM thapsigargin (T), a SERCA blocker, increased the CTRL concentration dependent contraction (Emax: CTRL .40 ± .08 vs CTRL+T .76 ± .09, p<0.001), but was not different in DM rings (Emax: DM .66 ± .10 vs DM+T .69 ± .06 g., ns), nor between groups (Emax DM+T .69 ± .07 vs CTRL+T .76 ± .08 g., ns).ConclusionsDuring STZ‐induced DM, endothelial cells release a contractile prostaglandin, perhaps TXA2, that induces vascular hypercontractility.Supported by: P/PIFI‐2010‐24MSU0011E‐13.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
