Premium
Small skeletal muscle veins exhibit substantial myogenic response, which is mediated by hydrogen peroxide‐induced activation of TP receptors
Author(s) -
Debreczeni Béla Zoltán,
Gara Edit,
Veresh Zoltán,
Tamás Róbert,
Hamar János,
Koller Ákos
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.858.1
Subject(s) - myogenic contraction , myograph , chemistry , thromboxane a2 , catalase , medicine , prostaglandin , endocrinology , skeletal muscle , hydrogen peroxide , prostaglandin h2 , arachidonic acid , receptor , anatomy , vasodilation , biochemistry , biology , smooth muscle , oxidative stress , enzyme
We hypothesized that isolated small veins (similarly arterioles) develop an appreciable myogenic tone in response to elevation of intraluminal pressure and aimed to elucidate the constrictor mechanism(s) involved. Thus small veins were isolated from gracilis muscle of male Wistar rats, then cannulated and incubated in the presence of 10 mmHg of intraluminal pressure at T = 37°C in a special pressure myograph chamber. Isolated small veins developed a substantial myogenic tone in response to increases in intraluminal pressure (from 1 to 12 mmHg). Calculated maximum myogenic tone was 70 ( 5 % of PD at 10 mmHg. Presence of indomethacin or catalase or SQ 29,548 reduced significantly the pressure‐induced myogenic tone. Also, H2O2 (10‐9‐10‐5 M) elicited concentration dependent constrictions, which were inhibited by the indomethacin or SQ 29,548. Arachidonic acid (10‐7–10‐4M) elicited concentration dependent constrictions, which were inhibited by indomethacin or SQ 29,548. In conclusion, in isolated small veins, 1) increases in pressure and H2O2 elicit substantial constrictons, both of which are inhibited by catalase, indomethacin or SQ 29,548 suggesting that the myogenic mechanism is mediated by H2O2 ‐induced arachidonic acid derived constrictor metabolite(s) such as prostaglandin H2/thromboxane A2 acting on TP receptors. Support: AHA Founders Aff. 0855910D and Hungarian Sci. Res. Funds, OTKA‐T48376.