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Kengo Takahashi, Taiji Nagaoka, Tsuneaki Omae, Shinji Ono, Takayuki Kamiya, Akira Tanner, Akitoshi Yoshida; Thrombin causes biphasic regulation of vascular tone in porcine retinal arteries. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3030.
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© ARVO (1962-2015); The Authors (2016-present)
Thrombin, a serine protease, plays an important role in hemostasis by converting fibrinogen to fibrin. In the vasculature, thrombin had been reported to cause vasodilation, whereas a previous study reported that thrombin causes vasoconstriction in bovine retinal arteries. However, the effect of thrombin on the retinal microcirculation remains unclear. We examined the effects of thrombin on the retinal microvasculature and investigated the signaling mechanisms.
Porcine retinal arterioles were isolated, cannulated, and pressurized (55 cm H2O) without flow for this in vitro study. Videomicroscopic techniques were used to record the changes in diameter in the retinal arterioles in response to thrombin at concentrations of 0.001 mU/ml to 20 mU/ml.
Thrombin induced a concentration-dependent vascular response, i.e., initially vasoconstriction at a low concentration (<5 mU/mL) and then vasodilation at a high concentration (>5 mU/mL). Pretreatment with a protease-activated receptor (PAR)-1 inhibitor but not a PAR-2 or PAR-4 inhibitor significantly (p<0.01) suppressed thrombin-induced constriction. Endothelial denudation suppressed vasodilation caused by a high concentration of thrombin.
The current findings suggested that the low dose of thrombin causes vasoconstriction via a PAR-1 on smooth muscle, and the high dose of thrombin causes endothelium-dependent vasodilation in the retinal arterioles.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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