Blood flow-dependent prostaglandin F-2 alpha regulates intestinal glucose uptake from the blood

Intestinal glucose uptake (GU(i)) from blood increased when blood flow (BF) was increased. The increase in BF could elevate shear stress. Therefore, w e hypothesize that shear stress-induced release of autacoids mediates the i ncrease in GU(i). A surgically separated segment of small intestine was per fused in situ with the use of an arterial circuit in anesthetized cats. Art erial and portal blood samples were taken simultaneously for assessment of GU(i). Adenosine was used to elevate intestinal BF. The GU(i) increased by 45.0 +/- 18.3 from 25.3 +/-. 3.8 mu mol.min(-1).100 g tissue(-1) when the B F increased about four times. It was not a direct effect of adenosine becau se GU(i) was not altered if the flow was held constant. This increase was b locked by a cyclooxygenase inhibitor, indomethacin, but not by nitric oxide synthase blocker N-G-nitro-L-arginine methyl ester. Furthermore, prostagla ndin F-2 alpha (PGF(2 alpha)) but not PGE(2) or PGI(2) reversed the blockad e of the increase in GU(i) after indomethacin during elevated blood flow, w hereas they had no influence on basal uptake. The results suggest that shea r stress-induced release of PGF(2 alpha), mediated the increase in GU(i) wh en blood flow was elevated.