ISLET CAPILLARY BLOOD-PRESSURE INCREASE MEDIATED BY HYPERGLYCEMIA IN NIDDM GK RATS

This study was performed to measure pancreatic islet capillary pressur e under basal conditions and after an acute glucose stimulation of ins ulin release in normal rats. In addition, the islet capillary pressure was estimated in GK rats, an animal model of NIDDM. Hydrostatic press ure in single pancreatic islet capillaries was determined in vivo by d irect measurement using the micropuncture technique. The pancreatic is lets were visualized by injection of neutral red. This intravital stai ning had no effect on islet function, whole pancreatic and islet blood flow, and capillary blood pressure in the exocrine pancreas. Islet ca pillary blood pressure in normoglycemic Wistar F rats was estimated at 3.1 +/- 0.3 mmHg (n = 15). Administration of D-glucose (1 g/kg) doubl ed this value, whereas no effect was seen after injection of an equimo lar dose of the non-metabolizable glucose-derivative 3-O-methyl glucos e. In GK rats, basal islet capillary blood pressure was increased (5.7 +/- 0.4 mmHg; n = 10; P < 0.001) when compared with the control Wista r F rats. Reduction of blood glucose levels in GR rats with phlorizin treatment showed this increased basal islet capillary pressure in GR r ats to be glucose dependent and reversible. In the present study, we h ave for the first time shown that both acute and chronic hyperglycemia augment islet capillary pressure. The effects of a chronically increa sed islet capillary pressure on long-term islet function remain to be determined.