Diabetes, Vol 46, Issue 6 947-952, Copyright © 1997 by American Diabetes Association

ARTICLES

Islet capillary blood pressure increase mediated by hyperglycemia in NIDDM GK rats

PO Carlsson, L Jansson, CG Ostenson and O Kallskog
Department of Medical Cell Biology, Uppsala University, Sweden. per-ola.carlsson@medcellbiol.uu.se

This study was performed to measure pancreatic islet capillary pressure under basal conditions and after an acute glucose stimulation of insulin release in normal rats. In addition, the islet capillary pressure was estimated in GK rats, an animal model of NIDDM. Hydrostatic pressure in single pancreatic islet capillaries was determined in vivo by direct measurement using the micropuncture technique. The pancreatic islets were visualized by injection of neutral red. This intravital staining had no effect on islet function, whole pancreatic and islet blood flow, and capillary blood pressure in the exocrine pancreas. Islet capillary blood pressure in normoglycemic Wistar F rats was estimated at 3.1 +/- 0.3 mmHg (n = 15). Administration of D-glucose (1 g/kg) doubled this value, whereas no effect was seen after injection of an equimolar dose of the non-metabolizable glucose-derivative 3-O-methyl glucose. 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 Wistar F rats. Reduction of blood glucose levels in GK rats with phlorizin treatment showed this increased basal islet capillary pressure in GK rats to be glucose dependent and reversible. In the present study, we have for the first time shown that both acute and chronic hyperglycemia augment islet capillary pressure. The effects of a chronically increased islet capillary pressure on long-term islet function remain to be determined.
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