Elevated glucose blocks angiotensin-(1-7) and bradykinin interaction:: the role of cyclooxygenase products

The interaction between angiotensin-(1-7) [Ang-(1-7)] and bradykinin (BK) was studied in the isolated mesenteric arteriolar bed of control and diabetic rats perfused with either 5.5 or 22 mM of glucose. Prostanoids release after the administration of BK, Ang-(1-7) and Ang-(1-7) + BK was also studied. In control and diabetic preparations perfused with Krebs Henseleit solution with 5.5 MM of glucose, Ang-(1-7) potentiates BK-induced vasodilation. On the other hand, the potentiating effect disappeared in control and diabetic preparations perfused with 22 mM of glucose. Prostaglandin F-2alpha (PGF(2alpha)) release induced by BK and Ang-(1-7) + BK was increased in perfusates of diabetic preparations containing 22 mM of glucose. The release of thromboxane A(2) (TXA(2)) (measured as TXB2) or prostaglandin I-2 (PGI(2)) (measured as 6-keto-PGF(1alpha)) did not differ in control and diabetic preparations perfused with 5.5 and 22 nM of glucose. Our data allow us to suggest that hyperglycemia may be involved in the lack of potentiation in control and diabetic preparations; increase in PGF(2alpha) release, but not other cyclooxygenase products, may explain the absence of potentiation in diabetic preparations. (C) 2003 Elsevier Science Inc. All rights reserved.