Vascular reactivity to vasopressin during diabetes: gender and regional differences.

The isometric response to vasopressin of 2-mm-long segments of basilar, coronary, renal and tail arteries from male and female, control (normoglycemic) and streptozotocin-induced diabetic rats was studied. Vasopressin (10(-12)-3 x 10(-8) M) produced arterial concentration-dependent contraction, with a lower potency in coronary arteries from female than from male rats, and was similar for both genders in basilar, renal and tail arteries. This contraction was reduced by diabetes in basilar and coronary arteries, increased in renal arteries, and not modified in tail arteries, in both genders. Inhibition of nitric oxide synthesis with N(W)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) increased the contraction to vasopressin in coronary arteries from control female and diabetic female rats; as well as in renal arteries from control male and control female rats, but not in any other experimental group. Inhibition of cyclooxygenase with meclofenamate (10(-5) M) reduced the contraction to vasopressin in basilar arteries from diabetic female rats and in renal arteries from diabetic male rats, but not in any other experimental group. These results suggest that the response to vasopressin (a) has lower potency in female coronary arteries due to higher nitric oxide production; (b) is reduced by diabetes in basilar and coronary arteries from both genders, by mechanisms independent of nitric oxide and prostanoids; and (c) is increased by diabetes in renal arteries due to reduced production of nitric oxide in females, and to both reduced production of nitric oxide and increased production of prostanoids in males. Therefore, the effects of diabetes on vascular reactivity to vasopressin may differ between vascular beds, and the mechanisms underlay these effects may be distinct between genders.