Abstract

Diabetes is associated with altered autonomic activity, and both the peripheral and central nervous content of NPY is altered in diabetes suggesting that part of the cardiovascular dysfunction of diabetes may be associated with altered responses to NPY. We evaluated the mean arterial pressure (MAP), heart rate (HR) and regional blood flow (BF) in response to NPY in normal and diabetic rats. Male Wistar rats were made diabetic using streptozotocin and maintained without insulin treatment for 28-30 days. Normal and diabetic animals were anesthetized, the femoral artery cannulated, and flow probes placed around the iliac, renal and superior mesenteric arteries. Dose dependent responses to NPY infusion were determined for MAP, HR and BF. Conductance was calculated from BF/MAP. In normal rats NPY increased the MAP in a dose-dependent fashion but did not alter the HR. NPY decreased the BF in the iliac artery in a dose-dependent fashion while the renal BF was decreased only at the highest dose, and the superior mesenteric BF was not affected. The conductances in all vascular beds were decreased dose dependently. NPY in diabetic rats also increased MAP and did not affect HR. In diabetic rats NPY also decreased BF in iliac and renal arteries but contrastingly increased BF in the superior mesenteric artery. Again conductances in all three vascular beds were decreased by NPY. When comparing diabetic response to NPY to normals we noted that the MAP response was less in the diabetic, but the HR and regional BF were not different. The vascular conductances in response to NPY were attenuated in the diabetic vessels especially the iliac and superior mesenteric. We conclude that systemic NPY increases MAP as a result of decreased vascular conductance and this vasopressive effect of NPY is diminished in diabetics.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.