Hyporeactivity of renal artery to angiotensin II in septic rats.

Although reduced vascular reactivity to vasoconstrictors has been well documented, it is not clear whether renal blood flow (RBF) and renal vascular response exhibit the same pattern following sepsis. We examined RBF and renal vascular response during early sepsis. Male Sprague-Dawley rats underwent cecal ligation and puncture (CLP)-induced sepsis. At 5 h after CLP or sham operation, RBF and plasma nitric oxide (NO) concentration were measured. Moreover, angiotensin II (50 ng/kg body weight) was employed to evaluate the renal vascular response (n = 12 rats/group). The results showed that CLP caused higher heart rate (HR), RBF and lower renal vascular resistance (RVR). In addition, plasma nitrite-nitrate (NOx) increased significantly after CLP. After angiotensin II infusion, maximal response in mean blood pressure (MBP), RBF and RVR were less in CLP rats. Thus, we found that CLP induced hyporeactivity of renal artery together with overproduction of NO during an early stage of sepsis.