Neuronal nitric oxide synthase and splanchnic blood flow in anaesthetized rats

Abstract

To evaluate to what extent the neuronal form of constitutive nitric oxide synthase (nNOS) contributes to the blood perfusion of splanchnic organs, including the islets of Langerhans. The nNOS inhibitor 7-nitroindazole (300 mg kg(-1) i.p.) was administered to anaesthetized Sprague-Dawley rats, some of which were pre-treated with the ganglionic blocker hexamethonium (20 mg kg(-1) i.v.) The blood perfusion of the splanchnic organs, including the pancreatic islets was then measured with a microsphere technique. Nitroindazole decreased total pancreatic, duodenal and renal blood flow, whereas pancreatic islet, colonic and adrenal blood flows were unchanged. A slight increase in mean arterial blood pressure was seen after nitroindazole treatment. Nitroindazole did not affect blood glucose or serum insulin concentrations. In separate experiments, hexamethonium affected none of the studied blood flow values, suggesting that the effects of nNOS-inhibition were not mediated from the nervous system. Nitric oxide derived from the activity of nNOS contributes to the blood perfusion in the upper portions of the gastrointestinal tract, viz. the parts supplied by the cranial mesenteric artery, and the kidneys, whilst no effects are seen on colonic or adrenal blood flow. Pancreatic islet blood flow was unaffected by nNOS inhibition, thereby suggesting that NO derived from the other isoforms of NOS maintains the high basal islet blood perfusion.