THE EFFECT OF A NITRIC-OXIDE DONOR AND AN INHIBITOR OF NITRIC-OXIDE SYNTHASE ON BLOOD-FLOW AND VASCULAR-RESISTANCE IN FELINE SUBMANDIBULAR,PAROTID AND PANCREATIC GLANDS

The aim was to examine whether (1) blood flow and vascular resistance are altered in response to exogenous nitric oxide and (2) whether endo genous synthesis of nitric oxide participates in the haemodynamic regu lation of the submandibular, parotid and pancreatic glands. Experiment s were performed on anaesthetized, artificially ventilated cats. Mean arterial blood pressure, heart rate, blood gases, cardiac output and t issue blood flow were determined before and 15 min after intravenous a dministration of either the nitric oxide donor SIN-1 (3-morpholinosydn onimine, I mg/kg, n = 10) or the competitive nitric oxide synthase inh ibitor NOLA (N-G-nitro-L-arginine, 30 mg/kg, n = 9). Blood flow was me asured by a radioactive-labelled microsphere method. In the SIN-I grou p, in spite of a serious decrease in mean arterial blood pressure (p < 0.001), the blood flow in the glands remained unchanged. The vascular resistance decreased after SIN-I in the submandibular and pancreatic glands (p < 0.001 and p < 0.05, respectively), and was slightly reduce d in the parotid. The NOLA increased mean arterial blood pressure (p < 0.01) and reduced the blood flow in the submandibular and pancreatic glands (p < 0.01 and p < 0.001, respectively), but the decrease in the parotid was not significant. Vascular resistance increased after NOLA in all three glands (p < 0.05, p < 0.001 and p < 0.05). These finding s suggest that basal nitric oxide production in these exocrine glands is sufficient to modulate vascular resistance. Moreover, the release o f endogenous NO from the nerves and/or endothelium is probably involve d in the regulation of vascular tone. The nitric oxide-dependent compo nent of blood-flow regulation, however, seems to be less pronounced in the parotid gland. Copyright (C) 1996 Elsevier Science Ltd.