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 endogenous synthesis of nitric oxide participates in the haemodynamic regulation of the submandibular, parotid and pancreatic glands. Experiments were performed on anaesthetized, artificially ventilated cats. Mean arterial blood pressure, heart rate, blood gases, cardiac output and tissue blood flow were determined before and 15 min after intravenous administration of either the nitric oxide donor SIN-1 (3-morpholinosydnonimine, 1 mg/kg, n = 10) or the competitive nitric oxide synthase inhibitor NOLA (NG-nitro-L-arginine, 30 mg/kg, n = 9) blood flow was measured by a radioactive-labelled microsphere method. In the SIN-1 group, 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-1 in the submandibular and pancreatic glands (p < 0.001 and p < 0.05, respectively), and was slightly reduced 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 findings suggest that basal nitric oxide production in these exocrine glands is sufficient to modulate vascular resistance. Moreover, the release of endogenous NO from the nerves and/or endothelium is probably involved in the regulation of vascular tone. The nitric oxide-dependent component of blood-flow regulation, however, seems to be less pronounced in the parotid gland.
Lohinai
Z
Z
Experimental Research Department-2nd Institute of Physiology, Semmelweis University Medical School, Budapest, Hungary. Lohinai@elet2.sote.hu
Balla
I
I
Marczis
J
J
Vass
Z
Z
Kovách
A G
AG
D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D004730:Endothelium, Vascular / Q000201:enzymology / Q000294:innervation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005088:Exocrine Glands / Q000098:blood supply* / Q000201:enzymology; D006439:Hemodynamics / Q000187:drug effects*; D008297:Male; D008981:Molsidomine / Q000031:analogs & derivatives / Q000494:pharmacology; D009412:Nerve Fibers / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019335:Nitroarginine / Q000494:pharmacology; D010179:Pancreas / Q000098:blood supply / Q000201:enzymology; D010306:Parotid Gland / Q000098:blood supply / Q000201:enzymology; D012039:Regional Blood Flow / Q000187:drug effects; D013363:Submandibular Gland / Q000098:blood supply / Q000201:enzymology; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D019335:Nitroarginine; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine; D019001:Nitric Oxide Synthase