Vascular distribution of nitric oxide synthase and vasodilation in the Australian lungfish, Neoceratodus forsteri

• Published in: Comparative biochemistry and physiology. Part A, Molecular & integrative physiology Molecular & integrative physiology, 2008-12, Vol.151 (4), p.590-595
• Main Authors: Jennings, Brett L., Blake, Rachel E., Joss, Jean M.P., Donald, John A.
• Format: Article
• Language: English
• Subjects: Animals; Australia; Blood Vessels - enzymology; Brachial Artery - drug effects; Brachial Artery - physiology; Endothelium, Vascular - enzymology; Enzyme Inhibitors - pharmacology; Female; Fishes - physiology; Freshwater; Guanylate Cyclase - antagonists & inhibitors; Guanylate Cyclase - metabolism; Immunohistochemistry; In Vitro Techniques; Lungfish; Male; NADPH Dehydrogenase - metabolism; Neoceratodus forsteri; Nitric oxide; Nitric Oxide - physiology; Nitric Oxide Donors - pharmacology; Nitric oxide synthase; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type I - metabolism; Prostaglandins; Signal Transduction; Tissue Distribution; Vasodilation - drug effects; Vasodilation - physiology
• ISSN: 1095-6433; 1531-4332
• DOI: 10.1016/j.cbpa.2008.07.018

The presence of nitric oxide synthase (NOS) and role of nitric oxide (NO) in vascular regulation was investigated in the Australian lungfish, Neoceratodus forsteri. No evidence was found for NOS in the endothelium of large and small blood vessels following processing for NADPH-diaphorase histochemistry. However, both NADPH-diaphorase histochemistry and neural NOS immunohistochemistry demonstrated a sparse network of nitrergic nerves in the dorsal aorta, hepatic artery, and branchial arteries, but there were no nitrergic nerves in small blood vessels in tissues. In contrast, nitrergic nerves were found in non-vascular tissues of the lung, gut and kidney. Dual-wire myography was used to determine if NO signalling occurred in the branchial artery of N. forsteri. Both SNP and SIN-1 had no effect on the pre-constricted branchial artery, but the particulate guanylyl cyclase (GC) activator, C-type natriuretic peptide, always caused vasodilation. Nicotine mediated a dilation that was not inhibited by the soluble GC inhibitor, ODQ, or the NOS inhibitor, L-NNA, but was blocked by the cyclooxygenase inhibitor, indomethacin. These data suggest that NO control of the branchial artery is lacking, but that prostaglandins could be endothelial relaxing factors in the vasculature of lungfish.