Mechanisms of nitric oxide-mediated, neurogenic vasodilation in mesenteric resistance arteries of toad Bufo marinus

2010 ◽  
Vol 298 (3) ◽  
pp. R767-R775 ◽  
Author(s):  
Brett L. Jennings ◽  
John A. Donald
Keyword(s):  
Nitric Oxide ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Bufo Marinus ◽  
Mesenteric Arteries ◽  
Induced Response ◽  
Resistance Arteries ◽  
Nos Inhibitors ◽  
Toad Bufo ◽  
Neurogenic Vasodilation

This study determined the role of nitric oxide (NO) in neurogenic vasodilation in mesenteric resistance arteries of the toad Bufo marinus . NO synthase (NOS) was anatomically demonstrated in perivascular nerves, but not in the endothelium. ACh and nicotine caused TTX-sensitive neurogenic vasodilation of mesenteric arteries. The ACh-induced vasodilation was endothelium-independent and was mediated by the NO/soluble guanylyl cyclase signaling pathway, inasmuch as the vasodilation was blocked by the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and the NOS inhibitors Nω-nitro-l-arginine methyl ester and Nω-nitro-l-arginine. Furthermore, the ACh-induced vasodilation was significantly decreased by the more selective neural NOS inhibitor N5-(1-imino-3-butenyl)-l-ornithine. The nicotine-induced vasodilation was endothelium-independent and mediated by NO and calcitonin gene-related peptide (CGRP), inasmuch as pretreatment of mesenteric arteries with a combination of Nω-nitro-l-arginine and the CGRP receptor antagonist CGRP-(8–37) blocked the vasodilation. Clotrimazole significantly decreased the ACh-induced response, providing evidence that a component of the NO vasodilation involved Ca2+-activated K+ or voltage-gated K+ channels. These data show that NO control of mesenteric resistance arteries of toad is provided by nitrergic nerves, rather than the endothelium, and implicate NO as a potentially important regulator of gut blood flow and peripheral blood pressure.

Nitric oxide regulation of the central aortae of the toad Bufo marinus occurs independently of the endothelium

2002 ◽  
Vol 205 (19) ◽  
pp. 3093-3100 ◽  
Author(s):  
Brad R. S. Broughton ◽  
John A. Donald
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylyl Cyclase ◽  
Rat Aorta ◽  
Bufo Marinus ◽  
Organ Bath ◽  
Perivascular Nerves ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Toad Bufo

SUMMARY Nitric oxide (NO) signalling pathways were examined in the lateral aortae and dorsal aorta of the cane toad Bufo marinus. NADPH diaphorase histochemistry and nitric oxide synthase (NOS) immunohistochemistry found no evidence for endothelial NOS in the endothelium of toad aortae, but it could be readily demonstrated in rat aorta that was used as a control. Immunohistochemistry using a specific neural NOS antibody showed the presence of neural NOS immunoreactivity in the perivascular nerves of the aortae. The anatomical data was supported by in vitro organ bath physiology,which demonstrated that the vasodilation mediated by applied acetylcholine(10-5 mol l-1) was not dependent on the presence of the vascular endothelium; however, it was significantly reduced in the presence of a neural NOS inhibitor, vinyl-L-NIO (10-4 mol l-1). In addition, atropine (10-6 mol l-1) (a muscarinic receptor inhibitor), L-NNA (10-4 mol l-1) (a NOS inhibitor) and ODQ (10-5 mol l-1) (an inhibitor of soluble guanylyl cyclase) abolished the vasodilatory effect of applied acetylcholine. In conclusion, we propose that an endothelial NO system is absent in toad aortae and that NO generated by neural NOS in perivascular nerves mediates vasodilation.

scholarly journals Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin in Clione limacina Central Pattern Generator Swim Interneurons

2020 ◽  
Author(s):  
Thomas J Pirtle ◽  
Richard A Satterlie
Keyword(s):  
Nitric Oxide ◽  
Central Pattern Generator ◽  
Guanylyl Cyclase ◽  
Signal Transduction Pathway ◽  
Soluble Guanylyl Cyclase ◽  
Cyclic Guanosine Monophosphate ◽  
Pattern Generator ◽  
Guanosine Monophosphate ◽  
Cellular Changes ◽  
Clione Limacina

Abstract Typically, the marine mollusk, Clione limacina, exhibits a slow, hovering locomotor gait to maintain its position in the water column. However, the animal exhibits behaviorally relevant locomotor swim acceleration during escape response and feeding behavior. Both nitric oxide and serotonin mediate this behavioral swim acceleration. In this study, we examine the role that the second messenger, cGMP, plays in mediating nitric oxide and serotonin-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of soluble guanylyl cyclase decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in Clione. Because nitric oxide has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in Clione swim interneurons that are consistent with cellular changes produced by serotonin application, we hypothesize that both nitric oxide and serotonin function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates nitric oxide-induced but not serotonin-induced swim acceleration in Clione.

scholarly journals Nitric Oxide Activates the β2Subunit of Soluble Guanylyl Cyclase in the Absence of a Second Subunit

2001 ◽  
Vol 276 (33) ◽  
pp. 30737-30743 ◽  
Author(s):  
Markus Koglin ◽  
Kai Vehse ◽  
Lars Budaeus ◽  
Hasso Scholz ◽  
Sönke Behrends
Keyword(s):  
Nitric Oxide ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase

Maturational changes in the regulation of pulmonary vascular tone by nitric oxide in neonatal rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1261-L1270 ◽  
Author(s):  
Louis G. Chicoine ◽  
Michael L. Paffett ◽  
Mark R. Girton ◽  
Matthew J. Metropoulus ◽  
Mandar S. Joshi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guanylyl Cyclase ◽  
Vascular Tone ◽  
Age Groups ◽  
Soluble Guanylyl Cyclase ◽  
No Production ◽  
Sprague Dawley ◽  
No Donor ◽  
Early Postnatal Development ◽  
Old Rats

Nitric oxide (NO) is an important regulator of vasomotor tone in the pulmonary circulation. We tested the hypothesis that the role NO plays in regulating vascular tone changes during early postnatal development. Isolated, perfused lungs from 7- and 14-day-old Sprague-Dawley rats were studied. Baseline total pulmonary vascular resistance (PVR) was not different between age groups. The addition of KCl to the perfusate caused a concentration-dependent increase in PVR that did not differ between age groups. However, the nitric oxide synthase (NOS) inhibitor Nω-nitro-l-arginine augmented the K+-induced increase in PVR in both groups, and the effect was greater in lungs from 14-day-old rats vs. 7-day-old rats. Lung levels of total endothelial, inducible, and neuronal NOS proteins were not different between groups; however, the production rate of exhaled NO was greater in lungs from 14-day-old rats compared with those of 7-day-old rats. Vasodilation to 0.1 μM of the NO donor spermine NONOate was greater in 14-day lungs than in 7-day lungs, and lung levels of both soluble guanylyl cyclase and cGMP were greater at 14 days than at 7 days. Vasodilation to 100 μM of the cGMP analog 8-(4-chlorophenylthio)guanosine-3′,5′-cyclic monophosphate was greater in 7-day lungs than in 14-day lungs. Our results demonstrate that the pulmonary vascular bed depends more on NO production to modulate vascular tone at 14 days than at 7 days of age. The observed differences in NO sensitivity may be due to maturational increases in soluble guanylyl cyclase protein levels.

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