Prolonged relaxation consistent with persistent soluble guanylyl cyclase activation in canine pulmonary artery following brief treatment with nitric oxide donors

Life Sciences ◽  
2006 ◽  
Vol 79 (21) ◽  
pp. 2001-2009 ◽  
Author(s):  
Young L. Kwak ◽  
Keith A. Jones ◽  
David O. Warner ◽  
William J. Perkins
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Artery ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Nitric Oxide Donors ◽  
Brief Treatment ◽  
Cyclase Activation

Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide

2007 ◽  
Vol 293 (1) ◽  
pp. L84-L95 ◽  
Author(s):  
William J. Perkins ◽  
Miwa Taniguchi ◽  
David O. Warner ◽  
Eduardo N. Chini ◽  
Keith A. Jones
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Artery ◽  
Protein Expression ◽  
Guanylyl Cyclase ◽  
Soluble Protein ◽  
Specific Activity ◽  
Soluble Guanylyl Cyclase ◽  
Prolonged Treatment ◽  
Camp Phosphodiesterase ◽  
Porcine Pulmonary Artery

In a newly characterized cultured porcine pulmonary artery (PA) preparation, 24-h treatment with the nitric oxide (NO) donor ( Z)-1-[ N-(2-aminoethyl)- N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) decreased the response to acutely applied DETA-NO compared with 24-h control (−log EC50 6.55 ± 0.12 and 5.02 ± 0.21, respectively). Treatment of PA with the cell-permeable superoxide dismutase mimetic, Mn(III) tetra(4-benzoic acid) porphyrin chloride, did not change NO responsiveness in either freshly prepared or 24-h DETA-NO-treated PA. cGMP and cAMP phosphodiesterase activities were approximately equal in PA. Twenty-four-hour DETA-NO treatment did not change either cGMP or cAMP phosphodiesterase activities. Twenty-four hours in culture had no significant effect on soluble guanylyl cyclase (sGC) subunit mRNA expression, but 24-h DETA-NO treatment significantly decreased the expression of both sGCα1 and sGCβ1. sGCβ1 protein expression was 42 ± 4 ng/mg soluble protein. Twenty-four hours in culture without and with DETA-NO reduced sGCβ1 protein expression (36 ± 3 and 31 ± 3 ng/mg soluble protein, respectively, P < 0.025). Basal tissue cGMP [(cGMP)i] was significantly increased, and NO-induced (cGMP)i was significantly decreased by 24-h DETA-NO treatment. (cGMP)i normalized to the amount of sGC protein expressed in PA was significantly lower in PA treated for 24 h with DETA-NO compared with both freshly isolated and 24-h cultured PA. We conclude that prolonged NO treatment induces decreased acute NO responsiveness in part by decreasing both sGC expression and sGC-specific activity.

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 Insights into Soluble Guanylyl Cyclase Activation Derived from Improved Heme-Mimetics

2013 ◽  
Vol 56 (21) ◽  
pp. 8948-8952 ◽  
Author(s):  
Margarete von Wantoch Rekowski ◽  
Vijay Kumar ◽  
Zongmin Zhou ◽  
Johann Moschner ◽  
Antonia Marazioti ◽  
...  
Keyword(s):  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Cyclase Activation

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
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