Activation of Soluble Guanylate Cyclase by Carbon Monoxide and Nitric Oxide: A Mechanistic Model

Methods ◽  
1999 ◽  
Vol 19 (4) ◽  
pp. 494-505 ◽  
Author(s):  
Vijay S. Sharma ◽  
Douglas Magde
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Mechanistic Model

scholarly journals In vivo exposure to carbon monoxide causes delayed impairment of activation of soluble guanylate cyclase by nitric oxide in rat brain cortex and cerebellum

2004 ◽  
Vol 89 (5) ◽  
pp. 1157-1165 ◽  
Author(s):  
Mariluz Hernandez-Viadel ◽  
Anna F. Castoldi ◽  
Teresa Coccini ◽  
Luigi Manzo ◽  
Slaven Erceg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Rat Brain ◽  
Guanylate Cyclase ◽  
Brain Cortex ◽  
Soluble Guanylate Cyclase ◽  
Rat Brain Cortex

Comparative efficiency of three gasotransmitters (nitric oxide, hydrogen sulfide and carbon monoxide): Analysis on the model of red blood cell micro rheological responses

2020 ◽  
pp. 1-9
Author(s):  
A.V. Muravyov ◽  
I.A. Tikhomirova ◽  
P.V. Avdonin ◽  
S.V. Bulaeva ◽  
Ju.V. Malisheva
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Red Blood Cells ◽  
Guanylate Cyclase ◽  
Blood Cells ◽  
Soluble Guanylate Cyclase ◽  
Comparative Efficiency ◽  
Rbc Aggregation ◽  
Endogenous Synthesis

BACKGROUND: It is now known regulatory effect of gaseous mediators in many bodily functions. These mediators include nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S). However, detailed data on the regulatory role of each of these gasotransmitters (GTs) are still not sufficiently studied. OBJECTIVE: The aim of this study was to investigate on models of microrheological behaviour of intact red blood cells and their recovered ghosts of cellular responses to all three known gasotransmitters: NO, H2S, and CO. METHODS: In experiments with intact red blood cells (RBCs) and their recovered ghosts (filled with an isotonic solution of known viscosity), deformability (RBCD) and aggregation (RBCA) were recorded after incubation of cells with GT donors or stimulators of their endogenous synthesis. RESULTS: It was found that all three GT donors moderately increased the deformability of both intact RBCs and their recovered ghosts (by 5–10%, p <  0.05). In addition GT donors and substrates of their endogenous synthesis significantly reduced RBCA, from 20 to 37%(p <  0.01). Experiments with inhibition of soluble guanylate cyclase (s-GC) almost completely eliminated the RBCD increasing effect of GT donors CONCLUSION: In present study it was demonstrated that all three known gaseous mediators: NO, CO and H2S cause moderate statistically significant positive alterations in RBC deformability as well as a noticeable decrease in RBC aggregation. This was confirmed both in experiments with gasotransmitter donors and stimulators of GT endogenous synthesis. In addition, the data obtained suggest that RBC microrheological responses to the actions of all three GTs are associated with activation of the guanylate cyclase signalling cascade.

A novel role for carbon monoxide as a potent regulator of intracellular Ca2+and nitric oxide in rat pancreatic acinar cells

2014 ◽  
Vol 307 (11) ◽  
pp. C1039-C1049 ◽  
Author(s):  
Amira Moustafa ◽  
Yoshiaki Habara
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Acinar Cells ◽  
Pancreatic Acinar Cells ◽  
Amylase Secretion ◽  
No Production ◽  
Dependent Manner ◽  
Nos Inhibitor

Carbon monoxide (CO) is known as an essential gaseous messenger that regulates a wide array of physiological and pathological processes, similar to nitric oxide (NO) and hydrogen sulfide. The aim of the present study was to elucidate the potential role of CO in Ca2+homeostasis and to explore the underlying mechanisms in pancreatic acinar cells. The exogenous application of a CO-releasing molecule dose-dependently increased intracellular Ca2+concentration ([Ca2+]i). A heme oxygenase (HO) inducer increased [Ca2+]iin a concentration-dependent manner, and the increase was diminished by an HO inhibitor. The CO-induced [Ca2+]iincrease persisted in the absence of extracellular Ca2+, indicating that Ca2+release is the initial source for the increase. The inhibition of G protein, phospholipase C (PLC), and inositol 1,4,5-trisphosphate (IP3) receptor diminished the CO-induced [Ca2+]iincrease. CO upregulated endothelial nitric oxide synthase (eNOS) expression and stimulated NO production, and NOS inhibitor, calmodulin inhibitor, or the absence of extracellular Ca2+eliminated the latter response. Blocking the phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) pathway abolished CO-induced NO production. Pretreatment with an NOS inhibitor, NO scavenger, or soluble guanylate cyclase inhibitor, did not affect the CO-induced [Ca2+]iincrease, indicating that NO, soluble guanylate cyclase, and cyclic guanosine 5′-monophosphate are not involved in the CO-induced [Ca2+]iincrease. CO inhibited the secretory responses to CCK-octapeptide or carbachol. We conclude that CO acts as a regulator not only for [Ca2+]ihomeostasis via a PLC-IP3-IP3receptor cascade but also for NO production via the calmodulin and PI3K-Akt/PKB pathway, and both CO and NO interact. Moreover, CO may provide potential therapy to ameliorate acute pancreatitis by inhibiting amylase secretion.

Vasoactivity of the gasotransmitters hydrogen sulfide and carbon monoxide in the chicken ductus arteriosus

2011 ◽  
Vol 301 (4) ◽  
pp. R1186-R1198 ◽  
Author(s):  
Saskia van der Sterren ◽  
Pamela Kleikers ◽  
Luc J. I. Zimmermann ◽  
Eduardo Villamor
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Guanylate Cyclase ◽  
Vascular Tone ◽  
Soluble Guanylate Cyclase ◽  
Ductus Arteriosus ◽  
No Synthase ◽  
Mechanical Responses ◽  
Synthase Inhibitor

Besides nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H2S) is a third gaseous messenger that may play a role in controlling vascular tone and has been proposed to serve as an O2 sensor. However, whether H2S is vasoactive in the ductus arteriosus (DA) has not yet been studied. We investigated, using wire myography, the mechanical responses induced by Na2S (1 μM–1 mM), which forms H2S and HS− in solution, and by authentic CO (0.1 μM-0.1 mM) in DA rings from 19-day chicken embryos. Na2S elicited a 100% relaxation (pD2 4.02) of 21% O2-contracted and a 50.3% relaxation of 62.5 mM KCl-contracted DA rings. Na2S-induced relaxation was not affected by presence of the NO synthase inhibitor l-NAME, the soluble guanylate cyclase (sGC) inhibitor ODQ, or the K+ channel inhibitors tetraethylammonium (TEA; nonselective), 4-aminopyridine (4-AP, KV), glibenclamide (KATP), iberiotoxin (BKCa), TRAM-34 (IKCa), and apamin (SKCa). CO also relaxed O2-contracted (60.8% relaxation) and KCl-contracted (18.6% relaxation) DA rings. CO-induced relaxation was impaired by ODQ, TEA, and 4-AP (but not by l-NAME, glibenclamide, iberiotoxin, TRAM-34 or apamin), suggesting the involvement of sGC and KV channel stimulation. The presence of inhibitors of H2S or CO synthesis as well as the H2S precursor l-cysteine or the CO precursor hemin did not significantly affect the response of the DA to changes in O2 tension. Endothelium-dependent and -independent relaxations were also unaffected. In conclusion, our results indicate that the gasotransmitters H2S and CO are vasoactive in the chicken DA but they do not suggest an important role for endogenous H2S or CO in the control of chicken ductal reactivity.

Nitric oxide-independent stimulation of soluble guanylate cyclase reduces organ damage in experimental low-renin and high-renin models

2010 ◽  
Vol 28 (8) ◽  
pp. 1666-1675 ◽  
Author(s):  
Yuliya Sharkovska ◽  
Philipp Kalk ◽  
Bettina Lawrenz ◽  
Michael Godes ◽  
Linda Sarah Hoffmann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Organ Damage ◽  
Stimulation Of
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