scholarly journals Role of Cyclic Guanosine Monophosphate in Late Preconditioning in Conscious Rabbits

Circulation ◽  
2002 ◽  
Vol 105 (25) ◽  
pp. 3046-3052 ◽  
Author(s):  
Eitaro Kodani ◽  
Yu-Ting Xuan ◽  
Hitoshi Takano ◽  
Ken Shinmura ◽  
Xian-Liang Tang ◽  
...  
Keyword(s):  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Late Preconditioning ◽  
Conscious Rabbits

scholarly journals Current Modulation of Guanylate Cyclase Pathway Activity—Mechanism and Clinical Implications

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3418
Author(s):  
Grzegorz Grześk ◽  
Alicja Nowaczyk
Keyword(s):  
Guanylate Cyclase ◽  
Natriuretic Peptides ◽  
Soluble Guanylate Cyclase ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Pharmacological Intervention ◽  
First Line ◽  
Phosphodiesterase Type ◽  
Activity Mechanism

For years, guanylate cyclase seemed to be homogenic and tissue nonspecific enzyme; however, in the last few years, in light of preclinical and clinical trials, it became an interesting target for pharmacological intervention. There are several possible options leading to an increase in cyclic guanosine monophosphate concentrations. The first one is related to the uses of analogues of natriuretic peptides. The second is related to increasing levels of natriuretic peptides by the inhibition of degradation. The third leads to an increase in cyclic guanosine monophosphate concentration by the inhibition of its degradation by the inhibition of phosphodiesterase type 5. The last option involves increasing the concentration of cyclic guanosine monophosphate by the additional direct activation of soluble guanylate cyclase. Treatment based on the modulation of guanylate cyclase function is one of the most promising technologies in pharmacology. Pharmacological intervention is stable, effective and safe. Especially interesting is the role of stimulators and activators of soluble guanylate cyclase, which are able to increase the enzymatic activity to generate cyclic guanosine monophosphate independently of nitric oxide. Moreover, most of these agents are effective in chronic treatment in heart failure patients and pulmonary hypertension, and have potential to be a first line option.

Sustainability and Chaos in the Abiotic Polymerization of 3′,5′ Cyclic Guanosine Monophosphate: The Role of Aggregation

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Giovanna Costanzo ◽  
Judit E. Šponer ◽  
Jiří Šponer ◽  
Angela Cirigliano ◽  
Piero Benedetti ◽  
...  
Keyword(s):  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate

scholarly journals Bifunctional Role of Protein Tyrosine Kinases in Late Preconditioning Against Myocardial Stunning in Conscious Rabbits

1999 ◽  
Vol 85 (12) ◽  
pp. 1154-1163 ◽  
Author(s):  
Buddhadeb Dawn ◽  
Yu-Ting Xuan ◽  
Yumin Qiu ◽  
Hitoshi Takano ◽  
Xian-Liang Tang ◽  
...  
Keyword(s):  
Tyrosine Kinases ◽  
Myocardial Stunning ◽  
Protein Tyrosine Kinases ◽  
Protein Tyrosine ◽  
Late Preconditioning ◽  
Conscious Rabbits

scholarly journals cGAS-mediated autophagy protects the liver from ischemia-reperfusion injury independently of STING

2018 ◽  
Vol 314 (6) ◽  
pp. G655-G667 ◽  
Author(s):  
Zhao Lei ◽  
Meihong Deng ◽  
Zhongjie Yi ◽  
Qian Sun ◽  
Richard A. Shapiro ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Adenosine Monophosphate ◽  
Cyclic Guanosine Monophosphate ◽  
Protective Role ◽  
Guanosine Monophosphate ◽  
Independent Manner

Liver ischemia-reperfusion (I/R) injury occurs through induction of oxidative stress and release of damage-associated molecular patterns (DAMPs), including cytosolic DNA released from dysfunctional mitochondria or from the nucleus. Cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) synthase (cGAS) is a cytosolic DNA sensor known to trigger stimulator of interferon genes (STING) and downstream type 1 interferon (IFN-I) pathways, which are pivotal innate immune system responses to pathogen. However, little is known about the role of cGAS/STING in liver I/R injury. We subjected C57BL/6 (WT), cGAS knockout (cGAS−/−), and STING-deficient (STINGgt/gt) mice to warm liver I/R injury and that found cGAS−/− mice had significantly increased liver injury compared with WT or STINGgt/gt mice, suggesting a protective effect of cGAS independent of STING. Liver I/R upregulated cGAS in vivo and also in vitro in hepatocytes subjected to anoxia/reoxygenation (A/R). We confirmed a previously published finding that hepatocytes do not express STING under normoxic conditions or after A/R. Hepatocytes and liver from cGAS−/− mice had increased cell death and reduced induction of autophagy under hypoxic conditions as well as increased apoptosis. Protection could be restored in cGAS−/− hepatocytes by overexpression of cGAS or by pretreatment of mice with autophagy inducer rapamycin. Our findings indicate a novel protective role for cGAS in the regulation of autophagy during liver I/R injury that occurs independently of STING. NEW & NOTEWORTHY Our studies are the first to document the important role of cGAS in the acute setting of sterile injury induced by I/R. Specifically, we provide evidence that cGAS protects liver from I/R injury in a STING-independent manner.

Reduced Natriuretic Effect of Atrial Natriuretic Peptide in Nephrotic Syndrome: A Possible Role of Decreased Cyclic Guanosine Monophosphate

Nephron ◽  
1995 ◽  
Vol 71 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Bente Jespersen ◽  
Hans Eiskjœr ◽  
Carl E. Mogensen ◽  
Søren S. Sørensen ◽  
Erling Bjerregaard Pedersen
Keyword(s):  
Nephrotic Syndrome ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Natriuretic Effect ◽  
Atrial Natriuretic

scholarly journals Endothelin in health and disease

2004 ◽  
Vol 4 (3) ◽  
pp. 31-34 ◽  
Author(s):  
Emina Nakaš-Ićindić ◽  
Asija Začiragić ◽  
Almira Hadžović ◽  
Nešina Avdagić
Keyword(s):  
Nitric Oxide ◽  
Amino Acids ◽  
Calcium Ions ◽  
Potential Role ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Health And Disease ◽  
Endothelin 3 ◽  
Stimulation Of

Endothelin is a recently discovered peptide composed of 21 amino acids. There are three endothelin isomers: endothelin -1 (ET-1), endothelin -2 (ET-2) and endothelin - 3 (ET-3). In humans and animals levels of ET-1, ET-2, ET-3 and big endothelin in blood range from 0,3 to 3 pg/ml. ET-1, ET-2 and ET-3 act by binding to receptors. Two main types of the receptors for endothelins exist and they are referred to as A and B type receptors. Different factors can stimulate or inhibit production of endothelin by endothelial cells. Mechanical stimulation of endothehum, thrombin, calcium ions, epinephrine, angiotensin II, vasopressin, dopamine, cytokines, growth factors stimulate the production of endothelin whereas nitric oxide, cyclic guanosine monophosphate, atrial natriuretic peptide, prostacyclin, bradykinin inhibit its production. Endothelins have different physiological roles in human body but at the same time their actions are involved in the pathogenesis of many diseases.The aim of this review was to present some of, so far, the best studied physiological roles of endothelin and to summarize evidence supporting the potential role of ET in the pathogenesis of certain diseases.

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