guanylate cyclase
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RSC Advances ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 251-264
Author(s):  
Ko-Hua Yu ◽  
Hsin-Yi Hung

Since 1994, YC-1 (Lificiguat) has been synthesized, and many targets for special bioactivities have been explored, such as stimulation of platelet-soluble guanylate cyclase, indirect elevation of platelet cGMP levels, and inhibition of HIF-1 and NF-κB.


2022 ◽  
Vol 124 (1) ◽  
pp. 151811
Author(s):  
Chengfeng Xing ◽  
Tao Zhang ◽  
Xiaolin Liu ◽  
Canmei Li ◽  
Gang Yang ◽  
...  

Pharmacology ◽  
2021 ◽  
pp. 1-6
Author(s):  
Masashi Tawa ◽  
Takashi Shimosato ◽  
Keisuke Nakagawa ◽  
Tomio Okamura ◽  
Mamoru Ohkita

Soluble guanylate cyclase (sGC) plays an important role in nitric oxide (NO)-mediated regulation of vascular tone; however, NO bioavailability is often reduced in diseased blood vessels. Accumulating evidence suggests that a shift of sGC from the NO-sensitive form to the NO-insensitive form could be an underlying cause contributing to this reduction. Herein, we investigated the impact of renovascular hypertension on NO-sensitive and NO-insensitive sGC-mediated relaxation in rat aortas. Renovascular hypertension was induced by partially clipping the left renal artery (2-kidneys, 1-clip; 2K1C) for 10 weeks. Systolic, diastolic, and mean arterial pressures were significantly increased in the 2K1C group when compared with the sham group. In addition, plasma thiobarbituric acid reactive substances and aortic superoxide generation were significantly enhanced in the 2K1C group when compared with those in the sham group. The vasorelaxant response of isolated aortas to the sGC stimulator BAY 41-2272 (NO-sensitive sGC agonist) was comparable between the sham and 2K1C groups. Likewise, the sGC activator BAY 60-2770 (NO-insensitive sGC agonist)-induced relaxation did not differ between the sham and 2K1C groups. In addition, the cGMP mimetic 8-Br-cGMP (protein kinase G agonist) induced similar relaxation in both groups. Furthermore, there were no differences in BAY 41-2272-stimulated and BAY 60-2770-stimulated cGMP generation between the groups. These findings suggest that the balance between NO-sensitive and NO-insensitive forms of sGC is maintained during renovascular hypertension. Therefore, sGC might not be responsible for the reduced NO bioavailability observed during renovascular hypertension.


2021 ◽  
Vol 77 (10) ◽  
pp. 615-621
Author(s):  
Beata Jacuś ◽  
Mirosława Kowalkowska ◽  
Paweł Miękus ◽  
Grzegorz Grześk

2021 ◽  
Author(s):  
S.O. Svitko ◽  
K.S. Koroleva ◽  
G.F. Sitdikova ◽  
K.A. Petrova

Nitric oxide (NO) is a gaseous signaling molecule that regulates a number of physiological functions, including its role in the formation of migraine has been established. NO is endogenously produced in the body from L-arginine by NO synthase. The NO donor, nitroglycerin, is a trigger of migraine in humans and is widely used in the modeling of this disease in animals, which suggests the involvement of components of the NO signaling cascade in the pathogenesis of migraine. Based on the results obtained, it was found that an increase in the concentration of both the substrate for the synthesis of NO, L-arginine, and the NO donor, sodium nitroprusside, has a pro-nociceptive effect in the afferents of the trigeminal nerve. In this case, the effect of sodium nitroprusside is associated with the activation of intracellular soluble guanylate cyclase. Key words: nitric oxide, migraine, trigeminal nerve, L-arginine, guanylate cyclase, sodium nitroprusside, nociception.


Author(s):  
Stuart M. Brierley ◽  
Luke Grundy ◽  
Joel Castro ◽  
Andrea M. Harrington ◽  
Gerhard Hannig ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maximilian W. Schenk ◽  
Sam Humphrey ◽  
A. S. Md Mukarram Hossain ◽  
Mitchell Revill ◽  
Sarah Pearsall ◽  
...  

AbstractSmall cell lung cancer (SCLC) has a 5-year survival rate of <7%. Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. We exploit six paired pre-treatment and post-chemotherapy circulating tumour cell patient-derived explant (CDX) models from donors with extensive stage SCLC to investigate changes at disease progression after chemotherapy. Soluble guanylate cyclase (sGC) is recurrently upregulated in post-chemotherapy progression CDX models, which correlates with acquired chemoresistance. Expression and activation of sGC is regulated by Notch and nitric oxide (NO) signalling with downstream activation of protein kinase G. Genetic targeting of sGC or pharmacological inhibition of NO synthase re-sensitizes a chemoresistant CDX progression model in vivo, revealing this pathway as a mediator of chemoresistance and potential vulnerability of relapsed SCLC.


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