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Journal articles on the topic 'Soluble guanylyl cyclase stimulator'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Zuo, Zhiyi, and Roger A. Johns. "Halothane, Enflurane, and Isoflurane Do Not Affect the Basal or Agonist-stimulated Activity of Partially Isolated Soluble and Particulate Guanylyl Cyclases of Rat Brain." Anesthesiology 83, no. 2 (1995): 395–404. http://dx.doi.org/10.1097/00000542-199508000-00020.

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Background Evidence suggests that inhalational anesthetics interact with the nitric oxide-guanylyl cyclase signaling pathway in the central nervous system and that the inhibitation of this pathway in brain may result in an anesthetic, analgesic, or sedative effect. The mechanism of the effects inhalational anesthetics on this signaling pathway is not clear. This study attempted to determine whether inhalational anesthetics directly affect soluble or particulate guanylyl cyclase activity in a partially isolated enzyme system. Methods The effects of halothane (0.44-4.4%), enflurane (1.34-6.7%),

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2

Grześk, Grzegorz, Adrianna Witczyńska, Magdalena Węglarz, et al. "Soluble Guanylyl Cyclase Activators—Promising Therapeutic Option in the Pharmacotherapy of Heart Failure and Pulmonary Hypertension." Molecules 28, no. 2 (2023): 861. http://dx.doi.org/10.3390/molecules28020861.

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Endogenous nitric oxide (NO)-dependent vascular relaxation plays a leading role in the homeostasis of the cardiovascular, pulmonary, and vascular systems and organs, such as the kidneys, brain, and liver. The mechanism of the intracellular action of NO in blood vessels involves the stimulation of the activity of the soluble cytosolic form of guanylyl cyclase (soluble guanylyl cyclase, sGC), increasing the level of cyclic 3′-5′—guanosine monophosphate (cGMP) in smooth muscle and subsequent vasodilation. In recent years, a new group of drugs, soluble guanylyl cyclase stimulators, has found its w

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3

Krizhanovsky, Valery, Orly Agamy, and Michael Naim. "Sucrose-stimulated subsecond transient increase in cGMP level in rat intact circumvallate taste bud cells." American Journal of Physiology-Cell Physiology 279, no. 1 (2000): C120—C125. http://dx.doi.org/10.1152/ajpcell.2000.279.1.c120.

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Initial sweet taste transduction is expected to occur in the subsecond time range. We demonstrate a rapid and transient (75–250 ms) increase of cGMP (but not cAMP) level in rat intact circumvallate taste cells after stimulation by sucrose. This rapid increase does not occur in nonsensory epithelial cells. Pretreatment with a nonspecific phosphodiesterase (PDE) inhibitor (IBMX), a specific cAMP-PDE4 inhibitor (denbufylline), or an adenylyl cyclase activator (forskolin) all increased basal cAMP and abolished the sucrose-stimulated cGMP increase at 150 ms. Pretreatment with a soluble guanylyl cyc

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4

Johns, Roger A., Alexandra Tichotsky, Michael Muro, James P. Spaeth, Timothy D. Le Cras, and Appavoo Rengasamy. "Halothane and Isoflurane Inhibit Endothelium-derived Relaxing Factor-dependent Cyclic Guanosine Monophosphate Accumulation in Endothelial Cell-Vascular Smooth Muscle Co-cultures Independent of an Effect on Guanylyl Cyclase Activation." Anesthesiology 83, no. 4 (1995): 823–34. http://dx.doi.org/10.1097/00000542-199510000-00023.

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Background Interaction of inhalational anesthetics with the nitric oxide signaling pathway and the mechanism of such effects are controversial. The aim of this study was to clarify the sites and mechanism of inhalational anesthetic interaction with the vascular nitric oxide and guanylyl cyclase signaling pathway. Methods To specifically study the mechanism of anesthetic interaction with the nitric oxide-guanylyl cyclase pathway, cultured vascular smooth muscle and endothelial cell-vascular smooth muscle (EC-VSM) co-culture models were chosen. Monolayer cultures of VSM with or without cultured

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5

Liu, Zhenguo, Kanji Nakatsu, James F. Brien, E. Danielle Beaton, Gerald S. Marks, and Donald H. Maurice. "Selective sequestration of nitric oxide by subcellular components of vascular smooth muscle and platelets: relationship to nitric oxide stimulation of the soluble guanylyl cyclase." Canadian Journal of Physiology and Pharmacology 71, no. 12 (1993): 938–45. http://dx.doi.org/10.1139/y93-142.

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Sequestration of nitric oxide (NO) by subcellular fractions isolated from bovine pulmonary arterial medial layer (BPA) and rabbit platelets (RP) was studied utilizing a novel chemiluminescence – headspace gas technique. Sequestration in all fractions was similarly rapid (5 min) and remained constant for at least 30 min. When incubated with 108 pmol of NO, the BPA mitochondrial, microsomal, and nuclear fractions sequestered 22.8 ± 1.9, 20.5 ± 2.2 and 15.2 ± 3.6% of the NO, respectively (n = 14). However, significantly more of the 108 pmol of NO, 36.8 ± 2.8 and 32.9 ± 3.6%, respectively, was seq

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6

Mace, Eric H., Melissa J. Kimlinger, Frederic T. Billings, and Marcos G. Lopez. "Targeting Soluble Guanylyl Cyclase during Ischemia and Reperfusion." Cells 12, no. 14 (2023): 1903. http://dx.doi.org/10.3390/cells12141903.

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Ischemia and reperfusion (IR) damage organs and contribute to many disease states. Few effective treatments exist that attenuate IR injury. The augmentation of nitric oxide (NO) signaling remains a promising therapeutic target for IR injury. NO binds to soluble guanylyl cyclase (sGC) to regulate vasodilation, maintain endothelial barrier integrity, and modulate inflammation through the production of cyclic-GMP in vascular smooth muscle. Pharmacologic sGC stimulators and activators have recently been developed. In preclinical studies, sGC stimulators, which augment the reduced form of sGC, and

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7

Hempel, A., T. Noll, A. Muhs, and H. M. Piper. "Functional antagonism between cAMP and cGMP on permeability of coronary endothelial monolayers." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 4 (1996): H1264—H1271. http://dx.doi.org/10.1152/ajpheart.1996.270.4.h1264.

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The role of the intracellular second messengers guanosine 3', 5'-cyclic monophosphate (cGMP) and adenosine 3', 5'-cyclic monophosphate (cAMP) in the control of macromolecule permeability was studied in cultured monolayers of microvascular coronary endothelial cells from rat. Macromolecule permeability was determined as passage of fluorescein isothiocyanate (FITC)-labeled albumin across the monolayers. Activation of adenylyl cyclase by the beta-adrenoceptor agonist isoproterenol (Iso; 10(-5) M) and the A2-adenosine receptor agonist 5'-(N-ethylcarboxamido)-adenosine (NECA; 10(-7) M) induced an i

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8

Veltman, Douwe M., Jeroen Roelofs, Ruchira Engel, Antonie J. W. G. Visser, and Peter J. M. Van Haastert. "Activation of Soluble Guanylyl Cyclase at the Leading Edge during Dictyostelium Chemotaxis." Molecular Biology of the Cell 16, no. 2 (2005): 976–83. http://dx.doi.org/10.1091/mbc.e04-08-0701.

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Dictyostelium contains two guanylyl cyclases, GCA, a 12-transmembrane enzyme, and sGC, a homologue of mammalian soluble adenylyl cyclase. sGC provides nearly all chemoattractant-stimulated cGMP formation and is essential for efficient chemotaxis toward cAMP. We show that in resting cells the major fraction of the sGC-GFP fusion protein localizes to the cytosol, and a small fraction is associated to the cell cortex. With the artificial substrate Mn2+/GTP, sGC activity and protein exhibit a similar distribution between soluble and particulate fraction of cell lysates. However, with the physiolog

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9

Ben Aissa, Manel, Alycia F. Tipton, Zachariah Bertels, et al. "Soluble guanylyl cyclase is a critical regulator of migraine-associated pain." Cephalalgia 38, no. 8 (2017): 1471–84. http://dx.doi.org/10.1177/0333102417737778.

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Background Nitric oxide (NO) has been heavily implicated in migraine. Nitroglycerin is a prototypic NO-donor, and triggers migraine in humans. However, nitroglycerin also induces oxidative/nitrosative stress and is a source of peroxynitrite – factors previously linked with migraine etiology. Soluble guanylyl cyclase (sGC) is the high affinity NO receptor in the body, and the aim of this study was to identify the precise role of sGC in acute and chronic migraine. Methods We developed a novel brain-bioavailable sGC stimulator (VL-102), and tested its hyperalgesic properties in mice. We also dete

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Piggott, Leslie A., Kathryn A. Hassell, Zuzana Berkova, Andrew P. Morris, Michael Silberbach, and Thomas C. Rich. "Natriuretic Peptides and Nitric Oxide Stimulate cGMP Synthesis in Different Cellular Compartments." Journal of General Physiology 128, no. 1 (2006): 3–14. http://dx.doi.org/10.1085/jgp.200509403.

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Cyclic nucleotide-gated (CNG) channels are a family of ion channels activated by the binding of cyclic nucleotides. Endogenous channels have been used to measure cyclic nucleotide signals in photoreceptor outer segments and olfactory cilia for decades. Here we have investigated the subcellular localization of cGMP signals by monitoring CNG channel activity in response to agonists that activate either particulate or soluble guanylyl cyclase. CNG channels were heterologously expressed in either human embryonic kidney (HEK)-293 cells that stably overexpress a particulate guanylyl cyclase (HEK-NPR

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11

Rho, Edwin H., William J. Perkins, Robert R. Lorenz, David O. Warner, and Keith A. Jones. "Differential effects of soluble and particulate guanylyl cyclase on Ca2+ sensitivity in airway smooth muscle." Journal of Applied Physiology 92, no. 1 (2002): 257–63. http://dx.doi.org/10.1152/jappl.2002.92.1.257.

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Maximal relaxation of airway smooth muscle (ASM) in response to atrial natriuretic peptide (ANP), which stimulates particulate guanylyl cyclase (pGC), is less than that produced by nitric oxide (NO) and other compounds that stimulate soluble guanylyl cyclase (sGC). We hypothesized that stimulation of pGC relaxes ASM only by decreasing intracellular Ca2+ concentration ([Ca2+]i), whereas stimulation of sGC decreases both [Ca2+]i and the force developed for a given [Ca2+]i (i.e., the Ca2+ sensitivity) during muscarinic stimulation. We measured the relationship between force and [Ca2+]i (using fur

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12

Zamir, N., D. Barkan, N. Keynan, Z. Naor, and H. Breitbart. "Atrial natriuretic peptide induces acrosomal exocytosis in bovine spermatozoa." American Journal of Physiology-Endocrinology and Metabolism 269, no. 2 (1995): E216—E221. http://dx.doi.org/10.1152/ajpendo.1995.269.2.e216.

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The induction of acrosomal exocytosis in capacitated bull spermatozoa by atrial natriuretic peptide (ANP) was studied in vitro. ANP markedly stimulated acrosomal exocytosis in a calcium-dependent manner. Typically, ANP exerts its action via activation of the ANP receptor (ANPR-A), a particulate guanylyl cyclase-linked receptor, and subsequent formation of guanosine 3',5'-cyclic monophosphate (cGMP). We found that the ANP-induced acrosome reaction was inhibited by the competitive ANPR-A receptor antagonist-anantin, indicating a receptor-mediated effect. We could mimic the effect of ANP on the a

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13

Beste, Kerstin Y., та Roland Seifert. "cCMP, cUMP, cTMP, cIMP and cXMP as possible second messengers: Development of a hypothesis based on studies with soluble guanylyl cyclase α1β1". Biological Chemistry 394, № 2 (2013): 261–70. http://dx.doi.org/10.1515/hsz-2012-0282.

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Abstract Adenosine 3′,5′-cyclic monophosphate and guanosine 3′,5′-cyclic monophosphate are second messengers that regulate multiple physiological functions. The existence of additional cyclic nucleotides in mammalian cells was postulated many years ago, but technical problems hampered development of the field. Using highly specific and sensitive mass spectrometry methods, soluble guanylyl cyclase has recently been shown to catalyze the formation of several cyclic nucleotides in vitro. This minireview discusses the broad substrate-specificity of soluble guanylyl cyclase and the possible second

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Huttl, Martina, Matus Miklovic, Olga Gawrys, et al. "The treatment with soluble guanylate cyclase stimulator BAY41-8543 prevents malignant hypertension and associated organ damage." Journal of hypertension 43, no. 6 (2025): 1030–41. https://doi.org/10.1097/HJH.0000000000004009.

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Objective:Despite availability of an array of antihypertensive drugs, malignant hypertension remains a life-threatening condition, and new therapeutic strategies for the treatment of malignant hypertension and malignant hypertension-associated organ damage are needed. The aim of the present study was to assess the effects of nitric oxide (NO)-independent soluble guanylyl cyclase (sGC) stimulator on the course of malignant hypertension. The second aim was to investigate if the treatment with sodium-glucose cotransporter type 2 (SGLT2) inhibitor would augment the expected beneficial actions of t

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15

Jiang, Yonghua, та Stanko S. Stojilkovic. "Molecular cloning and characterization of α1-soluble guanylyl cyclase gene promoter in rat pituitary cells". Journal of Molecular Endocrinology 37, № 3 (2006): 503–15. http://dx.doi.org/10.1677/jme.1.02180.

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Soluble guanylyl cyclase is a cytosolic enzyme which catalyzes conversion of GTP to the second messenger cyclic GMP. The transcriptional regulation at the promoter levels of four soluble guanylyl cyclase subunits, termed α1, α2, β1, and β2, is largely unknown. In this study, we identified the transcription start site of α1-soluble guanylyl cyclase gene in rat pituitary cells and cloned the 3.5 kb 5′-promoter. Sequence analysis of this TATA-less promoter revealed the presence of several putative-binding sites for transcriptional factors, including CCAAT site at −41 to −32 and Sp1 site at −34 to

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16

Zhuo, Min, Jarmo T. Laitinen, Xiao-Ching Li, and Robert D. Hawkins. "On the Respective Roles of Nitric Oxide and Carbon Monoxide in Long-Term Potentiation in the Hippocampus." Learning & Memory 5, no. 6 (1998): 467–80. http://dx.doi.org/10.1101/lm.5.6.467.

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Perfusion of hippocampal slices with an inhibitor of nitric oxide (NO) synthase-blocked induction of long-term potentiation (LTP) produced by a one-train tetanus and significantly reduced LTP by a two-train tetanus, but only slightly reduced LTP by a four-train tetanus. Inhibitors of heme oxygenase, the synthetic enzyme for carbon monoxide (CO), significantly reduced LTP by either a two-train or four-train tetanus. These results suggest that NO and CO are both involved in LTP but may play somewhat different roles. One possibility is that NO serves a phasic, signaling role, whereas CO provides

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Zhuo, Min, Jarmo T. Laitinen, Xiao-Ching Li, and Robert D. Hawkins. "On the Respective Roles of Nitric Oxide and Carbon Monoxide in Long-Term Potentiation in the Hippocampus." Learning & Memory 6, no. 1 (1999): 63–76. http://dx.doi.org/10.1101/lm.6.1.63.

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Perfusion of hippocampal slices with an inhibitor nitric oxide (NO) synthase blocked induction of long-term potentiation (LTP) produced by a one-train tetanus and significantly reduced LTP by a two-train tetanus, but only slightly reduced LTP by a four-train tetanus. Inhibitors of heme oxygenase, the synthetic enzyme for carbon monoxide (CO), significantly reduced LTP by either a two-train or four-train tetanus. These results suggest that NO and CO are both involved in LTP but may play somewhat different roles. One possibility is that NO serves a phasic, signaling role, whereas CO provides ton

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18

McDowell, K. A., R. L. Chevalier, B. A. Thornhill, and L. L. Norling. "Unilateral ureteral obstruction increases glomerular soluble guanylyl cyclase activity." Journal of the American Society of Nephrology 6, no. 5 (1995): 1498–503. http://dx.doi.org/10.1681/asn.v651498.

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RBF and GFR are decreased in kidneys after ipsilateral unilateral ureteral obstruction (UUO) for 24 h. Despite net vasoconstriction, vasodilatory mechanisms respond to counterbalance the vasoconstriction: the inhibition of nitric oxide synthase activity is associated with a greater reduction in RBF with ipsilateral UUO. To determine whether the stimulation of soluble guanylyl cyclase differs between glomeruli from obstructed kidneys and normal kidneys, cGMP was measured after stimulation by 10(-3) M sodium nitroprusside (SNP) in glomeruli isolated from the kidneys of Sprague-Dawley rats after

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Su, Jun, Qihang Zhang, Jacob Moalem, James Tse, Peter M. Scholz, and Harvey R. Weiss. "Functional effects of C-type natriuretic peptide and nitric oxide are attenuated in hypertrophic myocytes from pressure-overloaded mouse hearts." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (2005): H1367—H1373. http://dx.doi.org/10.1152/ajpheart.00880.2004.

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Increases in the myocardial level of cGMP usually exert negative inotropic effects in the mammalian hearts. We tested the hypothesis that the negative functional effects caused by nitric oxide (NO) or C-type natriuretic peptide (CNP) through cGMP would be blunted in hypertrophied cardiac myocytes. Contractile function, guanylyl cyclase activity, cGMP-dependent protein phosphorylation, and calcium transients were assessed in ventricular myocytes from aortic stenosis-induced hypertrophic and age-matched control mice. Basal percentage shortening was similar in control and hypertrophic myocytes. S

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Egemnazarov, Bakytbek, Akylbek Sydykov, Ralph T. Schermuly, et al. "Novel soluble guanylyl cyclase stimulator BAY 41-2272 attenuates ischemia-reperfusion-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 3 (2009): L462—L469. http://dx.doi.org/10.1152/ajplung.90377.2008.

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The protective effects of nitric oxide (NO), a physiological activator of soluble guanylyl cyclase (sGC), have been reported in ischemia-reperfusion (I/R) syndrome of the lung. Therefore, we studied the effects of BAY 41-2272, a novel sGC stimulator, on I/R injury of the lung in an isolated intact organ model. Lung injury was assessed by measuring weight gain and microvascular permeability (capillary filtration coefficient, Kfc). Release of reactive oxygen species (ROS) into the perfusate was measured during early reperfusion by electron spin resonance (ESR) spectroscopy. Rabbit lungs were tre

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Zhang, Guoying, Binggang Xiang, Anping Dong, et al. "Biphasic roles for soluble guanylyl cyclase (sGC) in platelet activation." Blood 118, no. 13 (2011): 3670–79. http://dx.doi.org/10.1182/blood-2011-03-341107.

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AbstractNitric oxide (NO) stimulates cGMP synthesis by activating its intracellular receptor, soluble guanylyl cyclase (sGC). It is a currently prevailing concept that No and cGMP inhibits platelet function. However, the data supporting the inhibitory role of NO/sGC/cGMP in platelets have been obtained either in vitro or using whole body gene deletion that affects vessel wall function. Here we have generated mice with sGC gene deleted only in megakaryocytes and platelets. Using the megakaryocyte- and platelet-specific sGC-deficient mice, we identify a stimulatory role of sGC in platelet activa

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Hamad, Ahmed M., Simon Range, Elaine Holland, and Alan J. Knox. "Regulation of cGMP by soluble and particulate guanylyl cyclases in cultured human airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 4 (1997): L807—L813. http://dx.doi.org/10.1152/ajplung.1997.273.4.l807.

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Although guanosine 3′,5′-cyclic monophosphate (cGMP) acts as a relaxant second messenger, the regulation of intracellular cGMP has not been comprehensively studied in human airway smooth muscle. We studied the production of cGMP by cultured human airway smooth muscle cells (HASMC) after stimulation with activators of soluble guanylyl cyclase [sodium nitroprusside (SNP) and S-nitroso- N-acetylpenicillamine (SNAP)] and particulate guanylyl cyclase [atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and Escherichia coli heat stable enterotoxin (ST

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Sandner, Peter. "From molecules to patients: exploring the therapeutic role of soluble guanylate cyclase stimulators." Biological Chemistry 399, no. 7 (2018): 679–90. http://dx.doi.org/10.1515/hsz-2018-0155.

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AbstractNitric oxide (NO) signaling represents one of the major regulatory pathways for cardiovascular function. After the discovery of NO, awarded with the Nobel Prize in 1998, this signaling cascade was stepwise clarified. We now have a good understanding of NO production and NO downstream targets such as the soluble guanylyl cyclases (sGCs) which catalyze cGMP production. Based on the important role of NO-signaling in the cardiovascular system, intense research and development efforts are currently ongoing to fully exploit the therapeutic potential of cGMP increase. Recently, NO-independent

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Miyashiro, Joy, Asha Pant, Boris Tchernychev, et al. "The Effect of the Soluble Guanylyl Cyclase Stimulator Olinciguat on ƴ-Globin Gene Induction in K562 Cells." Blood 132, Supplement 1 (2018): 1078. http://dx.doi.org/10.1182/blood-2018-99-116011.

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Abstract Induction of fetal hemoglobin (HbF: α2ƴ2) is a recognized mode of action of hydroxyurea, the sickle cell disease (SCD) standard of care in SCD, and has been shown to prevent red blood cell (RBC) sickling. Discovery of novel HbF inducers is underway and several therapeutics with the potential to increase HbF expression are currently at different stages of preclinical and clinical development. Soluble guanylyl cyclase (sGC) is a heterodimeric heme-containing enzyme whose catalytic activity is regulated by nitric oxide (NO). Binding of NO to heme activates the catalytic domain of sGC, en

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van Haastert, Peter J. M., Ineke Keizer-Gunnink, Henderikus Pots, et al. "Forty-five years of cGMP research in Dictyostelium: understanding the regulation and function of the cGMP pathway for cell movement and chemotaxis." Molecular Biology of the Cell 32, no. 20 (2021): ar8. http://dx.doi.org/10.1091/mbc.e21-04-0171.

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Chemoattractants induce a fast cGMP response in Dictyostelium. The cGMP signaling pathway consists of a soluble guanylyl cyclase sGC, a cGMP-stimulated PDE, and the cGMP-target protein GbpC. Here we combine published and many unpublished experiments performed in the past 45 years on the regulation and function of the cGMP signaling pathway.

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Ogawa, Naoto, Asami Mori, Masami Hasebe, et al. "Nitric oxide dilates rat retinal blood vessels by cyclooxygenase-dependent mechanisms." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 4 (2009): R968—R977. http://dx.doi.org/10.1152/ajpregu.91005.2008.

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It has been suggested that nitric oxide (NO) stimulates the cyclooxygenase (COX)-dependent mechanisms in the ocular vasculature; however, the importance of the pathway in regulating retinal circulation in vivo remains to be elucidated. Therefore, we investigated the role of COX-dependent mechanisms in NO-induced vasodilation of retinal blood vessels in thiobutabarbital-anesthetized rats with and without neuronal blockade (tetrodotoxin treatment). Fundus images were captured with a digital camera that was equipped with a special objective lens. The retinal vascular response was assessed by meas

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Bačová, Barbara Szeiffová, Matúš Sýkora, Adriana Martišková, Olga Gawrys, Narcisa Tribulová, and Luděk Červenka. "P164 SOLUBLE GUANYLATE CYCLASE STIMULATORS: AN EMERGING OPTION IN THE TREATMENT OF PRESSURE AND VOLUME OVERLOAD INDUCED CHRONIC HEART FAILURE." Journal of Hypertension 42, Suppl 3 (2024): e120. http://dx.doi.org/10.1097/01.hjh.0001063528.01284.cf.

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Pressure and volume overload-induced chronic heart failure (HF) is associated with characteristic cardiac remodeling and ventricular myocardial proteomic alterations, that can lead to the formation of a substrate for arrhythmias. Antiarrhythmic drug therapy is still suboptimal and current therapies are not efficacious enough. The purpose of the current study was therefore to examine the efficiency of nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) stimulator. We used as an experimental model male hypertensive Ren-2 transgenic rats (TGR) (n = 16), normoten

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Amirjanians, Matthieu, Bakytbek Egemnazarov, Akylbek Sydykov, et al. "Chronic intratracheal application of the soluble guanylyl cyclase stimulator BAY 41-8543 ameliorates experimental pulmonary hypertension." Oncotarget 8, no. 18 (2017): 29613–24. http://dx.doi.org/10.18632/oncotarget.16769.

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Jabs, A., M. Oelze, Y. Mikhed, et al. "Effect of soluble guanylyl cyclase activator and stimulator therapy on nitroglycerin-induced nitrate tolerance in rats." Vascular Pharmacology 71 (August 2015): 181–91. http://dx.doi.org/10.1016/j.vph.2015.03.007.

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Wales, Jessica A., Cheng-Yu Chen, Linda Breci, et al. "Discovery of stimulator binding to a conserved pocket in the heme domain of soluble guanylyl cyclase." Journal of Biological Chemistry 293, no. 5 (2017): 1850–64. http://dx.doi.org/10.1074/jbc.ra117.000457.

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Badejo, Adeleke M., Vaughn E. Nossaman, Edward A. Pankey, et al. "Pulmonary and systemic vasodilator responses to the soluble guanylyl cyclase stimulator, BAY 41-8543, are modulated by nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 4 (2010): H1153—H1159. http://dx.doi.org/10.1152/ajpheart.01101.2009.

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BAY 41-8543 is a nitric oxide (NO)-independent stimulator of soluble guanylyl cyclase (sGC). Responses to intravenous injections of BAY 41-8543 were investigated under baseline and elevated tone conditions and when NO synthase (NOS) was inhibited with Nω-nitro-l-arginine methyl ester (l-NAME). Under baseline conditions, intravenous injections of BAY 41-8543 caused small decreases in pulmonary arterial pressure, larger decreases in systemic arterial pressure, and increases in cardiac output. When pulmonary arterial pressure was increased to ∼30 mmHg with an intravenous infusion of U-46619, intr

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Leinders-Zufall, T., and F. Zufall. "Block of cyclic nucleotide-gated channels in salamander olfactory receptor neurons by the guanylyl cyclase inhibitor LY83583." Journal of Neurophysiology 74, no. 6 (1995): 2759–62. http://dx.doi.org/10.1152/jn.1995.74.6.2759.

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1. Using whole cell voltage-clamp recordings, the guanylyl cyclase inhibitor LY83583 [6-(phenylamino)-5,8-quinolinedione] is shown to act as a potent blocker of cyclic nucleotide-gated (CNG) channels in isolated olfactory receptor neurons (ORNs) of the tiger salamander. 2. Under our experimental conditions, onset of the blockade by LY83583 occurs on the time scale of seconds and is completely reversed upon wash-out of the drug. Dose-response curves reveal a Kd of 1.4 microM (at -60 mV). Other data suggest that LY83583 acts within the CNG channel pore and that the channels must be in an activat

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Gawrys, Olga, Petr Kala, Janusz Sadowski, Vojtech Melenovsky, Peter Sandner, and Ludek Cervenka. "Soluble guanylyl cyclase stimulators and activators: Promising drugs for the treatment of hypertension?" European journal of pharmacology 2025, no. 987 (2025): 177175. https://doi.org/10.1016/j.ejphar.2024.177175.

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Nitric oxide (NO)-stimulated cyclic guanosine monophosphate (cGMP) is a key regulator of cardiovascular health, as NO-cGMP signalling is impaired in diseases like pulmonary hypertension, heart failure and chronic kidney disease. The development of NO-independent sGC stimulators and activators provide a novel therapeutic option to restore altered NO signalling. sGC stimulators have been already approved for the treatment of pulmonary arterial hypertension (PAH), chronic thromboembolic pulmonary hypertension (CTEPH), and chronic heart failure (HFrEF), while sGC activators are currently in phase-

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RUSSWURM, Michael, Soenke BEHRENDS, Christian HARTENECK, and Doris KOESLING. "Functional properties of a naturally occurring isoform of soluble guanylyl cyclase." Biochemical Journal 335, no. 1 (1998): 125–30. http://dx.doi.org/10.1042/bj3350125.

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Soluble guanylyl cyclase (sGC), the target enzyme of the signalling molecule NO, contains one prosthetic haem group and consists of an α and a β subunit. So far, only the α1β1 heterodimer has been shown to exist in different cells and tissues, and most biochemical studies of sGC have been performed with the α1β1 heterodimer. Here we demonstrate for the first time the natural occurrence of the α2 subunit on the protein level. The α2 subunit co-precipitated with the β1 subunit from human placenta, showing the existence of the α2β1 isoform in vivo. The new enzyme was expressed in and purified fro

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Gonzalez-Iglesias, Arturo E., Yonghua Jiang, Melanija Tomić, et al. "Dependence of Electrical Activity and Calcium Influx-Controlled Prolactin Release on Adenylyl Cyclase Signaling Pathway in Pituitary Lactotrophs." Molecular Endocrinology 20, no. 9 (2006): 2231–46. http://dx.doi.org/10.1210/me.2005-0363.

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Abstract Pituitary lactotrophs in vitro fire extracellular Ca2+-dependent action potentials spontaneously through still unidentified pacemaking channels, and the associated voltage-gated Ca2+ influx (VGCI) is sufficient to maintain basal prolactin (PRL) secretion high and steady. Numerous plasma membrane channels have been characterized in these cells, but the mechanism underlying their pacemaking activity is still not known. Here we studied the relevance of cyclic nucleotide signaling pathways in control of pacemaking, VGCI, and PRL release. In mixed anterior pituitary cells, both VGCI-inhibi

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Friebe, Andreas, Peter Sandner, and Achim Schmidtko. "cGMP: a unique 2nd messenger molecule – recent developments in cGMP research and development." Naunyn-Schmiedeberg's Archives of Pharmacology 393, no. 2 (2019): 287–302. http://dx.doi.org/10.1007/s00210-019-01779-z.

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AbstractCyclic guanosine monophosphate (cGMP) is a unique second messenger molecule formed in different cell types and tissues. cGMP targets a variety of downstream effector molecules and, thus, elicits a very broad variety of cellular effects. Its production is triggered by stimulation of either soluble guanylyl cyclase (sGC) or particulate guanylyl cyclase (pGC); both enzymes exist in different isoforms. cGMP-induced effects are regulated by endogenous receptor ligands such as nitric oxide (NO) and natriuretic peptides (NPs). Depending on the distribution of sGC and pGC and the formation of

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Bischoff, E., M. Schramm, A. Straub, A. Feurer, and J. P. Stasch. "BAY 41-2272: a stimulator of soluble guanylyl cyclase induces nitric oxide-dependent penile erection in vivo." Urology 61, no. 2 (2003): 464–67. http://dx.doi.org/10.1016/s0090-4295(02)02121-0.

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Nossaman, Bobby, Edward Pankey, and Philip Kadowitz. "Stimulators and Activators of Soluble Guanylate Cyclase: Review and Potential Therapeutic Indications." Critical Care Research and Practice 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/290805.

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The heme-protein soluble guanylyl cyclase (sGC) is the intracellular receptor for nitric oxide (NO). sGC is a heterodimeric enzyme withαandβsubunits and contains a heme moiety essential for binding of NO and activation of the enzyme. Stimulation of sGC mediates physiologic responses including smooth muscle relaxation, inhibition of inflammation, and thrombosis. In pathophysiologic states, NO formation and bioavailability can be impaired by oxidative stress and that tolerance to NO donors develops with continuous use. Two classes of compounds have been developed that can directly activate sGC a

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Antošová, Martina, Anna Strapková, and Tomáš Turčan. "Exogenous Irritant-Induced Airway Hyperreactivity and Inhibition of Soluble Guanylyl Cyclase." Biological Research For Nursing 10, no. 2 (2008): 93–101. http://dx.doi.org/10.1177/1099800408323846.

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The majority of nitric oxide (NO) effects in the respiratory system are caused by stimulation of soluble guanylyl cyclase (sGC) with subsequent increase of cyclic guanosine monophosphate (cGMP) production. The importance of this mechanism of NO action in airway hyperreactivity (AHR) pathogenesis is unknown. Therefore, the aim of our experiment was to examine the changes of airway reactivity enhanced by toluene vapor exposure in the presence or inhibition of sGC activity in guinea pigs. Animals were treated with a nonspecific sGC inhibitor, methylene blue, in a dose of 50 or 100 mg/kg body weig

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Goulopoulou, Styliani, Johanna L. Hannan, Takayuki Matsumoto, Safia Ogbi, Adviye Ergul, and R. Clinton Webb. "Reduced vascular responses to soluble guanylyl cyclase but increased sensitivity to sildenafil in female rats with type 2 diabetes." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 2 (2015): H297—H304. http://dx.doi.org/10.1152/ajpheart.00079.2015.

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Impaired nitric oxide (NO), soluble guanylyl cyclase (sGC), and cyclic guanosine monophosphate (cGMP) signaling (NO-sGC-cGMP) has been implicated in the pathogenesis of diabetic vascular dysfunction. Efforts to directly target this signaling have led to the development of sGC agonists that activate the heme group of sGC (stimulators) or preferentially activate sGC when the heme is oxidized (activators). In this study, we hypothesized that resistance arteries from female rats with spontaneous type 2 diabetes (Goto-Kakizaki rats, GK) would have reduced vasodilatory responses to heme-dependent sG

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Kostic, Tatjana S., Silvana A. Andric, and Stanko S. Stojilkovic. "Spontaneous and Receptor-Controlled Soluble Guanylyl Cyclase Activity in Anterior Pituitary Cells." Molecular Endocrinology 15, no. 6 (2001): 1010–22. http://dx.doi.org/10.1210/mend.15.6.0648.

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Abstract Nitric oxide (NO)-dependent soluble guanylyl cyclase (sGC) is operative in mammalian cells, but its presence and the role in cGMP production in pituitary cells have been incompletely characterized. Here we show that sGC is expressed in pituitary tissue and dispersed cells, enriched lactotrophs and somatotrophs, and GH3 immortalized cells, and that this enzyme is exclusively responsible for cGMP production in unstimulated cells. Basal sGC activity was partially dependent on voltage-gated calcium influx, and both calcium-sensitive NO synthases (NOS), neuronal and endothelial, were expre

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Schmidt, Eric P., Mahendra Damarla, Otgonchimeg Rentsendorj, et al. "Soluble guanylyl cyclase contributes to ventilator-induced lung injury in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 6 (2008): L1056—L1065. http://dx.doi.org/10.1152/ajplung.90329.2008.

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High tidal volume (HVT) ventilation causes pulmonary endothelial barrier dysfunction. HVT ventilation also increases lung nitric oxide (NO) and cGMP. NO contributes to HVT lung injury, but the role of cGMP is unknown. In the current study, ventilation of isolated C57BL/6 mouse lungs increased perfusate cGMP as a function of VT. Ventilation with 20 ml/kg VT for 80 min increased the filtration coefficient ( Kf), an index of vascular permeability. The increased cGMP and Kf caused by HVT were attenuated by nitric oxide synthase (NOS) inhibition and in lungs from endothelial NOS knockout mice. Inhi

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Mangmool, Supachoke, Ratchanee Duangrat, Warisara Parichatikanond, and Hitoshi Kurose. "New Therapeutics for Heart Failure: Focusing on cGMP Signaling." International Journal of Molecular Sciences 24, no. 16 (2023): 12866. http://dx.doi.org/10.3390/ijms241612866.

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Current drugs for treating heart failure (HF), for example, angiotensin II receptor blockers and β-blockers, possess specific target molecules involved in the regulation of the cardiac circulatory system. However, most clinically approved drugs are effective in the treatment of HF with reduced ejection fraction (HFrEF). Novel drug classes, including angiotensin receptor blocker/neprilysin inhibitor (ARNI), sodium-glucose co-transporter-2 (SGLT2) inhibitor, hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker, soluble guanylyl cyclase (sGC) stimulator/activator, and cardiac

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Huang, Xinxin, Bin Guo, Maegan L. Capitano, and Hal E. Broxmeyer. "Nitric Oxide Promotes Human Hematopoietic Stem Cell Homing and Engraftment Via cGMP-Pkg Signaling." Blood 132, Supplement 1 (2018): 807. http://dx.doi.org/10.1182/blood-2018-99-112993.

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Abstract The success of hematopoietic stem cell (HSC) transplantation relies on adequate homing and long-term engraftment of HSC into the bone marrow (BM). The free radical nitric oxide (NO) is a gaseous molecule that plays important roles in a variety of physiological regulations. NO can freely diffuse across cellular membranes and activate an enzyme, soluble guanylyl cyclase, to produce cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). cGMP binding activates cGMP-dependent protein kinase (PKG) and other proteins to regulate many biological processes. However, the roles

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Lau, K. S., O. Nakashima, G. R. Aalund, et al. "TNF-alpha and IFN-gamma induce expression of nitric oxide synthase in cultured rat medullary interstitial cells." American Journal of Physiology-Renal Physiology 269, no. 2 (1995): F212—F217. http://dx.doi.org/10.1152/ajprenal.1995.269.2.f212.

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Cytokines increase the expression of the inducible (type II) nitric oxide synthase (NOS) in macrophages, liver, and renal epithelial cells. Previously, we found that cultured rat medullary interstitial cells (RMIC) contain high levels of soluble guanylyl cyclase. To determine whether these cells can also produce NO, we studied the effects of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) on NO production, NOS II mRNA, and NOS II protein expression. Both TNF-alpha and IFN-gamma, in the presence of a low concentration of the other cytokine, caused dose-dependent increas

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Schwabl, P., K. Brusilovskaya, P. Königshofer, et al. "Molecular effects of the soluble guanylyl cyclase stimulator Riociguat in experimental cirrhosis and impact on transaminases in patients." Zeitschrift für Gastroenterologie 55, no. 05 (2017): e28-e56. http://dx.doi.org/10.1055/s-0037-1603432.

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Baracat, Juliana S., Cleber E. Teixeira, Cristina E. Okuyama, et al. "Relaxing effects induced by the soluble guanylyl cyclase stimulator BAY 41-2272 in human and rabbit corpus cavernosum." European Journal of Pharmacology 477, no. 2 (2003): 163–69. http://dx.doi.org/10.1016/j.ejphar.2003.08.012.

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Schwabl, P., K. Brusilovskaya, P. Königshofer, et al. "Molecular effects of the soluble guanylyl cyclase stimulator riociguat on biliary cirrhosis and effects on transaminases in patients." Journal of Hepatology 66, no. 1 (2017): S74—S75. http://dx.doi.org/10.1016/s0168-8278(17)30411-7.

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Andresen, Bradley T., Kuntala Shome, Edwin K. Jackson, and Guillermo G. Romero. "AT2 receptors cross talk with AT1 receptors through a nitric oxide- and RhoA-dependent mechanism resulting in decreased phospholipase D activity." American Journal of Physiology-Renal Physiology 288, no. 4 (2005): F763—F770. http://dx.doi.org/10.1152/ajprenal.00323.2004.

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ANG II activation of phospholipase D (PLD) is required for ERK and NAD(P)H oxidase activation, both of which are involved in hypertension. Previous findings demonstrate that ANG II stimulates PLD activity through AT1 receptors in a RhoA-dependent mechanism. Additionally, endogenous AT2 receptors in preglomerular smooth muscle cells attenuate ANG II-mediated PLD activity. In the present study, we examined the signal transduction mechanisms used by endogenous AT2 receptors to modulate ANG II-induced PLD activity through either PLA2 generation of lysophosphatidylethanolamine or Gαi-mediated gener

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Zhang, Guoying, Binggang Xiang, Radek C. Skoda, Susan S. Smyth, Xiaoping Du, and Zhenyu Li. "Biphasic Roles for the Soluble Guanylyl Cyclase (sGC) In Platelet Activation In Mice." Blood 116, no. 21 (2010): 486. http://dx.doi.org/10.1182/blood.v116.21.486.486.

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Abstract Abstract 486 The role of intracellular secondary messenger cGMP in platelet activation has been controversial, with both stimulatory and inhibitory roles reported. The platelet cGMP is believed to be predominantly synthesized by soluble guanylyl cyclase (sGC), which is activated by nitric oxide (NO). To specifically determine the role of sGC-dependent cGMP synthesis in platelet function and in vivo thrombosis and hemostasis, we produced mice harboring a “floxed” sGC beta1 allele. In the “floxed” sGC beta1 mice (sGC beta1fl/fl), the exons 7 and 8 of sGC beta1 gene and an inserted Neo c

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