Guanylate Cyclase Activators Influence Reactivity of Human Mesenteric Superior Arteries Retrieved and Preserved in the Same Conditions as Transplanted Kidneys

Słupski, Maciej; Szadujkis-Szadurski, Leszek; Grześk, Grzegorz; Szadujkis-Szadurski, Rafał; Szadujkis-Szadurska, Katarzyna; Włodarczyk, Zbigniew; Masztalerz, M.; Piotrowiak, Ilona; Jasiński, Miłosz

doi:10.1016/j.transproceed.2007.02.079

Cited by 14 publications

(10 citation statements)

References 13 publications

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“…Acetylocholine decreases arterial tension due to the release of NO from endothelial cells, thus it stimulates the NO/cGMP signaling pathway (23). Cyclic nucleotides, e.g., cAMP and cGMP, which regulate the function of ion channels and calcium levels in the cell through the appropriate protein kinases exhibit functional antagonism of calcium ions in smooth muscle (24,25). In experiments performed on mouse lung slices NO-induced relaxation was enhanced by selective inhibitors of cGMP-specific phosphodiesterase-5 (zaprinast or vardenafil), but was blocked by ODQ and by Rp-8-pCPT-cGMPS, an inhibitor of protein kinase G. NOC-5 (nitric oxide donor), cGMP analogues and selective PKG activators 8Br-cGMP and 8pCPT-cGMP were found to induce airway relaxation and decrease the frequency of Ca 2+ oscillations (26).…”

Section: Discussionmentioning

confidence: 99%

Role of acetylcholine and calcium ions in three vascular contraction models: Angiotensin II, phenylephrine and caffeine

Szadujkis-Szadurska

Grześk

Szadujkis-Szadurski

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to determine the role of acetylcholine and calcium ions in modulating the vascular contraction induced by angiotensin II (ANG II), phenylephrine (PHE) and caffeine. The study was performed on perfunded Wistar rat tail arteries. The contraction caused by ANG II, PHE and caffeine with the participation of intracellular [in free physiological salt solution (FPSS)] and extracellular [in physiological salt solution (PSS), after emptying the cellular stores] pools of calcium ions and the addition of L-NNA (NOSe inhibitor) or ODQ (GC inhibitor) was studied. Then the effect of acetylcholine on the contraction responses was analyzed. ANG II, PHE and caffeine induced an increase in perfusion pressure in PSS and FPSS. Acetylcholine reduced the contraction resulting from the presence of ANG II and PHE, but not caffeine. L-NNA and ODQ abolished the spasmolytic action of acetylcholine. Both pools of calcium ions mediated the action of ANG II and PHE, and caffeine induced the contraction with the participation of calcium released from intracellular stores. The spasmolytic effect of acetylcholine on responses stimulated by ANG II and PHE indicates the participation of nitric oxide in modulating the reactivity of the arteries on the studied agonists of the metabotropic receptors. No observed acetylcholine effect on caffeine suggests that the pathway associated with nitric oxide does not interfere with the contraction induced by the ryanodin receptor.

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Section: Discussionmentioning

confidence: 99%

Role of acetylcholine and calcium ions in three vascular contraction models: Angiotensin II, phenylephrine and caffeine

Szadujkis-Szadurska

Grześk

Szadujkis-Szadurski

et al. 2012

Experimental and Therapeutic Medicine

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“…It should be noted that although it is well accepted that YC-1 is an effective HIF-1α inhibitor, it was originally characterized as a cGMP inducer because it stimulates soluble guanylyl cyclase activation in response to nitric oxide or carbon monoxide in some cells [47] ; only low concentrations of YC-1 (1-20 µmol/L) are required for anti-HIF-1α activity, whereas cGMP elevation requires higher concentrations (>50 µmol/L) [48,49] . It has been reported that no serious toxicity is observed in nude mice treated with YC-1 over a 2-week period [46] .…”

Section: Wwwchinapharcom Jiang H Et Almentioning

confidence: 99%

Inhibition of hypoxia inducible factor-1α ameliorates lung injury induced by trauma and hemorrhagic shock in rats

Hong

Huang

et al. 2012

Acta Pharmacol Sin

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Aim: Ischemia/reperfusion is an initial triggering event that leads to gut-induced acute lung injury (ALI). In this study, we investigated whether hypoxia inducible factor-1α (HIF-1α) played a role in the pathogenesis of lung injury induced by trauma and hemorrhagic shock (T/HS). Methods: Male Wistar rats underwent laparotomy and hemorrhagic shock for 60 min. Sham-shock animals underwent laparotomy but without hemorrhagic shock. After resuscitation for 3 h, the rats were sacrificed. Morphologic changes of the lungs and intestines were examined. Bronchoalveolar lavage fluid (BALF) was collected. Lung water content, pulmonary myeloperoxidase (MPO) activity and the levels of malondialdehyde (MDA), nitrite/nitrate, TNF-α, IL-1β, and IL-6 in the lungs were measured. The gene expression of pulmonary HIF-1α and iNOS, and HIF-1α transcriptional activity in the lungs were also assessed. The apoptosis in the lungs was determined using TUNEL assay and cleaved caspase-3 expression. Results: Lung and intestinal injuries induced by T/HS were characterized by histological damages and a significant increase in lung water content. Compared to the sham-shock group, the BALF cell counts, the pulmonary MPO activity and the MDA, nitrite/nitrate, TNF-α, IL-1β, and IL-6 levels in the T/HS group were significantly increased. Acute lung injury was associated with a higher degree of pulmonary HIF-1α and iNOS expression as well as apoptosis in the lungs. Intratracheal delivery of HIF-1α inhibitor YC-1 (1 mg/kg) significantly attenuated lung injury, and reduced pulmonary HIF-1α and iNOS expression and HIF-1α transcriptional activity in the T/HS group. Conclusion: Local inhibition of HIF-1α by YC-1 alleviates the lung injury induced by T/HS. Our results provide novel insight into the pathogenesis of T/HS-induced ALI and a potential therapeutic application.

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“…This is supported by the finding that NOS inhibition elevated the resistance to treatment with CaCl 2 , which mimics hypoxic stress and leads to the influx of calcium (4,6,22). Treatment with 300 µM CaCl 2 is commonly used to mimic hypoxic insults in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 92%

“…Mobilization tissues and the influx of calcium has long been considered as a major mechanism of ischemic cell death induced by different means, including ischemia (7,(19)(20)(21). The increased concentration of cytoplasmic free Ca 2+ following hypoxia is derived from an influx and release from intracellular storage, such as ER and mitochondria (6,8,22).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the post-mortem interval on the effect of vascular responses to the activation of ionotropic and metabotropic receptors

Bloch-Bogusławska

Grześk

2014

Biomedical Reports

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The contractibility of blood vessels depends on their normal structure and the availability of calcium ions; it changes under the influence of numerous contracting and relaxing factors, which control the activities of various pathways of intracellular and intercellular signaling. The main aim of the study was to investigate, by means of perfusion pressure in rat tail arteries, the role of Ca in vascular response to α-1 adrenoceptor activation by phenylephrine (PHE) and Bay K8644 agonist of the L-type calcium channel and caffeine before and after a post-mortem interval (PMI) of 2, 4, 6 and 8 h. A phasic increase of perfusion pressure in rat tail arteries, as induced by PHE or caffeine, in Ca-free solutions was used as an indicator of intracellular Ca release through the inositol 1,4,5-triphosphate and ryanodine receptor pathways, respectively. In Ca-free-ethylene glycol tetraacetic acid (EGTA)-poly(sodium styrenesulfonate) (PSS) and in Ca-EGTA-PSS, the PHE induced elevation of perfusion pressure significantly decreased. Vascular responses to caffeine (20 mmol/1) in Ca-free-EGTA-PSS, with an increase of PMI from 2-8 h, did not change significantly. A similar effect was observed with vascular responses to KCl 40 mmol/1 in Ca-EGTA-PSS. To confirm whether the inhibitory effect of 2, 4, 6 and 8 h PMI was mediated through the formation of NO, nitro-L-arginine (L-NNA), a potent NO synthase inhibitor, was used. Exposure to L-NNA (10 M) blocked the inhibition induced by an increase of PMI. The blocked effects of L-NNA were reversed by L-arginine (10 M). In conclusion, these patterns of change in artery responses provide insight into the post-mortem change in the receptor-mediated signaling components in epithelial and smooth muscle cells, and support the further study of post-mortem vascular responses triggered by G protein-coupled receptors (metabotropic) and channel-linked receptors (ionotropic) as potential markers for estimating short and long-term PMIs, respectively.

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Guanylate Cyclase Activators Influence Reactivity of Human Mesenteric Superior Arteries Retrieved and Preserved in the Same Conditions as Transplanted Kidneys

Cited by 14 publications

References 13 publications

Role of acetylcholine and calcium ions in three vascular contraction models: Angiotensin II, phenylephrine and caffeine

Role of acetylcholine and calcium ions in three vascular contraction models: Angiotensin II, phenylephrine and caffeine

Inhibition of hypoxia inducible factor-1α ameliorates lung injury induced by trauma and hemorrhagic shock in rats

Comparison of the post-mortem interval on the effect of vascular responses to the activation of ionotropic and metabotropic receptors

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