The interaction of l -cysteine/H 2 S pathway and muscarinic acetylcholine receptors (mAChRs) in mouse corpus cavernosum

Aydinoglu, Fatma; Dalkir, Fatma Tugce; Demirbağ, Hatice Oruç; Ogulener, Nuran

doi:10.1016/j.niox.2017.08.005

Cited by 13 publications

(6 citation statements)

References 25 publications

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“…Although relaxation induced by interactions of H 2 S with NO has been described previously [ 31 , 71 , 75 , 76 ], in our hands, following Pb exposition and NaHS treatment, no differences in endothelial NO-dependent relaxation promoted by ACh were observed. However, when relaxation was triggered by ACh in the presence of NOS inhibitor L-NAME, a relaxation around 40% was reached in aortic rings from animals of Pb + NaHS group.…”

Section: Discussioncontrasting

confidence: 55%

Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

Possomato-Vieira

Gonçalves-Rizzi

Nascimento

et al. 2018

BioMed Research International

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Lead- (Pb-) induced hypertension has been shown in humans and experimental animals and cardiovascular effects of hydrogen sulfide (H2S) have been reported previously. However, no studies examined involvement of H2S in Pb-induced hypertension. We found increases in diastolic blood pressure and mean blood pressure in Pb-intoxicated humans followed by diminished H2S plasmatic levels. In order to expand our findings, male Wistar rats were divided into four groups: Saline, Pb, NaHS, and Pb + NaHS. Pb-intoxicated animals received intraperitoneally (i.p.) 1st dose of 8 μg/100 g of Pb acetate and subsequent doses of 0.1 μg/100 g for seven days and sodium hydrosulfide- (NaHS-) treated animals received i.p. NaHS injections (50 μmol/kg/twice daily) for seven days. NaHS treatment blunted increases in systolic blood pressure, increased H2S plasmatic levels, and diminished whole-blood lead levels. Treatment with NaHS in Pb-induced hypertension seems to induce a protective role in rat aorta which is dependent on endothelium and seems to promote non-NO-mediated relaxation. Pb-intoxication increased oxidative stress in rats, while treatment with NaHS blunted increases in plasmatic MDA levels and increased antioxidant status of plasma. Therefore, H2S pathway may be involved in Pb-induced hypertension and treatment with NaHS exerts antihypertensive effect, promotes non-NO-mediated relaxation, and decreases oxidative stress in rats with Pb-induced hypertension.

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Section: Discussioncontrasting

confidence: 55%

Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

Possomato-Vieira

Gonçalves-Rizzi

Nascimento

et al. 2018

BioMed Research International

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“…Thus, the blunted hyperreactivity to PHE in HTN‐Preg+NaHS could be related to the re‐establishment of endothelial relaxant responses. Interactions between H 2 S and NO have been described, and this interaction could explain the re‐established sensitivity to PHE in HTN‐Preg+NaHS animals. To test this hypothesis, ACh‐induced relaxation curves that trigger the release of endothelial NO, have been performed.…”

Section: Discussionmentioning

confidence: 96%

Increases in placental nitric oxide, but not nitric oxide‐mediated relaxation, underlie the improvement in placental efficiency and antihypertensive effects of hydrogen sulphide donor in hypertensive pregnancy

Possomato-Vieira

Chimini

Silva

et al. 2018

Clin Exp Pharma Physio

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Dysregulation of hydrogen sulphide (H S) producing enzymes has been related to hypertensive pregnancy, and H S donor, sodium hydrosulphide (NaHS) exerts antihypertensive effects, modulates angiogenic factors production and acts as an antioxidant. Moreover, reduction in nitric oxide (NO) bioavailability is related to hypertensive pregnancy and H S may interact with NO, modulating its production. We aimed to investigate the NaHS effects in hypertension-in-pregnancy and also in feto-placental parameters. Female Wistar rats (200-250 g) were mated and desoxycorticosterone acetate injections followed by replacement of water by 0.9% saline solution were used to induce hypertensive pregnancy. Rats were divided into four groups: normal pregnant (Norm-Preg), pregnant + NaHS (Preg+NaHS), hypertensive pregnant (HTN-Preg) and HTN-Preg+NaHS. Systolic blood pressure was increased in HTN-Preg and this increase was blunted in HTN-Preg+NaHS. Fetal and placental weights were decreased in HTN-Preg animals, while fetal growth restriction was improved in HTN-Preg+NaHS. Placental weight was lower in HTN-Preg+NaHS than in HTN-Preg; however, placental efficiency was re-established in HTN-Preg+NaHS rats. We observed that a partial contribution of placental NO, but not changes in anti-angiogenic factors may mediate the increases in placental efficiency in HTN-Preg+NaHS. HTN-Preg presented thoracic aorta hyperreactivity to phenylephrine while NaHS treatment blunted this hyperreactivity, which seems not to be related to NO-mediated relaxation induced by acetylcholine. Therefore, changes in vascular responsiveness promoted by NaHS treatment may underlie the beneficial effects in systolic blood pressure and feto-placental parameters in our study.

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“…As illustrated in Figure 1E, the production of H 2 S was 31.96 ± 1.88 nmol/g protein × min -1 ( n = 4), 65.09 ± 5.45 nmol/g protein × min -1 ( n = 4) and 72.39 ± 3.02 nmol/g protein × min -1 ( n = 4) in caput, corpus and cauda epididymis, respectively. The synthesis of H 2 S was significantly suppressed when pretreated the tissue homogenate with AOAA (1 mM), the inhibitor of CBS, or/and PAG (10 mM), the inhibitor of CSE (Aydinoglu et al, 2017). These results indicated that the epididymis possessed increasing ability to generate the endogenous H 2 S from caput to cauda regions.…”

Section: Resultsmentioning

confidence: 99%

Cellular Mechanism Underlying Hydrogen Sulfide Mediated Epithelial K+ Secretion in Rat Epididymis

Gao

Qin

et al. 2019

Front. Physiol.

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As a novel gasotransmitter, hydrogen sulfide (H2S) elicits various physiological actions including smooth muscle relaxation and promotion of transepithelial ion transport. However, the pro-secretory function of H2S in the male reproductive system remains largely unclear. The aim of this study is to elucidate the possible roles of H2S in modulating rat epididymal intraluminal ionic microenvironment essential for sperm storage. The results revealed that endogenous H2S-generating enzymes cystathionine β-synthetase (CBS) and cystathionine γ-lyase (CSE) were both expressed in rat epididymis. CBS located predominantly in epithelial cells whilst CSE expressed primarily in smooth muscle cells. The relative expression level of CBS and CSE escalated from caput to cauda regions of epididymis, which was paralleled to the progressively increasing production of endogenous H2S. The effect of H2S on epididymal epithelial ion transportation was investigated using short-circuit current (ISC), measurement of intracellular ion concentration and in vivo rat epididymal microperfusion. Our data showed that H2S induced transepithelial K+ secretion via adenosine triphosphate-sensitive K+ (KATP) channel and large conductance Ca2+-activated K+ (BKCa) channel. Transient receptor potential vanilloid 4 (TRPV4) channel-mediated Ca2+ influx was implicated in the activation of BKCa channel. In vivo studies further demonstrated that H2S promoted K+ secretion in rat epididymal epithelium. Inhibition of endogenous H2S synthesis caused a significant decrease in K+ concentration of cauda epididymal intraluminal fluid. Moreover, our data demonstrated that high extracellular K+ concentration actively depressed the motility of cauda epididymal sperm in a pH-independent manner. Collectively, the present study demonstrated that H2S was vital to the formation of high K+ concentration in epididymal intraluminal fluid by promoting the transepithelial K+ secretion, which might contribute to the maintenance of the cauda epididymal sperm in quiescent dormant state before ejaculation.

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The interaction of l -cysteine/H 2 S pathway and muscarinic acetylcholine receptors (mAChRs) in mouse corpus cavernosum

Cited by 13 publications

References 25 publications

Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

Increases in placental nitric oxide, but not nitric oxide‐mediated relaxation, underlie the improvement in placental efficiency and antihypertensive effects of hydrogen sulphide donor in hypertensive pregnancy

Cellular Mechanism Underlying Hydrogen Sulfide Mediated Epithelial K+ Secretion in Rat Epididymis

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