Possible Roles of Nitric Oxide and Vasoactive Intestinal Polypeptide on Relaxation Induced by Isoprenaline in Isolated Muscle Strips of the Mouse Gastric Fundus

The possible role of nitric oxide (NO) and vasoactive intestinal polypeptide on isoprenaline-induced relaxation of the mouse longitudinal gastric fundal strips precontracted with 5.4 x 10(-7) M carbachol was investigated. Isoprenaline (5 x 10(-7) M, 10(-6) M and 5 x 10(-6) M) produced a concentration-dependent relaxations. NG-nitro L-arginine (10(-4) M) partly inhibited isoprenaline-induced relaxation. The inhibitory action of NG-nitro L-arginine was reversed by 4 x 10(-4) M L-arginine but not by 4 x 10(-4) M D-arginine. NG-nitro L-arginine (10(-4) M) did not affect the relaxation caused by sodium nitroprusside (10(-6) M). Vasoactive intestinal polypeptide antibody 7913 (1:160 dilution) partly inhibited isoprenaline-induced relaxation. This inhibition was greater on the response to the higher isoprenaline concentration (5 x 10(-6) M) than to the lower concentration (10(-6) M). The combination of vasoactive intestinal polypeptide antibody and NG-nitro L-arginine significantly enhanced the inhibition on 10(-6) M isoprenaline action. These results suggest that nitric oxide and vasoactive intestinal polypeptide may partly contribute to the relaxation induced by isoprenaline in the mouse gastric fundus precontracted with carbachol.</p

The investigation of the relaxant mechanism of hydrogen sulfide in isolated mice corpus cavernosum

3rd European Conference on the Biology of Hydrogen Sulfide (H2S) -- MAY 03-06, 2015 -- Athens, GREECEWOS: 000353313900047

Antioxidant effect of quercetin on the nitrergic neurotansmitter in the mouse gastric fundus

WOS: 000239590003610

Involvement of RhoA/Rho-kinase in L-cysteine/H2S pathway-induced inhibition of agonist-mediated corpus cavernosal smooth muscle contraction

WOS: 000460714100008PubMed ID: 30768962Rho-kinase activity is a key regulator in the maintenance of corporal vasoconstriction and penile detumescense. Also, importance of L-cysteine/H2S pathway in erectile tissue has been shown; however it is currently unknown the role RhoA/Rho-kinase pathway in H2S-induced inhibition in cavernosal tissue. We investigated the role of RhoA/Rho-kinase pathway in the inhibitory effect of L-cysteine and NaHS, as endogenous and exogenous H2S, respectively, on phenylephrine-induced contractions of mouse cavernosal strips. Phenylephrine, alpha(1) receptor agonist, (10 nM-100 mu M) induced a concentration-dependent contraction in CC. L-cysteine (endogenous H2S substrate; 10 mM) and exogenous H2S (NaHS; 1 mM) significantly inhibited the contractile response to phenylephrine (P < 0.05). Inhibition of CSE and CBS enzymes by PAG (10 mM) and AOAA (1 mM), respectively, significantly reversed the inhibitory effects of L-cysteine on phenylephrine-induced contraction (P < 0.05). Y-27632 (1 mu M), a specific Rho-kinase inhibitor, significantly augmented the inhibitory effect of L-cysteine and NaHS on phenylephrine-induced contraction, and this inhibition was reversed by PAG and AOAA (P < 0.05). In addition, the formation of H2S was increased by approximately 1.8 fold over basal values after incubation of tissue homogenates with L-cysteine. Y-27632 significantly increased both basal and L-cysteine-induced H2S formation and this augmentation diminished by PAG and AOAA (P < 0.05). Furthermore, the pMYPT-1 expression was significantly decreased by L-cysteine, NaHS or Y-27632 alone. Also, pMYPT-1 expression was completely abolished by the L-cysteine/NaHS plus Y-27632 combination, and this inhibition was reversed by PAG and AOAA (P < 0.05). These results suggest that there is an interaction between Rho-kinase and H2S pathways. Rho-kinase may be, at least in part, inhibits CSE/CBS enzymes in mouse corpus cavernosal tissue; however, it is not excluded the other kinases such as PKC and Zip-kinase.Cukurova University Research FoundationCukurova University [TF2013BAP2]This study was supported by Cukurova University Research Foundation (TF2013BAP2)

Effects of ethanol treatment on the neurogenic and endothelium-dependent relaxation of corpus cavernosum smooth muscle in the mouse

WOS: 000261363900016PubMed ID: 19066420The relaxation of cavernous smooth muscle is critical for inducing and maintaining a penile erection. The neurogenic- and endothelium-dependent relaxation of corpus cavernosum smooth muscle and the degenerative effect of subacute ethanol treatment on the endothelial cells of corpus cavernosum was investigated in mice. In the cavernous strips contracted with phenylephrine, electrical field Stimulation (EFS), acetylcholine and exogenous nitric oxide (NO) induced relaxations in the control group. Ethanol treatment abolished the endothelium-dependent relaxations induced by acetylcholine but failed to alter the relaxation to EFS and NO. L-nitroarginine, a NO synthase inhibitor, reduced relaxations induced by EFS and acetylcholine, but not those induced by NO in control and ethanol-treated mice. L-arginine prevented the response inhibited by L-nitroarginine. ODQ, a guanylyl cyclase inhibitor, inhibited relaxations in response to EFS, NO and acetylcholine in control and ethanol-treated mice, Corpus cavernosum tissues were investigated using electron microscopy and endothelial damage was observed in ethanol-treated mice. These results suggest that ethanol impairs the endothelial function of corpus cavernosum, in mouse, and it may lead to erectile dysfunction through a reduced NO release via endothelial impairment.Cukurova University Research FoundationCukurova University [TF.2005YLS]This work was supported by the Cukurova University Research Foundation (TF.2005YLS)