The role of nitric oxide in the inhibitory effect of ghrelin against penicillin-induced epileptiform activity in rat

We examined in vitro the source and role of basal nitric oxide (NO) in proximal segments of guinea pig taenia caeci in nonadrenergic, noncholinergic (NANC) conditions. Using electron paramagnetic resonance (EPR), we measured the effect of the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10–4 M), the neuronal blocker tetrodotoxin (TTX, 10–6 M), or both on spontaneous contractions and on the production of basal NO. Both l-NAME and TTX, when tested alone, increased the amplitude and frequency of contractions. NO production was abolished by l-NAME and was inhibited by 38% by TTX. When tested together, l-NAME in the presence of TTX or TTX in the presence of l-NAME had no further effect on the amplitude or frequency of spontaneous contractions, and the NO production was inhibited. These findings suggest that basal NO consists of TTX-sensitive and TTX-resistant components. The TTX-sensitive NO has an inhibitory effect on spontaneous contractions; the role of TTX-resistant NO is unknown.

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Role of S-Nitrosation of Cysteine Residues in Long-Lasting Inhibitory Effect of Nitric Oxide on Arterial Tone

Molecular Pharmacology ◽

10.1124/mol.63.5.1148 ◽

2003 ◽

Vol 63 (5) ◽

pp. 1148-1158 ◽

Cited By ~ 32

Author(s):

Jacicarlos L. Alencar ◽

Irina Lobysheva ◽

Michel Geffard ◽

Mamadou Sarr ◽

Christa Schott ◽

...

Keyword(s):

Nitric Oxide ◽

Inhibitory Effect ◽

Cysteine Residues ◽

Arterial Tone

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Nitric oxide synthase acutely regulates progesterone production by in vitro cultured rabbit corpora lutea

Journal of Endocrinology ◽

10.1677/joe.0.1600275 ◽

1999 ◽

Vol 160 (2) ◽

pp. 275-283 ◽

Cited By ~ 32

Author(s):

A Gobbetti ◽

C Boiti ◽

C Canali ◽

M Zerani

Keyword(s):

Nitric Oxide ◽

In Vitro Release ◽

Inhibitory Effect ◽

Corpora Lutea ◽

No Donor ◽

Nos Inhibitor ◽

Oxide Synthase ◽

Vitro Release

We examined the presence and the regulation of nitric oxide (NO) synthase (NOS) using in vitro cultured corpora lutea (CL) obtained from rabbits at days 4 and 9 of pseudopregnancy. The role of NO and NOS on steroidogenesis was also investigated using the same CL preparations after short-term incubations (30 min and 2 h) with the NO donor, sodium nitroprusside (NP), the NOS inhibitor, Nomega-nitro-l-arginine methyl ester (l-NAME) and prostaglandin (PG) F-2alpha. The basal NOS activity was greater in CL at day 4 than at day 9, and was also differently modulated by PGF-2alpha, depending on the age of the CL. The addition of PGF-2alpha to day 4 CL had no effect, but PGF-2alpha on day 9 caused a threefold increase in NOS activity. NP caused a two- to fivefold decrease in release of progesterone from CL of both ages, and this inhibitory effect on steroidogenesis was reversed by l-NAME. All treatments failed to modify basal androgens and 17beta-oestradiol was not detectable in either control or treated CL. These results suggest that NO is effectively involved in the regulation process of steroidogenesis, independently of 17beta-oestradiol. PGF-2alpha had no effect on day 4, but induced luteolysis on day 9, by reducing progesterone (P</=0. 01) to about 18% of control. The luteolytic action of PGF-2alpha was completely reversed by co-incubation with l-NAME, thus supporting the hypothesis that luteolysis is mediated by NO. The addition of NP or l-NAME did not modify the in vitro release of PGF-2alpha. We hypothesised that PGF-2alpha upregulates NOS activity and, consequently, the production of NO, which acutely inhibits progesterone release from day 9 CL of pseudopregnant rabbits.

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Inhibitory effect of experimental colitis on fluid absorption in rat jejunum: role of the enteric nervous system, VIP, and nitric oxide

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00271.2005 ◽

2006 ◽

Vol 290 (2) ◽

pp. G262-G268 ◽

Cited By ~ 24

Author(s):

Fadi H. Mourad ◽

Kassem A. Barada ◽

Nadine A. Bou Rached ◽

Carmen I. Khoury ◽

Nayef E. Saadé ◽

...

Keyword(s):

Nitric Oxide ◽

Nervous System ◽

Enteric Nervous System ◽

Experimental Colitis ◽

Inhibitory Effect ◽

Fluid Absorption ◽

Receptor Antagonism ◽

Chemical Colitis

Impairment of small intestinal absorption has been described in patients with ulcerative colitis and in animal models of experimental colitis. The pathophysiology of this dysfunction has not been elucidated. The aim of this study was to investigate the effect of chemical colitis on jejunal fluid absorption and determine the role of the enteric nervous system and some putative neurotransmitters. In a rat model of iodoacetamide-induced colitis, jejunal net fluid absorption was evaluated by the in vivo single-pass perfusion technique. The effects of 1) tetrodotoxin (TTX), 2) benzylalkonium chloride (BAC), 3) capsaicin, 4) vasoactive intestinal polypeptide (VIP) antagonism, 5) nitric oxide (NO) synthase (NOS) inhibition, and 6) 5-hydroxytryptamine type 3 and 4 (5-HT3 and 5-HT4) receptor antagonism on the changes in fluid movement were investigated. A significant decrease in jejunal net fluid absorption was found 2 and 4 days after colitis induction: 26 (SD 14) and 28 (SD 19) μl·min−1·g dry intestinal wt−1, respectively [ P < 0.0002 compared with sham rats at 61 (SD 6.5) μl·min−1·g dry intestinal wt−1]. No histological changes were evident in jejunal sections. TTX and BAC reversed this decrease in fluid absorption: 54 (SD 13) and 44 (SD 14) μl·min−1·g dry intestinal wt−1 ( P = 0.0005 and P = 0.019, respectively, compared with colitis). Ablation of capsaicin-sensitive primary afferent fibers had a partial effect: 45 (SD 5) μl·min−1·g dry intestinal wt−1 ( P = 0.001 and P = 0.003 compared with colitis and sham, respectively). Constitutive and neuronal NOS inhibition and VIP antagonism returned jejunal net fluid absorption to normal values: 66 (SD 19), 61 (SD 5), and 56 (SD 14) μl·min−1·g dry intestinal wt−1, respectively. 5-HT3 and 5-HT4 receptor antagonism had no effect. Chemical colitis is associated with a significant decrease in jejunal net fluid absorption. This decrease is neurally mediated and involves VIP- and NO-related mechanisms.

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Role of Nitric Oxide/Cyclic GMP Pathway in the Inhibitory Effect of GABA and Dopamine on Prolactin Release

Journal of Neuroendocrinology ◽

10.1111/j.1365-2826.1996.tb00820.x ◽

1996 ◽

Vol 8 (12) ◽

pp. 909-913 ◽

Cited By ~ 24

Author(s):

Beatriz H. Duvilanski ◽

Carolina Zambruno ◽

Mercedes Lasaga ◽

Daniel Pisera ◽

Adriana Seilicovich

Keyword(s):

Nitric Oxide ◽

Cyclic Gmp ◽

Inhibitory Effect ◽

Prolactin Release

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Modulation of glomerular arteriolar tone by nitric oxide synthase inhibitors.

Journal of the American Society of Nephrology ◽

10.1681/asn.v451127 ◽

1993 ◽

Vol 4 (5) ◽

pp. 1127-1132

Author(s):

R M Edwards ◽

W Trizna

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Inhibitory Effect ◽

Lumen Diameter ◽

Nitric Oxide Synthase Inhibitors ◽

Afferent Arterioles ◽

Arteriolar Tone ◽

Oxide Synthase

The inhibition of nitric oxide production has been shown to reduce RBF. The effects of the nitric oxide synthase inhibitors, N omega-nitro-L-arginine and NG-monomethyl-L-arginine, on afferent and efferent arterioles isolated from rabbit kidneys were examined. Under basal conditions, N omega-nitro-L-arginine (10(-7) to 10(-3) M) had no effect on efferent arteriole lumen diameter but caused a 40% decrease in the lumen diameter of afferent arterioles. In afferent and efferent arterioles precontracted with norepinephrine, N omega-nitro-L-arginine and NG-monomethyl-L-arginine (3 x 10(-4) M) markedly attenuated the vasorelaxant effects of the endothelium-dependent vasodilator acetylcholine. In both arterioles, the inhibitory effect of N omega-nitro-L-arginine on acetylcholine-induced relaxation could be reversed by L- but not D-arginine (10(-3) M). However, N omega-nitro-L-arginine had no effect on the relaxation produced by the endothelium-independent vasodilators prostaglandin E2 (afferent) and dopamine (efferent). These observations demonstrate that under the in vitro conditions used in this study, afferent arterioles but not efferent arterioles synthesize and release nitric oxide in the basal state. However, both arterioles release nitric oxide in response to an endothelium-dependent vasodilator. The results of this study provide further evidence for an important role of nitric oxide in the regulation of renal hemodynamics.

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Role of phosphodiesterase and protein kinase G on nitric oxide-induced inhibition of prolactin release from the rat anterior pituitary

Acta Endocrinologica ◽

10.1530/eje.0.1430279 ◽

2000 ◽

pp. 279-284 ◽

Cited By ~ 20

Author(s):

MO Velardez ◽

A De Laurentiis ◽

M del Carmen Diaz ◽

M Lasaga ◽

D Pisera ◽

...

Keyword(s):

Nitric Oxide ◽

Protein Kinase ◽

Anterior Pituitary ◽

Inhibitory Effect ◽

Male Rats ◽

Protein Kinase G ◽

Camp Concentration ◽

Prolactin Release ◽

Pituitary Glands

OBJECTIVE: In order to determine the mechanism by which nitric oxide (NO) inhibits prolactin release, we investigated the participation of cGMP-dependent cAMP-phosphodiesterases (PDEs) and protein kinase G (PKG) in this effect of NO. METHODS: Anterior pituitary glands of male rats were incubated with inhibitors of PDE and PKG with or without sodium nitroprusside (NP). Prolactin release, and cAMP and cGMP concentrations were determined by RIA. RESULTS AND CONCLUSIONS: The inhibitory effect of NP (0.5 mmol/l) on prolactin release and cAMP concentration was blocked by EHNA (10(-4)mol/l) and HL-725 (10(-4)mol/l), inhibitors of cGMP-stimulated cAMP-PDE (PDE2). 8-Br-cGMP (10(-4) and 10(-3)mol/l), which mimics cGMP as a mediator of NP effects on prolactin release, also decreased cAMP concentration. Zaprinast (10(-4)mol/l), a selective inhibitor of specific cGMP-PDE (PDE5), potentiated the NP effect on cAMP concentration. Rp-8-[(4-chlorophenyl)thio]-cGMP triethylamine (Rp-8-cGMP, 10(-7)-10(-6)mol/l), an inhibitor of PKG, reversed the effect of NP on prolactin release. The present study suggests that several mechanisms are involved in the inhibitory effect of NO on prolactin release. The activation of PDE2 by cGMP may mediate the inhibitory effect of NO on cAMP concentration and therefore on prolactin release. NO-activated PKG may also be participating in the inhibitory effect of NO on prolactin release.

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Role of ETB receptors and nitric oxide in adrenal catecholamine secretion in anesthetized dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.277.4.r1051 ◽

1999 ◽

Vol 277 (4) ◽

pp. R1051-R1056 ◽

Cited By ~ 2

Author(s):

Akio Hosokawa ◽

Takahiro Nagayama ◽

Kimiya Masada ◽

Makoto Yoshida ◽

Mizue Suzuki-Kusaba ◽

...

Keyword(s):

Nitric Oxide ◽

Splanchnic Nerve ◽

Inhibitory Effect ◽

Catecholamine Secretion ◽

Anesthetized Dogs ◽

Nos Inhibitor ◽

Neuronal Nos ◽

Endothelin B ◽

Oxide Synthase

We examined the effects of sarafotoxin 6c (S6c), an endothelin-B (ETB) receptor agonist, on adrenal catecholamine secretion in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered intra-arterially into the adrenal gland through the phrenicoabdominal artery. Infusion of S6c attenuated increases in adrenal catecholamine output induced by splanchnic nerve stimulation. The inhibitory effect of S6c on the catecholamine secretion response was suppressed with a selective ETB receptor antagonist N- cis2,6-dimethylpiperidinocarbonyl-l-γ-methylleucyl-d-1-methoxycarbonyltryptophanyl-d-norleucine (BQ-788), a nitric oxide synthase (NOS) inhibitor N ω-nitro-l-arginine methyl ester, and a neuronal NOS inhibitor 7-nitroindazole monosodium salt (7-NINA). Similar results were obtained with the catecholamine secretion response induced by injection of ACh. 7-NINA alone did not affect these catecholamine secretion responses. These results suggest that ETB receptors play an inhibitory role in adrenal catecholamine secretion by activating neuronal NOS, whereas neuronal NOS is unlikely to be involved in regulation of adrenal catecholamine secretion in the absence of simultaneous ETB receptor stimulation.

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