Nitric oxide as a putative nonadrenergic noncholinergic inhibitory transmitter in the canine pylorus in vivo

1992 ◽  
Vol 262 (4) ◽  
pp. G695-G702 ◽  
Author(s):  
H. D. Allescher ◽  
G. Tougas ◽  
P. Vergara ◽  
S. Lu ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Neural Inhibition ◽  
Anesthetized Dogs ◽  
Inhibitory Transmitter

Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.

Characterization of acute reversible systemic hypertension in a model of heme protein-induced renal injury

1999 ◽  
Vol 277 (1) ◽  
pp. F58-F65 ◽  
Author(s):  
David H. Warden ◽  
Anthony J. Croatt ◽  
Zvonimir S. Katusic ◽  
Karl A. Nath
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Vessel Wall ◽  
Heme Proteins ◽  
Blood Vessel Wall ◽  
Vasodilatory Response

In the glycerol model of renal injury we describe an acute rise in systemic arterial pressure which is attended by a reduced vasodilatory response to acetylcholine in vivo; vasodilatory responses to verapamil, however, were not impaired. Neither arginine nor sodium nitroprusside diminished this rise in blood pressure; N ω-nitro-l-arginine methyl ester (l-NAME) elevated basal mean arterial pressure and markedly blunted the rise in mean arterial pressure following the administration of glycerol. Aortic rings from the glycerol-treated rat demonstrate an impaired vasodilatory response to acetylcholine, an effect not repaired by arginine; the vasodilatory responses to nitric oxide donors, sodium nitroprusside and SIN-1, were also impaired; 8-bromo-cGMP, at higher doses, evinced a vasodilatory response comparable to that observed in the control rings. This pattern of responses was not a nonspecific effect of aortic injury, since aortic rings treated with mercuric chloride, a potent oxidant, displayed an impaired vasodilatory response to acetylcholine but not to sodium nitroprusside. We conclude that in the glycerol model of heme protein-induced tissue injury, there is an acute elevation in mean arterial pressure attended by impaired endothelium-dependent vasodilatation in vitro and in vivo. We suggest that the acute scavenging of nitric oxide by heme proteins depletes the blood vessel wall of its endogenous vasodilator and permeation of heme proteins into the blood vessel wall may contribute to such sustained effects as observed in vitro.

Presynaptic inhibition of canine renal adrenergic nerves by acetylcholine in vivo

1979 ◽  
Vol 237 (3) ◽  
pp. H326-H331
Author(s):  
N. W. Robie
Keyword(s):  
Nerve Stimulation ◽  
Neurotransmitter Release ◽  
Intact Animal ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Renal Vasculature ◽  
Anesthetized Dogs ◽  
Renal Sympathetic

Experiments were performed in anesthetized dogs to determine whether previously reported in vitro inhibition of sympathetic neurotransmitter release by acetylcholine could be demonstrated in the renal vasculature of the intact animal. Vasoconstrictor responses to renal sympathetic nerve stimulation at varying frequencies were compared to intra-arterial injections of norepinephrine before and during intra-arterial infusions of acetylcholine, 2.5--80 micrograms/min. The vasoconstrictor responses to nerve stimulation were inhibited to a greater extent than were responses to norepinephrine during infusions of acetylcholine. The inhibitory effects of acetylcholine on nerve stimulation were dose and frequency dependent. The inhibition was blocked by atropine but not altered by physostigmine. Changes in renal blood flow per se did not contribute to the inhibitory effect of acetylcholine, since another vasodilator agent, sodium acetate, did not affect the nerve stimulation-norepinephrine vasocontriction relationship. Thus, acetylcholine produced inhibition of in vivo renal sympathetic vasoconstrictor responses, and the receptor involved appears to be muscarinic.

Hydrogen sulfide downregulates the aortic l-arginine/nitric oxide pathway in rats

2007 ◽  
Vol 293 (4) ◽  
pp. R1608-R1618 ◽  
Author(s):  
Bin Geng ◽  
Yuying Cui ◽  
Jing Zhao ◽  
Fang Yu ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Umbilical Vein ◽  
Transcript Abundance ◽  
Inhibitory Effect ◽  
Akt Phosphorylation ◽  
Enos Activity ◽  
Nos Inhibitors

The aim of the present study was to investigate the effect of hydrogen sulfide (H2S) signaling by nitric oxide (NO) in isolated rat aortas and cultured human umbilical vein endothelial cells (HUVECs). Both administration of H2S and NaHS, as well as endogenous H2S, reduced NO formation, endothelial nitric oxide synthase (eNOS) activity, eNOS transcript abundance, and l-arginine (l-Arg) transport (all P < 0.01). The kinetics analysis of eNOS activity and l-Arg transport showed that H2S reduced Vmax values (all P < 0.01) without modifying Km parameters. Use of selective NOS inhibitors verified that eNOS [vs. inducible NOS (iNOS) and neuronal NOS (nNOS)] was the specific target of H2S regulation. H2S treatment (100 μmol/l) reduced Akt phosphorylation and decreased eNOS phosphorylation at Ser1177. H2S reduced l-Arg uptake by inhibition of a system y+ transporter and decreased the CAT-1 transcript. H2S treatment reduced protein expression of eNOS but not of nNOS and iNOS. Pinacidil (KATP channel opener) exhibited the similar inhibitory effects on the l-Arg/NOS/NO pathway. Glibenclamide (KATP channel inhibitor) partly blocked the inhibitory effect of H2S and pinacidil. An in vivo experiment revealed that H2S downregulated the vascular l-Arg/eNOS/NO pathway after intraperitoneal injection of NaHS (14 μmol/kg) in rats. Taken together, our findings suggest that H2S downregulates the vascular l-Arg/NOS/NO pathway in vitro and in vivo, and the KATP channel could be involved in the regulatory mechanism of H2S.

scholarly journals Inhibitory effect of nitric oxide on the replication of a murine retrovirus in vitro and in vivo.

1995 ◽  
Vol 69 (11) ◽  
pp. 7001-7005 ◽  
Author(s):  
K Akarid ◽  
M Sinet ◽  
B Desforges ◽  
M A Gougerot-Pocidalo
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect

Inhibition of rat mesangial cell mitogenesis by nitric oxide-generating vasodilators

1989 ◽  
Vol 257 (1) ◽  
pp. F60-F66 ◽  
Author(s):  
U. C. Garg ◽  
A. Hassid
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Culture Medium ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Inhibitory Effect ◽  
Relaxing Factor ◽  
Growth Inhibitory ◽  
Endothelium Derived Relaxing Factor

Recent studies indicate that endothelium-derived relaxing factor (EDRF) may be identical with nitric oxide (NO). The purpose of this study was to investigate the antimitogenic effect of NO-generating drugs in cultured mesangial cells. S-nitroso-N-acetylpenicillamine, sodium nitroprusside, and isosorbide dinitrate, which generate NO, dose dependently inhibited serum-stimulated DNA synthesis. All three drugs also inhibited the rate of cell proliferation, whereas sodium nitroprusside and S-nitroso-N-acetylpenicillamine decreased cell density at confluence. The antimitogenic activity of S-nitroso-N-acetylpenicillamine was labile in culture medium and could be inhibited by hemoglobin, supporting the view that NO, in free or bound form, was the ultimate effector. All three vasodilators increased cellular guanosine 3',5'-cyclic monophosphate (cGMP) levels dose dependently; moreover, 8-bromo-cGMP mimicked the effects of the NO-generating drugs, suggesting that cGMP may be an intracellular mediator of antimitogenesis. The growth-inhibitory effect of S-nitroso-N-acetylpenicillamine was reversible and was not due to cell toxicity as shown by several criteria of cell viability. The results raise the possibility that EDRF/NO may be a modulator of mesangial cell growth in vivo.

Inhibitory function of VIP-PHI and galanin in canine pylorus

1989 ◽  
Vol 256 (4) ◽  
pp. G789-G797 ◽  
Author(s):  
H. D. Allescher ◽  
E. E. Daniel ◽  
J. Dent ◽  
J. E. Fox
Keyword(s):  
Field Stimulation ◽  
Intraduodenal Infusion ◽  
Inhibitory Function ◽  
Excitatory Pathways ◽  
Neural Inhibition ◽  
Before And After ◽  
Pyloric Muscle ◽  
Stimulation Of

Contractions of canine pylorus and adjacent muscles were recorded with antral and duodenal strain gauges and a Dent sleeve manometric assembly with additional side holes in the pylorus. In vivo, vasoactive intestinal polypeptide (VIP) and peptide histamine isoleucine (PHI) given through the gastroepiploic artery inhibited both spontaneous and acetylcholine-induced pyloric contractions, before and after neural blockade with tetrodotoxin. Galanin inhibited only nerve-stimulated contractions. VIP greater than PHI much greater than galanin inhibited pyloric motor activity initiated by field stimulation of duodenal intramural nerves or intraduodenal infusion of 0.1 N HCl. In vitro, forskolin or field stimulation of nerves inhibited contractions of the pyloric muscle induced by various agonists but VIP-PHI failed to inhibit these contractions on two-thirds of the strips. The in vivo results suggest that VIP (or PHI) may be an inhibitory mediator in the pylorus acting directly on smooth muscle. Galanin may inhibit neural excitatory pathways in the pylorus. However, the structures on which VIP and PHI act in vivo may have become nonfunctional in vitro and other mediators account for the neural inhibition observed in isolated strips.

scholarly journals Vasorelaxant-Mediated Antihypertensive Effect of the Leaf Aqueous Extract from Stephania abyssinica (Dillon & A. Rich) Walp (Menispermaceae) in Rat

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Chamberlin Fodem ◽  
Elvine Pami Nguelefack-Mbuyo ◽  
Magloire Kanyou Ndjenda II ◽  
Albert Kamanyi ◽  
Télesphore Benoit Nguelefack
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methylene Blue ◽  
Aqueous Extract ◽  
Calcium Release ◽  
Inhibitory Effect ◽  
Antihypertensive Activity ◽  
Phytochemical Analysis

Stephania abyssinica is a medicinal plant used in Cameroon alternative medicine to treat arterial hypertension (AHT). Previous in vitro studies demonstrated the endothelium nitric oxide-independent vasorelaxant property of the aqueous extract from Stephania abyssinica (AESA). But its effect on AHT is unknown. The present study was undertaken to explore other vasorelaxant mechanisms and to determine the antihypertensive effects of AESA in male Wistar rats. Phytochemical analysis of AESA was carried out using the liquid chromatography-mass spectrometry (LC-MS) method. The vasorelaxant effects of AESA (1-1000 μg/mL) were studied on rat isolated thoracic aorta rings, in the absence or presence of indomethacin (10 μM) or methylene blue (10 μM). The inhibitory effect of AESA on phenylephrine (PE, 10 μM) or KCl- (60 mM) induced contraction as well as the intracellular calcium release was also evaluated. The in vivo antihypertensive activity of AESA (43, 86, or 172 mg/kg/day) or captopril (20 mg/kg/day) administered orally was assessed in L-NAME- (40 mg/kg/day) treated rats. Blood pressure and heart rate (HR) were measured at the end of each week while serum or urinary nitric oxide (NO), creatinine, and glomerular filtration rate (GFR) were determined at the end of the 6 weeks of treatment, as well as histological analysis of the heart and the kidney. The LC-MS profiling of AESA identified 9 compounds including 7 alkaloids. AESA produced a concentration-dependent relaxation on contraction induced either by PE and KCl, which was significantly reduced in endothelium-denuded vessels, as well as in vessels pretreated with indomethacin and methylene blue. Moreover, AESA inhibited the intracellular Ca2+ release-induced contraction. In vivo, AESA reduced the AHT, heart rate (HR), and ventricular hypertrophy and increased serum NO, urine creatinine, and GFR. AESA also ameliorated heart and kidney lesions as compared to the L-NAME group. These findings supported the use of AESA as a potential antihypertensive drug.

scholarly journals A Review ofIn VitroandIn VivoStudies on the Efficacy of Herbal Medicines for Primary Dysmenorrhea

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Kyoung-Sun Park ◽  
Kang-In Park ◽  
Deok-Sang Hwang ◽  
Jin-Moo Lee ◽  
Jun-Bock Jang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Somatostatin Receptor ◽  
Herbal Medicines ◽  
Inhibitory Effect ◽  
Phospholipid Metabolism ◽  
Reproductive Age ◽  
Herbal Formula ◽  
Primary Dysmenorrhea

Purpose. Primary dysmenorrhea (PD) is a common gynecological complaint among adolescent girls and women of reproductive age. This study aims to review the findings of published articles on thein vitroandin vivoefficacy of herbal medicines for PD.Methods.In vitroandin vivostudies of herbal compounds, individual herbal extracts, or herbal formula decoctions published from their inception to April 2014 were included in this review.Results. A total of 18 studies involving herbal medicines exhibited their inhibitory effect on PD. The majority ofin vitrostudies investigated the inhibition of uterine contractions.In vivostudies suggest that herbal medicines exert a peripheral analgesic effect and a possible anti-inflammatory activity via the inhibition of prostaglandin (PG) synthesis. The mechanisms of herbal medicines for PD are associated with PG level reduction, suppression of cyclooxygenase-2 expression, superoxide dismutase activation and malondialdehyde reduction, nitric oxide, inducible nitric oxide synthase, and nuclear factor-kappa B reduction, stimulation of somatostatin receptor, intracellular Ca2+reduction, and recovery of phospholipid metabolism.Conclusions. Herbal medicines are thought to be promising sources for the development of effective therapeutic agents for PD. Further investigations on the appropriate herbal formula and their constituents are recommended.

Effects of Nitric Oxide Donors in Vitro on the Arachidonic Acid-Induced Platelet Release Reaction and Platelet Cyclic GMP Concentration in Pre-Eclampsia

1994 ◽  
Vol 86 (2) ◽  
pp. 195-202 ◽  
Author(s):  
E. Hardy ◽  
P. C. Rubin ◽  
E. H. Horn
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Cyclic Gmp ◽  
Phosphodiesterase Inhibitor ◽  
Nitric Oxide Donors ◽  
Release Reaction ◽  
Healthy Pregnancy ◽  
Platelet Release

1. Platelet activation in vivo occurs in healthy pregnancy and is more pronounced in pre-eclampsia. 2. This study has investigated: (i) the inhibitory potency of the nitric oxide donors 3-morpholinosydnonimine and sodium nitroprusside, on the platelet release reaction in vitro in non-pregnant, healthy pregnant and pre-eclamptic women; (ii) the concentration of cyclic GMP during incubation of washed platelets with sodium nitroprusside in a separate group of non-pregnant, healthy pregnant and pre-eclamptic women. 3. The half-maximal inhibitory concentration of sodium nitroprusside, in the presence of a phosphodiesterase inhibitor, for inhibition of the platelet release reaction was lower in the pre-eclamptic subjects than in the non-pregnant subjects (P < 0.05). 4. Several of the pre-eclamptic women were studied again postnatally. The half-maximal inhibitory concentrations of sodium nitroprusside and 3-morpholinosydnonimine were higher in the postnatal than in the antenatal sample (P < 0.02). 5. Peak platelet cyclic GMP responses to sodium nitroprusside were significantly higher in the pre-eclamptic women than in the healthy pregnant and non-pregnant women. 6. These results suggest that platelets are more sensitive to the inhibitory effects of nitric oxide donors in pre-eclampsia.

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