Macrophage-induced nitric oxide and prostanoid dependent relaxation of arterial smooth muscles

1997 ◽  
Vol 75 (7) ◽  
pp. 789-795 ◽  
Author(s):  
H Wang ◽  
R Mizuno ◽  
T Ohhashi
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscles

scholarly journals Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway

2021 ◽  
Author(s):  
Beata Modzelewska ◽  
Krzysztof Drygalski ◽  
Tomasz Kleszczewski ◽  
Andrzej Chomentowski ◽  
Krzysztof Koryciński ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Smooth Muscles ◽  
Nitric Oxide Pathway

Nitrergic Prejunctional Inhibition of Purinergic Neuromuscular Transmission in the Hamster Proximal Colon

2003 ◽  
Vol 89 (5) ◽  
pp. 2346-2353 ◽  
Author(s):  
Hayato Matsuyama ◽  
AbuBakr El-Mahmoudy ◽  
Yasutake Shimizu ◽  
Tadashi Takewaki
Keyword(s):  
Nitric Oxide ◽  
Nerve Stimulation ◽  
Smooth Muscles ◽  
Circular Muscle ◽  
Single Pulse ◽  
Proximal Colon ◽  
Paired Stimulus ◽  
Physiological Control ◽  
Purinergic Transmission ◽  
Intramural Nerve

Neurogenic ATP and nitric oxide (NO) may play important roles in the physiological control of gastrointestinal motility. However, the interplay between purinergic and nitrergic neurons in mediating the inhibitory neurotransmission remains uncertain. This study investigated whether neurogenic NO modulates the purinergic transmission to circular smooth muscles of the hamster proximal colon. Electrical activity was recorded from circular muscle cells of the hamster proximal colon by using the microelectrode technique. Intramural nerve stimulation with a single pulse evoked a fast purinergic inhibitory junction potential (IJP) followed by a slow nitrergic IJP. The purinergic component of the second IJP evoked by paired stimulus pulses at pulse intervals between 1 and 3 s became smaller than that of the first IJP. This purinergic IJP depression could be observed at pulse intervals <3 s, but not at longer ones, and failed to occur in the presence of NO synthase inhibitor. Exogenous NO (0.3–1 μM), at which no hyperpolarization is produced, inhibited purinergic IJPs, without altering the nitrergic IJP and exogenously applied ATP-induced hyperpolarization. In the presence of both purinoceptor antagonist and nitric oxide synthase (NOS) inhibitor, intramural nerve stimulation with 5 pulses at 20 Hz evoked vasoactive intestinal peptide (VIP)-associated IJPs, suggesting that VIP component may be masked in the IJPs of the hamster proximal colon. Our results suggest that neurogenic NO may modulate the purinergic transmission to circular smooth muscles of the hamster proximal colon via a prejunctional mechanism. In addition, VIP may be involved in the neurotransmitter in the hamster proximal colon.

scholarly journals Epithelium-dependent regulation of airways smooth muscle function. A histamine-nitric oxide pathway

1998 ◽  
Vol 7 (6) ◽  
pp. 409-411 ◽  
Author(s):  
Konstantinos Gourgoulianis ◽  
Zoe Iliodromitis ◽  
Apostolia Hatziefthimiou ◽  
Paschalis-Adam Molyvdas
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Airway Epithelium ◽  
Muscle Function ◽  
Smooth Muscles ◽  
Airways Smooth Muscle ◽  
Smooth Muscle Function ◽  
No Release ◽  
Nos Inhibitor

The airway epithelium is responsible for the production of a number of arachidonic acid and nonprostanoid inhibitory factors. Epithelium synthesises nitric oxide (NO) which may be important in regulating the function of airways smooth muscles. We studiedin vitrothe effect of histamine (100 nM100 μ M) which increases the NO release on rabbit airway smooth muscles induced by 80 mM KCl in the presence or not of 10-5Methylene blue (MB) (inactivator of guanylate cyclase) or N(G)-monomethyl L-arginine (L-NMMA), a NOS inhibitor. All experiments were done in tracheal muscle strips from 28 rabbits with epithelium and after epithelium removal. The additional use of histamine (1 μ M) on KCl contraction induced a relaxation of 10% of the initial contraction. The additional use of L-NMMA decreased the relaxation to 5% of initial contraction. MB rather than L-NMMA increased the contraction significantly(p<0.01). Epithelium removal increased the contraction induced by KCl (80 mM) and histamine (1 μ M) by about 30%(p<0.001). NO release especially from epithelium regulates the airways smooth muscle functions. Damage to the epithelium may contribute to an increase in airways sensitivity, observed in asthma.

Densities of nitric oxide synthesizing nerves in smooth muscles of human gut during fetal development

1997 ◽  
Vol 32 (9) ◽  
pp. 1314-1317 ◽  
Author(s):  
Carlos Teixeira Brandt ◽  
Andrew Graham ◽  
Pau Kwong Hang Tam
Keyword(s):  
Nitric Oxide ◽  
Fetal Development ◽  
Smooth Muscles ◽  
Human Gut

Role of Nitric Oxide Produced by Lactobacilli in Relaxation of Intestinal Smooth Muscles

2016 ◽  
Vol 160 (3) ◽  
pp. 343-346 ◽  
Author(s):  
D. R. Yarullina ◽  
R. O. Mikheeva ◽  
G. I. Sabirullina ◽  
P. V. Zelenikhin ◽  
O. N. Ilinskaya ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscles ◽  
Intestinal Smooth Muscles

scholarly journals Magnetic-laser influence on the system of nitric oxide and contractile activity of smooth muscles of rat aorta under hypertension

2012 ◽  
Vol 58 (6) ◽  
pp. 36-47
Author(s):  
SM Fedorov ◽  
◽  
OV Baziliuk ◽  
AV Kotsiuruba ◽  
IuP Korkach ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Rat Aorta

scholarly journals Nitric oxide as a second messenger in parathyroid hormone-related protein signaling

2001 ◽  
Vol 170 (2) ◽  
pp. 433-440 ◽  
Author(s):  
L Kalinowski ◽  
LW Dobrucki ◽  
T Malinski
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Parathyroid Hormone ◽  
Smooth Muscles ◽  
Calcium Ionophore ◽  
No Production ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
No Release ◽  
Pthrp Receptor

Parathyroid hormone (PTH)-related protein (PTHrP) is produced in smooth muscles and endothelial cells and is believed to participate in the local regulation of vascular tone. No direct evidence for the activation of endothelium-derived nitric oxide (NO) signaling pathway by PTHrP has been found despite attempts to identify it. Based on direct in situ measurements, it is reported here for the first time that the human PTH/PTHrP receptor analogs, hPTH(1--34) and hPTHrP(1--34), stimulate NO release from a single endothelial cell. A highly sensitive porphyrinic microsensor with a response time of 0.1 ms and a detection limit of 1 nmol/l was used for the measurement of NO. Both hPTH(1--34) and hPTHrP(1--34) stimulated NO release at nanomolar concentrations. The peak concentration of 0.1 micromol/l hPTH(1--34)- and 0.1 micromol/l hPTHrP(1--34)-stimulated NO release was 175+/-9 and 248+/-13 nmol/l respectively. This represents about 30%--40% of maximum NO concentration recorded in the presence of (0.1 micromol/l) calcium ionophore. Two competitive PTH/PTHrP receptor antagonists, 10 micromol/l [Leu(11),d -Trp(12)]-hPTHrP(7--34)amide and 10 micromol/l [Nle(8,18),Tyr(34)]-bPTH(3--34)amide, were equipotent in antagonizing hPTH(1--34)-stimulated NO release; [Leu(11),d -Trp(12)]-hPTHrP(7--34)amide was more potent than [Nle(8,18),Tyr(34)]-bPTH(3--34)amide in inhibiting hPTHrP(1--34)-stimulated NO release. The PKC inhibitor, H-7 (50 micromol/l), did not change hPTH(1--34)- and hPTHrP(1--34)-stimulated NO release, whereas the combined effect of 10 micromol/l of the cAMP antagonist, Rp-cAMPS, and 50 micromol/l of the calmodulin inhibitor, W-7, was additive. The present studies show that both hPTH(1--34) and hPTHrP(1--34) activate NO production in endothelial cells. The activation of NO release is through PTH/PTHrP receptors and is mediated via the calcium/calmodulin pathway.

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