Pregnancy-induced alterations of neurogenic constriction and dilation of human uterine artery

1995 ◽  
Vol 268 (4) ◽  
pp. H1694-H1701 ◽  
Author(s):  
S. H. Nelson ◽  
O. S. Steinsland ◽  
R. L. Johnson ◽  
M. S. Suresh ◽  
A. Gifford ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Uterine Artery ◽  
Electrical Field Stimulation ◽  
Physiological Mechanisms ◽  
Electrical Field ◽  
Uterine Arteries ◽  
Perivascular Nerves ◽  
Arterial Constriction ◽  
Contraction And Relaxation ◽  
Oxide Synthase

The responses to electrical field stimulation (EFS) of perivascular nerves in human uterine arteries were characterized. The arteries were removed from pregnant and nonpregnant patients undergoing hysterectomy. Tetrodotoxin, guanethidine, and phentolamine blocked EFS (2 min, 80 V, 0.1-ms duration)-induced constriction. The constrictions and the endogenous norepinephrine levels were lower (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. When arterial rings were precontracted, the response to EFS was biphasic, consisting of an initial constriction followed by a postconstriction relaxation. The EFS-induced relaxation was endothelium independent and was greater (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. The relaxation was enhanced by guanethidine and superoxide dismutase, inhibited by nitric oxide synthase inhibitors, blocked by tetrodotoxin, and unaffected by atropine, propranolol, or indomethacin. The results demonstrate that human uterine arteries respond to EFS with contraction and relaxation and that these responses may be mediated, respectively, by norepinephrine and, in part, by nitric oxide released from periarterial nerves. The decrease in neuronally mediated uterine arterial constriction and the increase in dilation could be physiological mechanisms for ensuring appropriate uteroplacental perfusion.

Involvement of nitric oxide synthetic pathway in inhibitory junction potentials in canine proximal colon

1991 ◽  
Vol 260 (5) ◽  
pp. G789-G792 ◽  
Author(s):  
H. H. Dalziel ◽  
K. D. Thornbury ◽  
S. M. Ward ◽  
K. M. Sanders
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Electrical Field Stimulation ◽  
Proximal Colon ◽  
Electrical Field ◽  
Nitric Oxide Synthase Inhibitor ◽  
Potential Oscillations ◽  
Synthetic Pathway ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Experiments were performed to determine the involvement of nitric oxide synthase in the generation of nonadrenergic, noncholinergic (NANC) inhibitory junction potentials (IJPs) in the canine proximal colon. Smooth muscle cells were impaled near the myenteric border between the circular and longitudinal layers. Cells exhibited rhythmic myenteric potential oscillations. IJPs were evoked with electrical field stimulation in the presence of drugs to block adrenergic and cholinergic neurotransmission. N omega-nitro-L-arginine, methyl ester (L-NAME), a nitric oxide synthase inhibitor, progressively reduced the amplitude of IJPs. The effect of L-NAME was reversed by L-Arg but not by the stereoisomer D-Arg. IJPs disrupt the regular pattern of myenteric potential oscillations. This effect was also blocked by L-NAME and reversed by L-Arg. These experiments suggest that a product of the nitric oxide synthetic pathway is involved in NANC neurotransmission in the canine proximal colon.

Effect of an inhibitor of nitric oxide synthase on neural relaxation of human bronchi

1993 ◽  
Vol 264 (5) ◽  
pp. L425-L430 ◽  
Author(s):  
T. R. Bai ◽  
A. M. Bramley
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Electrical Field Stimulation ◽  
Electrical Field ◽  
Maximal Inhibition ◽  
Low Frequencies ◽  
Before And After ◽  
Oxide Synthase ◽  
Human Bronchi

This study examines the roles of peptides and nitric oxide (NO) as mediators of inhibitory nonadrenergic, noncholinergic (NANCi) neurons in human and guinea pig airways in vitro. Tissues were contracted with 0.3 microM methacholine (MCh) and relaxation studied before and after the addition of the peptidase alpha-chymotrypsin (alpha-CT) (2 U/ml) and NG-nitro-L-arginine methyl ester (L-NAME 0.1-1.1 mM), an inhibitor of NO synthase, the enzyme catalyzing the formation of NO. alpha-CT alone, in comparison to parallel time controls, inhibited control relaxation to electrical field stimulation (EFS) by 29.2 +/- 8.6% in guinea pig tracheae (n = 9), whereas a small augmentation of relaxation was observed in human bronchi (n = 7). L-NAME inhibited the NANCi response in both guinea pig tracheae and human bronchi: in guinea pig tracheae, maximal inhibition of the alpha-CT-insensitive relaxation was 59.3 +/- 11.5% (SE, P = 0.003) at low frequencies (4-16 Hz) and 28.6 +/- 8.9% (P = 0.08) at 32 Hz; in human bronchi, the maximal inhibition was 37.7 +/- 9.3% (P = 0.008) at 8 or 16 Hz, and 37.9 +/- 5.9% (P = 0.005) at 32 Hz. Inhibition was greater after repeated baseline EFS for 90 min before initiation of contraction with MCh and addition of L-NAME (59.8 +/- 13.9% after repeated baseline EFS, n = 4; vs. 34.9 +/- 6.2% without repeated baseline EFS, n = 9, P = 0.025). Relaxant responses to sodium nitroprusside, vasoactive intestinal peptide, and isoproterenol were not affected by L-NAME. L-Arginine (10 mM), a precursor of NO, partially reversed the effect of L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitric Oxide is Involved in the Inhibitory Neurotransmission and Endothelium-Dependent Relaxations of Human Small Penile Arteries

1997 ◽  
Vol 92 (3) ◽  
pp. 269-275 ◽  
Author(s):  
ULF Simonsen ◽  
Dolores Prieto ◽  
Jose Angel Delgado ◽  
Medardo Hernández ◽  
Luis Resel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Corpus Cavernosum ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field ◽  
Small Arteries ◽  
Inhibitory Neurotransmission ◽  
Oxide Synthase ◽  
Penile Arteries

1. Alteration in the flow of blood to the penis is thought to be the most frequent organic cause of erectile dysfunction or impotence. However, information concerning the penile small arteries (helicine arteries) which control blood flow between the arterial systemic circulation and the cavernous sinusoids is scarce. Therefore, the purpose of the present study was to investigate the involvement of nitric oxide, which is considered to be the main neurotransmitter in corpus cavernosum, in both the non-adrenergic non-cholinergic inhibitory neurotransmission and the endothelium-dependent responses in human penile small arteries. 2. Penile small arteries (lumen diameter 200-700 μm), which were branches of the human deep penile arteries obtained either from patients undergoing penile surgery or from organ donors, were mounted in microvascular myographs for isometric tension recording and electrical field stimulation was performed in the presence of guanethidine and atropine to block adrenergic neurotranmission and muscarinic receptors, respectively. 3. In phenylephrine-contracted penile small arteries, electrical field stimulation (0.5–32 Hz) induced frequency-dependent relaxations of both endothelium-intact and -denuded preparations. The inhibitor of nitric oxide synthase, NG-nitro-l-arginine (3 × 10−5 mol/l), abolished the relaxations at the lowest frequencies, while slow-developing relaxations were still observed at high frequencies (16 and 32 Hz). The inhibitory effect of NG-nitro-l-arginine was reversed in the presence of l-arginine (3 × 10−3 mol/l). Tetrodotoxin totally abolished the relaxations to electrical field stimulation. In contracted small penile arteries in the presence of NG-nitro-l-arginine, the nitrovasodilator sodium nitroprusside induced potent relaxations. 4. The endothelium-dependent vasodilator acetylcholine induced relaxations of penile small arteries, which were only partially reduced in the presence of NG-nitro-l-arginine. In contrast, the relaxations to acetylcholine of trabecular corpus cavernosum preparations were almost abolished in the presence of NG-nitro-l-arginine. 5. The present study suggests that relaxations of human intracavernosal small penile arteries induced by non-adrenergic non-cholinergic nerve stimulation partially involve nitric oxide and also another inhibitory transmitter causing relaxations resistant to nitric oxide synthase blockade. In addition, endothelium-dependent relaxations in human small penile arteries are mediated by both nitric oxide and a factor resistant to NG-nitro-l-arginine.

Pharmacologic responses of the mouse urinary bladder

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 192-197 ◽  
Author(s):  
A. Canda ◽  
Christopher Chapple ◽  
Russ Chess-Williams
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Detrusor Muscle ◽  
Field Stimulation ◽  
Muscarinic Agonists ◽  
Electrical Field ◽  
M3 Receptor

AbstractThe aim of the study was to determine pathways involved in contraction and relaxation of the mouse urinary bladder. Mouse bladder strips were set up in gassed Krebs-bicarbonate solution and responses to various drugs and electrical field stimulation were obtained. Isoprenaline (b-receptor agonist) caused a 63% inhibition of carbachol precontracted detrusor (EC50=2nM). Carbachol caused contraction (EC50=0.3µM), responses were antagonised more potently by 4-DAMP (M3-antagonist) than methoctramine (M2-antagonist). Electrical field stimulation caused contraction, which was inhibited by atropine (60%) and less by guanethidine and α,β-methylene-ATP. The neurogenic responses were not potentiated by inhibition of nitric oxide synthase. Presence of an intact urothelium significantly depressed responses to carbachol (p=0.02) and addition of indomethacin and L-NNA to remove prostaglandin and nitric oxide production respectively did not prevent the inhibitory effect of the urothelium. In conclusion, b-receptor agonists cause relaxation and muscarinic agonists cause contraction via the M3-receptor. Acetylcholine is the main neurotransmitter causing contraction while nitric oxide has a minor role. The mouse and human urothelium are similar in releasing a factor that inhibits contraction of the detrusor muscle which is unidentified but is not nitric oxide or a prostaglandin. Therefore, the mouse may be used as a model to study the lower urinary tract.

Nitric oxide as modulator of cholinergic neurotransmission in gastric muscle of rabbits

1997 ◽  
Vol 273 (2) ◽  
pp. G456-G463 ◽  
Author(s):  
M. C. Baccari ◽  
C. Iacoviello ◽  
F. Calamai
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Substance P ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field ◽  
Prostaglandin F2 Alpha ◽  
Fast Relaxation ◽  
Gastric Muscle ◽  
Relaxant Response

The effects of the nitric oxide (NO) synthesis inhibitors, NG-nitro-L-arginine (L-NNA) and NG-nitro-L-arginine methyl ester (L-NAME), on the electrical field stimulation (EFS)-induced inhibitory responses were investigated. EFS caused, in strips contracted by means of substance P (SP), prostaglandin F2 alpha (PGF2 alpha), or carbachol (CCh), a fast relaxant response that, depending on stimulation frequency and strip tension, could be followed by a slower, sustained relaxation. The NO synthesis inhibitors blocked the EFS-induced fast relaxations and often reversed them into contractions; these effects were greatly counteracted in SP- or PGF2 alpha-treated strips by scopolamine or atropine. In CCh-precontracted strips, either L-NNA or L-NAME became progressively unable to block the EFS-induced fast relaxations as the CCh concentration was increased. The NO synthesis inhibitors greatly reduced the sustained relaxant responses elicited either by EFS or exogenous vasoactive intestinal polypeptide (VIP). The results indicate that the NO synthesis inhibitors abolish the neurally induced fast relaxation by interfering with the cholinergic excitatory pathway. The involvement of both VIP and NO in sustained relaxations is also suggested.

Nonadrenergic inhibitory nerves attenuate neurally mediated contraction in cat bronchi

1990 ◽  
Vol 69 (5) ◽  
pp. 1594-1598 ◽  
Author(s):  
T. Aikawa ◽  
K. Sekizawa ◽  
S. Itabashi ◽  
H. Sasaki ◽  
T. Takishima
Keyword(s):  
Contractile Response ◽  
Stimulus Frequency ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Inhibitory Effects ◽  
Electrical Field ◽  
Calcitonin Gene ◽  
Contraction And Relaxation ◽  
Biphasic Responses

Effects of nonadrenergic and noncholinergic (NANC) inhibitory nerves on cholinergic neurotransmission were examined in isolated bronchial segments from cats in the presence of propranolol (10(-6) M) and indomethacin (10(-6) M) by use of electrical field stimulation (EFS) techniques. EFS caused contraction alone in tissues at the baseline tension and biphasic responses (contraction and relaxation) in tissues precontracted with 5-hydroxytryptamine. Contraction was abolished by atropine (10(-6) M), and relaxation was abolished by tetrodotoxin (10(-6) M). At the baseline tension, EFS at frequencies greater than 10 Hz inhibited the subsequent (4 min later) contraction induced by EFS at 1-5 Hz. EFS-induced inhibition was stimulus frequency dependent and reached maximum at 20 Hz. However, EFS at 20 Hz did not inhibit the subsequent contractile response to acetylcholine (10(-7) to 10(-3) M). Exogenously applied vasoactive intestinal peptide mimicked EFS-induced inhibitory effects, but substance P and calcitonin gene-related peptide did not. The inhibitory effect of EFS at 20 Hz was not altered by pyrilamine, cimetidine, naloxone, methysergide, phentolamine, BW755C, AF-DX 116, or removal of epithelium. These results imply that the NANC transmitter acts via presynaptic cholinergic receptors.

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