ALTERATIONS IN THE NITRIC OXIDE SYNTHASE BINDING SITES AND NON-ADRENERGIC, NON-CHOLINERGIC MEDIATED SMOOTH MUSCLE RELAXATION IN THE DIABETIC RABBIT BLADDER OUTLET: POSSIBLE RELEVANCE TO THE PATHOGENESIS OF DIABETIC CYSTOPATHY

1999 ◽  
Vol 162 (2) ◽  
pp. 558-566 ◽  
Author(s):  
F.H. MUMTAZ ◽  
M.E. SULLIVAN ◽  
C.S. THOMPSON ◽  
M.R. DASHWOOD ◽  
K.M. NASEEM ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Binding Sites ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Diabetic Cystopathy ◽  
Diabetic Rabbit ◽  
Rabbit Bladder ◽  
Oxide Synthase

Inducible and neuronal nitric oxide synthase involvement in lipopolysaccharide-induced sphincteric dysfunction

2001 ◽  
Vol 280 (1) ◽  
pp. G32-G42 ◽  
Author(s):  
Ya-Ping Fan ◽  
Sushanta Chakder ◽  
Feng Gao ◽  
Satish Rattan
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
No Production ◽  
Muscarinic Agonist ◽  
Basal Tone ◽  
Before And After ◽  
Oxide Synthase ◽  
Nanc Relaxation

We examined the effect of endotoxin lipopolysaccharide (LPS) on the basal tone and on the effects of different stimuli and agonists and transcriptional and translational expression of nitric oxide (NO) synthase (NOS) isozymes in the lower esophageal sphincter (LES), pyloric sphincter (PS), and internal anal sphincter (IAS). NO release was also examined before and after LPS. LPS caused a dose-dependent fall in the basal tone and augmentation of the relaxation caused by nonadrenergic, noncholinergic (NANC) nerve stimulation in the LES and IAS. In the PS, LPS had no significant effect on the basal tone and caused an attenuation of the NANC relaxation and an augmentation of the contractile response of muscarinic agonist. Interestingly, the smooth muscle relaxation by atrial natriuretic factor was suppressed in the LES and IAS but not in the PS. These changes in the sphincteric function following LPS may be associated with increase in the inducible NOS (iNOS) expression since they were blocked by iNOS inhibitorl-canavanine. Augmentation of NANC relaxation in the LES and IAS smooth muscle by LPS may be due to the increased activity of neuronal NOS and NO production.

Relaxin exerts two opposite effects on mechanical activity and nitric oxide synthase expression in the mouse colon

2012 ◽  
Vol 303 (9) ◽  
pp. E1142-E1150 ◽  
Author(s):  
M. C. Baccari ◽  
C. Traini ◽  
R. Garella ◽  
G. Cipriani ◽  
M. G. Vannucchi
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Muscle Tone ◽  
Muscle Relaxation ◽  
Proximal Colon ◽  
Mechanical Activity ◽  
Enos Expression ◽  
Oxide Synthase

The hormone relaxin exerts a variety of functions on the smooth muscle of reproductive and nonreproductive organs, most of which occur through a nitric oxide (NO)-mediated mechanism. In the stomach and ileum, relaxin causes muscle relaxation by modulating the activity and expression of different nitric oxide synthase (NOS) isoforms region-dependently. Nothing is known on the effects of relaxin in the colon, the gut region expressing the highest number of neuronal (n) NOSβ-immunoreactive neurons and mainly involved in motor symptoms of pregnancy and menstrual cycle. Therefore, we studied the effects of relaxin exposure in the mouse proximal colon in vitro evaluating muscle mechanical activity and NOS isoform expression. The functional experiments showed that relaxin decreases muscle tone and increases amplitude of spontaneous contractions; the immunohistochemical results showed that relaxin increases nNOSβ and endothelial (e) NOS expression in the neurons and decreases nNOSα and eNOS expression in the smooth muscle cells (SMC). We hypothesized that, in the colon, relaxin primarily increases the activity and expression of nNOSβ and eNOS in the neurons, causing a reduction of the muscle tone. The downregulation of nNOSα and eNOS expression in the SMC associated with increased muscle contractility could be the consequence of continuous exposue of these cells to the NO of neuronal origin. These findings may help to better understand the physiology of NO in the gastrointestinal tract and the role that the “relaxin-NO” system plays in motor disorders such as functional bowel disease.

SIN-1 reverses attenuation of hypercapnic cerebrovasodilation by nitric oxide synthase inhibitors

1994 ◽  
Vol 267 (1) ◽  
pp. R228-R235 ◽  
Author(s):  
C. Iadecola ◽  
F. Zhang ◽  
X. Xu
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Co2 Response ◽  
No Donor ◽  
No Donors ◽  
Doppler Probe ◽  
Nos Inhibitor ◽  
Oxide Synthase

We sought to determine whether the attenuation of the hypercapnic cerebrovasodilation associated with inhibition of nitric oxide synthase (NOS) can be reversed by exogenous NO. Rats were anesthetized (halothane) and ventilated. Neocortical cerebral blood flow (CBF) was monitored by a laser-Doppler probe. The NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg iv) reduced resting CBF [-36 +/- 5% (SE); P < 0.01, analysis of variance] and attenuated the increase in CBF elicited by hypercapnia (partial pressure of CO2 = 50-60 mmHg) by 66% (P < 0.01). L-NAME reduced forebrain NOS catalytic activity by 64 +/- 3% (n = 10; P < 0.001). After L-NAME, intracarotid infusion of the NO donor 3-morpholinosydnonimine (SIN-1; n = 6) increased resting CBF and reestablished the CBF increase elicited by hypercapnia (P > 0.05 from before L-NAME). Similarly, infusion of the guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo-cGMP (n = 6) reversed the L-NAME-induced attenuation of the hypercapnic cerebrovasodilation. The NO-independent vasodilator papaverine (n = 6) increased resting CBF but did not reverse the attenuation of the CO2 response. SIN-1 did not affect the attenuation of the CO2 response induced by indomethacin (n = 6). The observation that NO donors reverse the L-NAME-induced attenuation of the CO2 response suggests that a basal level of NO is required for the vasodilation to occur. The findings are consistent with the hypothesis that NO is not the final mediator of smooth muscle relaxation in hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitric oxide contributes to vascular smooth muscle relaxation in contracting fast-twitch muscles

2001 ◽  
Vol 5 (1) ◽  
pp. 35-44 ◽  
Author(s):  
ROBERT W. GRANGE ◽  
EIJI ISOTANI ◽  
KIM S. LAU ◽  
KRISTINE E. KAMM ◽  
PAUL L. HUANG ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Control Value ◽  
Skeletal Muscle Contraction ◽  
Fast Twitch ◽  
Oxide Synthase

During skeletal muscle contraction, NO derived from neuronal nitric oxide synthase (nNOS) in skeletal muscle fibers or from endothelial cells (eNOS) may relax vascular smooth muscle contributing to functional hyperemia. To examine the relative importance of these pathways, smooth muscle myosin regulatory light chain (smRLC) phosphorylation was assessed as an index of vascular tone in isolated extensor digitorum longus (EDL) muscles from C57, nNOS−/−, and eNOS−/− mice. The smRLC phosphorylation (in mol phosphate per mol smRLC) in C57 resting muscles (0.12 ± 0.04) was increased 3.7-fold (0.44 ± 0.03) by phenylephrine (PE). Reversal of this increase with electrical stimulation (to 0.19 ± 0.03; P < 0.05) was partially blocked by Nω-nitro-l-arginine (NLA). In nNOS−/− EDL, the PE-induced increase in smRLC phosphorylation (0.10 ± 0.02 to 0.49 ± 0.04) was partially decreased by stimulation (0.25 ± 0.04). In eNOS−/− EDL, the control value for smRLC was increased (0.24 ± 0.04), and PE-induced smRLC phosphorylation (0.36 ± 0.06) was decreased by stimulation even in the presence of NLA (to 0.20 ± 0.02; P < 0.05). These results suggest that in addition to NO-independent mechanisms, NO derived from both nNOS and eNOS plays a role in the integrative vascular response of contracting skeletal muscle.

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