scholarly journals The Inhibition of Ureteral Motility by Periureteral Adipose Tissue

ISRN Urology ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-7
Author(s):  
Lyndsey M. Killian ◽  
Stuart J. Bund
Keyword(s):  
Nitric Oxide ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase Inhibitor ◽  
Perivascular Adipose Tissue ◽  
Contractile Responses ◽  
Tissue Removal ◽  
Male Wistar Rats ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Perivascular adipose tissue exerts an anticontractile influence on vascular smooth muscle. This study was conducted to determine whether periureteral adipose tissue (PUAT) could exert a similar influence upon ureteral smooth muscle. Acetylcholine-stimulated (10−7 M–10−4 M) contractile responses of ureteral segments obtained from male Wistar rats were recorded in the presence and absence of PUAT. Ureters with PUAT generated phasic contractile responses with significantly lower frequencies () and magnitudes () compared with ureters cleared of their periureteral adipose tissue. Removal of PUAT significantly increased the frequency () and magnitude () of the contractile responses. Bioassay experiments demonstrated that ureters with PUAT released a transferable factor that significantly reduced frequencies (), but not magnitudes, of the contractile responses of ureters cleared of PUAT. The nitric oxide synthase inhibitor L-NNA (10−4 M) did not significantly influence the anticontractile effect exerted by ureters with PUAT. This is the first study to demonstrate that ureteral motility is influenced by its surrounding adipose tissue. The PUAT has an anticontractile effect which is mediated by a transferable factor released from the PUAT. The identity of the factor is unknown but does not exert its effect through nitric oxide.

scholarly journals Tetramethoxystilbene-Loaded Liposomes Restore Reactive-Oxygen-Species-Mediated Attenuation of Dilator Responses in Rat Aortic Vessels Ex vivo

Molecules ◽  
2019 ◽  
Vol 24 (23) ◽  
pp. 4360 ◽  
Author(s):  
Azziza Zaabalawi ◽  
Cai Astley ◽  
Lewis Renshall ◽  
Frances Beards ◽  
Adam P. Lightfoot ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Ex Vivo ◽  
Antioxidant Properties ◽  
Young Male ◽  
Oxidase Inhibitor ◽  
Nitric Oxide Synthase Inhibitor ◽  
Male Wistar Rats ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The methylated analogue of the polyphenol resveratrol (RV), 2,3′,4,5′-tetramethoxystilbene (TMS) displays potent antioxidant properties and is an effective cytochrome P450 (CYP) 1B1 inhibitor. The bioavailability of TMS is low. Therefore, the use of liposomes for the encapsulation of TMS is a promising delivery modality for enhanced uptake into tissues. We examined the effect of delivery of TMS in liposomes on the restoration of vasodilator responses of isolated aortic vessels after acute tension elevation ex vivo. Aortic vessels from young male Wistar rats were isolated, and endothelial-dependent (acetylcholine, ACh) and -independent (sodium nitroprusside, SNP) responses assessed. Acute tension elevation (1 h) significantly reduced ACh dilator responses, which were restored following incubation with superoxide dismutase or apocynin (an NADPH oxidase inhibitor). Incubation with TMS-loaded liposomes (mean diameter 157 ± 6 nm; PDI 0.097) significantly improved the attenuated dilator responses following tension elevation, which was sustained over a longer period (4 h) when compared to TMS solution. Endothelial denudation or co-incubation with L-NNA (Nω-nitro-l-arginine; nitric oxide synthase inhibitor) resulted in loss of dilator function. Our findings suggest that TMS-loaded liposomes can restore attenuated endothelial-dependent dilator responses induced by an oxidative environment by reducing NADPH-oxidase-derived ROS and potentiating the release of the vasodilator nitric oxide. TMS-loaded liposomes may be a promising therapeutic strategy to restore vasodilator function in vascular disease.

scholarly journals L-arginine, a nitric oxide precursor, reduces dapsone-induced methemoglobinemia in rats

2012 ◽  
Vol 48 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Natália Valadares de Moraes ◽  
Mateus Machado Bergamaschi ◽  
Maria de Lourdes Pires Bianchi ◽  
Juliana Bordinassi Bragheto ◽  
Wilson Roberto Malfará ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Multiple Dose ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitric Oxide Formation ◽  
Oxide Precursor ◽  
P450 Enzyme ◽  
Male Wistar Rats ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Dapsone use is frequently associated to hematological side effects such as methemoglobinemia and hemolytic anemia, which are related to N-hydroxylation mediated by the P450 enzyme system. The aim of the present study was to evaluate the influence of L-arginine supplementation, a precursor for the synthesis of nitric oxide, as single or multiple dose regimens on dapsone-induced methemoglobinemia. Male Wistar rats were treated with L-arginine at 5, 15, 30, 60 and 180 mg/kg doses (p.o., gavage) in single or multiple dose regimens 2 hours prior to dapsone administration (40 mg/kg, i.p.). The effect of the nitric oxide synthase inhibitor L-NAME was investigated by treatment with multiple doses of 30 mg/kg (p.o., gavage) 2 hours before dapsone administration. Blood samples were collected 2 hours after dapsone administration. Erythrocytic methemoglobin levels were assayed by spectrophotometry. The results showed that multiple dose supplementations with 5 and 15 mg/kg L-arginine reduced dapsone-induced methemoglobin levels. This effect is mediated by nitric oxide formation, since the reduction in methemoglobin levels by L-arginine is blocked by simultaneous administration with L-NAME, a nitric oxide synthase inhibitor.

Glomerular and tubular interactions between renal adrenergic activity and nitric oxide

1995 ◽  
Vol 268 (6) ◽  
pp. F1004-F1008 ◽  
Author(s):  
F. B. Gabbai ◽  
S. C. Thomson ◽  
O. Peterson ◽  
L. Wead ◽  
K. Malvey ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Glomerular Filtration ◽  
Renal Nerves ◽  
Ang Ii ◽  
Nitric Oxide Synthase Inhibitor ◽  
Adrenergic Activity ◽  
Single Nephron ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Endothelium-dependent nitric oxide (EDNO) exerts control over the processes of glomerular filtration and tubular reabsorption. The importance of the renal nerves to the tonic influence of EDNO in the glomerular microcirculation and proximal tubule was tested by renal micropuncture in euvolemic adult male Munich-Wistar rats. The physical determinants of glomerular filtration and proximal reabsorption were assessed before and during administration of the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA), in control animals and in animals 5–9 days after either ipsilateral surgical renal denervation (DNX) or after either sham surgery (SHX). L-NMMA caused single-nephron glomerular filtration rate to decline in control and SHX animals but not in DNX rats. L-NMMA caused a reduction in proximal reabsorption in control and SHX rats, which was prevented by prior DNX. DNX did not alter urinary guanosine 3',5'-cyclic monophosphate excretion, and, although DNX upregulates glomerular angiotensin II (ANG II) receptors, prior DNX did not alter intrarenal ANG II content as evaluated by radioimmunoassay. Some component of renal adrenergic activity is required for the full expression of the glomerular and tubular effects of blockade of nitric oxide synthase.

Effects of Early Neuronal and Delayed Inducible Nitric Oxide Synthase Blockade on Cardiovascular, Renal, and Hepatic Function in Ovine Sepsis

2010 ◽  
Vol 113 (6) ◽  
pp. 1376-1384 ◽  
Author(s):  
Matthias Lange ◽  
Atsumori Hamahata ◽  
Daniel L. Traber ◽  
Yoshimitsu Nakano ◽  
Aimalohi Esechie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitrite Nitrate ◽  
Synthase Inhibitor ◽  
Plasma Nitrite ◽  
Oxide Synthase ◽  
Organ Dysfunctions ◽  
Inducible Nitric Oxide

Background Recent evidence suggests that nitric oxide produced via the neuronal nitric oxide synthase is involved mainly in the early response to sepsis, whereas nitric oxide derived from the inducible nitric oxide synthase is responsible during the later phase. We hypothesized that early neuronal and delayed inducible nitric oxide synthase blockade attenuates multiple organ dysfunctions during sepsis. Methods Sheep were randomly allocated to sham-injured, nontreated animals (n = 6); injured (48 breaths of cotton smoke and instillation of Pseudomonas aeruginosa into the lungs), nontreated animals (n = 7); and injured animals treated with a neuronal nitric oxide synthase inhibitor from 1 to 12 h and an inducible nitric oxide synthase inhibitor from 12 to 24 h postinjury (n = 6). Results The injury induced arterial hypotension, vascular leakage, myocardial depression, and signs of renal and hepatic dysfunctions. The treatment significantly attenuated, but did not fully prevent, the decreases in mean arterial pressure and left ventricular stroke work index. Although the elevation of creatinine levels was partially prevented, the decreases in urine output and creatinine clearance were not affected. The injury-related increases in bilirubin levels, international normalized ratio, and lipid peroxidation in liver tissue were significantly attenuated. Although plasma nitrite/nitrate levels were significantly increased versus baseline from 12-24 h in controls, plasma nitrite/nitrate levels were not increased in treated animals. Conclusions The combination treatment shows potential benefit on sepsis-related arterial hypotension and surrogate parameters of organ dysfunctions in sheep. It may be crucial to identify the time course of expression and activation of different nitric oxide synthase isoforms in future investigations.

Myogenic reactivity is reduced in small renal arteries isolated from relaxin-treated rats

2002 ◽  
Vol 283 (2) ◽  
pp. R349-R355 ◽  
Author(s):  
Jacqueline Novak ◽  
Rolando J. J. Ramirez ◽  
Robin E. Gandley ◽  
O. David Sherwood ◽  
Kirk P. Conrad
Keyword(s):  
Nitric Oxide ◽  
Virgin Female ◽  
Renal Arteries ◽  
Mesenteric Arteries ◽  
Blood Levels ◽  
Renal Circulation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Myogenic Responses ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Administration of the ovarian hormone relaxin to nonpregnant rats vasodilates the renal circulation comparable to pregnancy. This vasodilation is mediated by endothelin (ET), the ETB receptor, and nitric oxide. Furthermore, endogenous relaxin mediates the renal vasodilation and hyperfiltration that occur during gestation. The goal of this study was to investigate whether myogenic reactivity of small renal and mesenteric arteries is reduced in relaxin-treated rats comparable to the pregnant condition. Relaxin or vehicle was administered to virgin female Long-Evans rats for 5 days at 4 μg/h, thereby producing midgestational blood levels of the hormone. The myogenic responses of small renal arteries (200–300 μm in diameter) isolated from these animals were evaluated in an isobaric arteriograph system. Myogenic reactivity was significantly reduced in the small renal arteries from relaxin-treated compared with vehicle-treated rats. The reduced myogenic responses were mediated by the ETB receptor and nitric oxide since the selective ETB receptor antagonist RES-701–1 and the nitric oxide synthase inhibitor N G-nitro-l-arginine methyl ester restored myogenic reactivity to virgin levels. The influence of relaxin was not limited to the renal circulation because myogenic reactivity was also reduced in small mesenteric arteries isolated from relaxin-treated rats. Thus relaxin administration to nonpregnant rats mimics pregnancy, insofar as myogenic reactivity of small renal and mesenteric arteries is reduced in both conditions.

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