OBJECTIVETo study the early change of serum nitric oxide (NO) after acute heat exposure with trauma and the effect of NO on mean arterial pressure (MAP), thus to provide theoretical basis for studying the mechanism of NO effect in acute stress.

METHODSThe rabbit model of acute heat exposure combined with trauma was established. The animals were divided into four groups, including control, trauma, hyperthermia and hyperthermia combined with trauma. The levels of NO were measured at different time points: 0 h, 1 h, 2 h and MAP was monitored throughout the whole experiment.

RESULTSThe concentration of NO declined at first and then increased at 1 h or so after acute heat exposure and trauma. The levels of NO in hyperthermia with trauma group at 1 h, 2 h were (42.75 +/- 8.24), (59.54 +/- 9.05) micro mol/L respectively (P < 0.05), while those in control group were (56.63 +/- 3.79) and (55.22 +/- 7.15) micro mol/L, the difference at 1h between two groups was significant (P < 0.05). Under the circumstance of hyperthermia and trauma, the level of MAP declined to the lowest point at 60 - 70 min and then showed a transient rise, after that, the level declined rapidly.

CONCLUSIONSAt the early stage of acute heat exposure and trauma, the concentration of serum NO declined at first and then increased, and had certain relationship with the change of MAP.

Animals ; Blood Pressure ; Cytokines ; biosynthesis ; Hot Temperature ; Male ; Nitric Oxide ; blood ; Rabbits ; Wounds and Injuries ; blood ; physiopathology

The present study was aimed at investigating whether an altered role of nitric oxide (NO) is involved in chronic renal failure (CRF). Rats were subjected to 5/6 nephrectomy and kept for 6 weeks to induce CRF. On the experimental day, after measurement of arterial pressure under anesthesia, the arterial blood was collected, and thoracic aorta and kidney were rapidly taken. NO metabolites (NOx) were determined in the plasma, urine, aorta and kidney. The expression of NO synthase (NOS) isozymes was determined in the kidney and aorta by Western blot analysis. The expression of NOS mRNA in the glomeruli was also determined by RT-PCR. There were significant increases in arterial pressure and serum creatinine levels in CRF. Urine NOx levels were decreased in CRF, whereas plasma NOx levels were not altered. Aorta and kidney tissue NOx levels were also decreased in CRF. The expression of endothelial constitutive (ec) and inducible (i) isoforms of NOS proteins was decreased in the kidney and aorta in CRF. Accordingly, the expression of ecNOS and iNOS mRNA was decreased in the glomeruli in CRF. In conclusion, NO synthesis is decreased in the kidney and vasculature of CRF rats.
Animal ; Aorta, Thoracic/metabolism ; Comparative Study ; Enzyme Induction ; Isoenzymes/metabolism+ACo- ; Isoenzymes/genetics ; Kidney/metabolism ; Kidney Failure, Chronic/metabolism+ACo- ; Male ; Nephrectomy ; Nitrates/urine ; Nitrates/blood ; Nitric Oxide/deficiency+ACo- ; Nitric Oxide/biosynthesis ; Nitric-Oxide Synthase/metabolism+ACo- ; Nitric-Oxide Synthase/genetics ; Nitrites/urine ; Nitrites/blood ; Organ Specificity ; RNA, Messenger/biosynthesis ; Rats ; Rats, Sprague-Dawley

The present study was aimed at investigating whether an altered role of nitric oxide (NO) is involved in chronic renal failure (CRF). Rats were subjected to 5/6 nephrectomy and kept for 6 weeks to induce CRF. On the experimental day, after measurement of arterial pressure under anesthesia, the arterial blood was collected, and thoracic aorta and kidney were rapidly taken. NO metabolites (NOx) were determined in the plasma, urine, aorta and kidney. The expression of NO synthase (NOS) isozymes was determined in the kidney and aorta by Western blot analysis. The expression of NOS mRNA in the glomeruli was also determined by RT-PCR. There were significant increases in arterial pressure and serum creatinine levels in CRF. Urine NOx levels were decreased in CRF, whereas plasma NOx levels were not altered. Aorta and kidney tissue NOx levels were also decreased in CRF. The expression of endothelial constitutive (ec) and inducible (i) isoforms of NOS proteins was decreased in the kidney and aorta in CRF. Accordingly, the expression of ecNOS and iNOS mRNA was decreased in the glomeruli in CRF. In conclusion, NO synthesis is decreased in the kidney and vasculature of CRF rats.
Animal ; Aorta, Thoracic/metabolism ; Comparative Study ; Enzyme Induction ; Isoenzymes/metabolism+ACo- ; Isoenzymes/genetics ; Kidney/metabolism ; Kidney Failure, Chronic/metabolism+ACo- ; Male ; Nephrectomy ; Nitrates/urine ; Nitrates/blood ; Nitric Oxide/deficiency+ACo- ; Nitric Oxide/biosynthesis ; Nitric-Oxide Synthase/metabolism+ACo- ; Nitric-Oxide Synthase/genetics ; Nitrites/urine ; Nitrites/blood ; Organ Specificity ; RNA, Messenger/biosynthesis ; Rats ; Rats, Sprague-Dawley

Heat shock protein 27 belongs to the heat shock protein family in the small molecular weight family. This review collected a number of literature to analyze the expression meaning and mechanism of HSP27,expounded HSP27 with inhibition of NO production, maintenance of cell protein stability and accelerated cell damage repair function. At the same time, HSP27 also has a resistance to apoptosis, protecting mitochondria, inhibiting activation of nuclear factor and other related functions. The heat shock protein 27 has protection in spinal cord ischemia-reperfusion.
Apoptosis ; HSP27 Heat-Shock Proteins ; physiology ; Humans ; Nitric Oxide ; biosynthesis ; Reperfusion Injury ; prevention & control ; Spinal Cord ; blood supply

Platelets, small pieces of cytoplasm with biological activity, split and fall off the megakaryocytes and mature from the bone marrow. After stimulated, platelets produce nitric oxide to inhibit their own activation and aggregation. Pathologically, the injury of endothelial cells activates platelets and changes their functions. The release of inflammatory mediators and cytokines induces and enhances the development and progression of atherosclerosis, and thereby promotes the occurrence of erectile dysfunction. Besides, platelets and their related functional parameters may serve as important indicators in the diagnosis and treatment of erectile dysfunction.
Atherosclerosis ; etiology ; Blood Platelets ; physiology ; Cytokines ; metabolism ; Endothelial Cells ; Erectile Dysfunction ; etiology ; Humans ; Male ; Nitric Oxide ; biosynthesis ; Platelet Activation

The role of nitric oxide (NO) in the ocular surface remains unknown. We investigated the conditions leading to an increase of NO generation in tear and the main sources of NO in ocular surface tissue. We evaluated the dual action (cell survival or cell death) of NO depending on its amount. We measured the concentration of nitrite plus nitrate in the tears of ocular surface diseases and examined the main source of nitric oxide synthase (NOS). When cultured human corneal fibroblast were treated with NO producing donor with or without serum, the viabilities of cells was studied. We found that the main sources of NO in ocular surface tissue were corneal epithelium, fibroblast, endothelium, and inflammatory cells. Three forms of NOS (eNOS, bNOS, and iNOS) were expressed in experimentally induced inflammation. In the fibroblast culture system, the NO donor (SNAP, S-nitroso-N-acetyl-D, L-penicillamine) prevented the death of corneal fibroblast cells caused by serum deprivation in a dose dependent manner up to 500 micrometer SNAP, but a higher dose decreased cell viability. This study suggested that NO might act as a doubleedged sword in ocular surface diseases depending on the degree of inflammation related with NO concentration.
Animals ; Apoptosis/drug effects/physiology ; Aqueous Humor/metabolism ; Blood Proteins/pharmacology ; Cell Survival/drug effects/physiology ; Cells, Cultured ; Epithelium, Corneal/*cytology/*enzymology ; Fibroblasts/cytology/enzymology ; Humans ; Nitric Oxide/biosynthesis/*physiology ; Nitric Oxide Donors/pharmacology ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Penicillamine/*analogs & derivatives/pharmacology ; Peroxynitrous Acid/biosynthesis ; Rabbits ; Tears/metabolism ; Uveitis/metabolism

OBJECTIVETo observe effect of porcine relaxin(pRLX) on NO production of human microvascular endothelial cells(HMVECs) and discuss its possible mechanism.

METHODSiNOS and cNOS expression of HMVECs with or without pRLX were detected using western blotting. NO production of HMVECs with pRLX at different concentration or different time were determined by method of Griess. NO production of pRLX of HMVECs plus Non-selective NOS inhibitor NG-monomethyl-L-arginine(L-NMMA), selective iNOS inhibitor aminoguanidine(AG) or nuclear factors-kappaB (NF-kappaB) inhibitor pyrrolidine dithiocarbamate(PDTC) were also analysed.

RESULTSpRLX promoted iNOS protein expression of HMVECs, but not cNOS protein expression. NO production of HMVECs was promoted by pRLX on concentration-dependent pattern instead of time-dependent one. AG, L-NMMA and PDTC were showed to block the effect of pRLX on NO production of HMVECs.

CONCLUSIONpRLX promote iNOS expression and NO production of HMVECs.

Animals ; Dose-Response Relationship, Drug ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Lung ; blood supply ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase Type II ; biosynthesis ; Relaxin ; pharmacology ; Swine ; Time Factors

The endothelial nitric oxide synthase (eNOS) gene plays an important role in several biological functions. Polymorphisms of the eNOS gene have been associated with cancer. It has been suggested that the VNTR 4 a/b polymorphism may affect the expression of eNOS and contributes to tumor promotion in the mammary gland. We examined the role of the eNOS4 a/b polymorphism by comparing the genotypes of 281 healthy Mexican women with the genotypes of 429 Mexican women with breast cancer (BC). The observed genotype frequencies for control and BC patients were 0.6% and 0.7% for a/a (polymorphic); 87% and 77% for a/a (wild type); and 12% and 22% for a/b respectively. We found that the odds ratio (OR) was 1.9, with a 95% confidence interval (95%CI) of 1.29-2.95, P = 0.001 for genotypes a/a-a/b, b/c. The association was also evident when comparing the distribution of the a/a-a/b genotypes in patients with high levels of glutamate-oxaloacetate transaminase (SGOT) (OR, 1.93; 95% CI, 1.14-3.28; P = 0.015); undergoing menopause with high levels of SGOT (OR, 2.0; 95% CI, 1.1-3.84); and with high levels of glutamic-pyruvic transaminase (SGPT) (OR, 3.5; 95% CI, 1.56-8.22). The genotypes a/a-a/b are associated with BC susceptibility in the analyzed samples from the Mexican population.
Adult ; Alanine Transaminase/*blood ; Aspartate Aminotransferases/*blood ; Breast Neoplasms/*blood/*genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Mexico ; Middle Aged ; Nitric Oxide/biosynthesis/metabolism ; Nitric Oxide Synthase Type III/*genetics ; Polymorphism, Single Nucleotide

OBJECTIVES: The present study was aimed at exploring whether the pathogenesis of hypertension is related with an altered expression of nitric oxide synthase (NOS) isozymes, i.e., bNOS, iNOS and ecNOS. METHOD: By Western blot analysis, the expression of NOS isozymes were determined in the kidney isolated from spontaneously hypertensive rats (SHR) and their normotensive control, Wistar-Kyoto rats (WKY). The NOx (nitrite/nitrate) contents were also determined in the kidney and plasma. RESULTS: The plasma NOx was significantly increased in SHR compared with that in WKY. The basal level of NOx was higher in the medulla and cortex of the kidney in SHR compared with that in WKY rat. bNOS proteins were expressed higher in the outer medulla and cortex, and iNOS proteins were higher in the inner medulla, outer medulla and cortex in SHR. ecNOS expression did not significantly differ between the SHR and WKY. CONCLUSIONS: These results indicate that the NO generation may not be impaired, but rather increased. It is likely that the increased expression of NOS isozymes is a counter-reactive phenomenon secondary to the increased blood pressure in this model of hypertension.
Animal ; Hypertension/physiopathology ; Hypertension/enzymology* ; Isoenzymes/metabolism ; Kidney/enzymology* ; Male ; Nitrates/metabolism ; Nitrates/blood ; Nitric Oxide/biosynthesis ; Nitric-Oxide Synthase/metabolism* ; Nitrites/metabolism ; Nitrites/blood ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY

To examine the role and effect of nitric oxide synthase type II (NOS II) in cirrhotic rats, expression of NOS II mRNA was detected by real time RT-PCR. The enzymatic activity of nitric oxide synthase and the circulating levels of NO, systemic and portal hemodynamics and quantification of cirrhosis were measured. Chinese traditional medicine was used to treat cirrhotic rats and the effect of NO was evaluated. Double-blind method was used in experiment. Our results showed the concentration of NO and the enzymatic activity of NOS increased markedly at all stages of cirrhosis and iNOSmRNA was strongly expressed. Meanwhile, the portal-venous-pressure (PVP) and portal-venous-flow (PVF) were significantly increased. NO, NOS and iNOSmRNA were positively correlated to the degree of hepatic fibrosis. Tetrandrine significantly inhibited NO production and the expression of iNOSmRNA. Our results suggested that increased hepatic expression of NOS II is one of the important factors causing cirrhosis and portal hypertension. Tetrandrine can significantly ameliorate cirrhosis and portal hypertension.
Alkaloids ; pharmacology ; therapeutic use ; Animals ; Benzylisoquinolines ; pharmacology ; therapeutic use ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Hypertension, Portal ; drug therapy ; metabolism ; Liver ; enzymology ; pathology ; Liver Cirrhosis, Experimental ; drug therapy ; metabolism ; Male ; Nitric Oxide ; antagonists & inhibitors ; blood ; Nitric Oxide Synthase ; biosynthesis ; genetics ; Nitric Oxide Synthase Type II ; RNA, Messenger ; biosynthesis ; genetics ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction