AIMTo study the role of NO in the midbrain periaqueductal gray (PAG) in the development of stress-induced hypertension (SIH).

METHODSThe model of stress-induced hypertension (SIH) rat was established by electric-foot in company with noise, NADPH-d histochemistry technique was used to investigate the change of nitric oxide synthase (NOS) positive neurons. Selecting and using microinjection and radioimmunoassay, we studied the effects of blood pressure and the content of Ach in rostral ventrolateral medulla (RVLM) after microinjection of L-NNA into PAG.

RESULTS(1) The blood pressure increased, the cell number decreased and the grey degree value increased for the NOS positive neurons of PAG dorsolateral subdivision in SIH rats, and the content of Ach increased in RVLM. (2) Following microinjection of 100 mmol/L 0.1 microl L-NNA into PAG, the mean arterial pressure (MAP) and the content of Ach in RVLM increased in control rats, whereas the change of MAP was significantly smaller in SIH rats than control.

CONCLUSIONThe plastic change of NOS positive neurons of PAG in SIH rats may be involved in the development of SIH, which may be mediated by Ach in RVLM.

Animals ; Blood Pressure ; Hypertension ; etiology ; metabolism ; physiopathology ; Male ; Neurons ; metabolism ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Periaqueductal Gray ; metabolism ; Rats ; Rats, Wistar ; Stress, Psychological

AIMTo investigate the effect of taurine on nitric oxide synthase (NOS) activity and nitric oxide products (NO2 /NO3 ) content in myocardium and plasma during shock resuscitation.

METHODSTwenty-four rabbits were divided randomly into 3 groups (n=8): control group, shock group, taurine group. The model of hemorrhagic shock resuscitation was used. The activities of nitric oxide synthase (NOS), lactate dehydrogenase (LDH) and the contents of nitric oxide products (NO2- /NO3-) in plasma were observed before shock and shock 1.5 hours, after resuscitation 1 hour, 2 hours and 3 hours. The activities of NOS and the contents of NO2-/NO3- in myocardium homogenate were measured after resuscitation 3 hours. Meanwhile, pathologic samples treated routinely.

RESULTS(1) During resuscitation, the activities of NOS, LDH and the contents of NO2- /NO3- in plasma of shock group were significantly higher than that of before shock and shock 1.5 hours (P < 0.01). (2) After resuscitation 3 hours, the activity of NOS and the contents of NO2- / NO3 in myocardium of shock group were significantly higher than that of control group (P < 0.01). The cardiac myocyte appeared edema, fatty degeneration. (3) All the changes of above mentioned could be attenuated by intravenous injection taurine (40 mg/kg) (P < 0.01).

CONCLUSIONThese results suggest that the NOS activation and NO release may mediated myocardium injury induced by shock resuscitation, taurine can ameliorate the myocardium injury, which may be related to decreasing the generation of NO.

Animals ; Myocardium ; metabolism ; pathology ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Plasma ; metabolism ; Rabbits ; Resuscitation ; Shock, Hemorrhagic ; blood ; metabolism ; Taurine ; pharmacology

OBJECTIVETo study the changes of nitric oxide(NO) and nitric-oxide synthase(NOS) in the development of cold-induced hypertension (CIH).

METHODSSixty male Sprague-Dawley adult rats were used. Thirty were exposed to cold (4 +/- 1) degrees C as cold-treated group while the other 30 were at (25 +/- 1) degrees C as controls, 4 hours a day for 6 weeks for both groups. Systolic blood pressure (SBP) and heart rate were measured twice every week. Each group was further subdivided into three groups, 10 rats each. A subgroup of the cold-treated and control rats were sacrificed at 2, 4 and 6 week. Plasma was saved to measure superoxide dismutase (SOD) and malondiadehycle (MDA), while heart was homogenated to measure NO, NOS.

RESULTS1 SBP increased during 6 weeks of exposure to cold. From the second week, SBP of cold-treated group [(94.16 +/- 3.81) mm Hg] was significantly greater than that of control group [(88.77 +/- 4.45 mm Hg), P<0.01]. The highest SBP level was achieved at the sixth week [(116.78 +/- 3.79)mm Hg, P<0.01]. 2 Compared to the control group, SOD in cold-treated group decreased significantly from the second week, and maintained throughout the time of exposure to cold (P<0.05). MDA levels did not differ significantly between cold-treated and control groups though it increased mildly during 6 weeks of cold exposure (P>0.05). Heart NOS in cold-treated group decreased significantly from the fourth week to the sixth week. And a mild decrease was observed in heart NO of cold-treated group during 6 weeks of exposure (P>0.05).

CONCLUSIONCold-induced hypertension is induced in rats after repeated exposure to cold. The levels of NOS, NO decrease accordingly to the rise of blood pressure. This indicates that the dysfunction of NO and NOS is involved in the development of CIH.

Animals ; Cold Temperature ; adverse effects ; Disease Models, Animal ; Hypertension ; etiology ; metabolism ; Male ; Malondialdehyde ; blood ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood

OBJECTIVETo observe the effects of pravastatin on platelet-derived nitric oxide system in hypercholesterolemia (HC) and atherosclerosis (AS) in rabbits, and the relationship between these changes and atherosclerosis courses.

METHODSThirty male New Zealand white rabbits were randomly divided into three groups, 12 in group A, 12 in group B, and 6 in group C. All of them were fed daily with cholesterol-rich food during the first 12 weeks. In addition, in group A, pravastatin (10 mg) was orally administered daily. At the end of the 12th week, 6 in group A and B were killed randomly and their aortas were removed and the pathologic changes were observed. In the following 12 weeks, food enriched with cholesterol was substituted with normal food in all three groups. Pravastatin treatment was continued or started in the remaining members of group A and group B, but not in group C. At the end 24th week, all rabbits were killed and their aortas were examined for the fatty-streaks or atherosclerotic plaques. The expressions of endothelial NOS (eNOS) mRNA and inducible NOS (iNOS ) mRNA, NOS activity, NO production and the level of the serum lipids were measured at 0, 6th, 12th, 18th and 24th week.

RESULTSThe expression levels of platelet-derived NOS mRNA, eNOS mRNA ratio in group A had no difference at above time points, while in group B were reduced significantly at 6th week and 12th week compared with at 0 week (P <0.01), and increased at 18th week and 24th week compared with 12th week (P <0.05). The expression levels of eNOS mRNA in group C were reduced at 6th, 12th and 18th, 24th week compared with 0 week (P <0.05 and P <0.01, respectively), and were reduced in groups B and C compared with group A at 6th ,12th week (P < 0.05) and increased in group A and B compared with group C at 18th, 24th week (P <0.01). The expression levels of iNOS/mRNA among the three groups had no difference. Pathologic finding of the arteries: AS was not found in group A from the 12th to 24th week. While in group B, there were a lot of fatty-streaks on the entire intima of all large arteries at the 12th week. There were also fatty-streaks in the ascending aorta, but were improved at the 24th week. In group C, there were marked plaques in the entire aorta at the 24th week.

CONCLUSIONSThe expressions of platelet-derived eNOS mRNA, NOS activity, NO production are decreased in HC or AS rabbits. Pravastatin can up-regulate expressions of platelet-derived eNOS mRNA, NOS activity, leading to preventing or improving the pathological courses of AS.

Animals ; Atherosclerosis ; blood ; pathology ; Blood Platelets ; metabolism ; Disease Models, Animal ; Male ; Nitric Oxide ; blood ; genetics ; Nitric Oxide Synthase ; blood ; genetics ; Pravastatin ; pharmacology ; RNA, Messenger ; genetics ; Rabbits

OBJECTIVETo study the levels of nitric oxide synthase (NOS) and nitric oxide (NO) in patients with coronary heart disease (CHD), and the factors affecting them.

METHODSConcentrations of NO and the activities of NOS in plasma in 136 patients and 206 controls using the corresponding Kits were measured. The data were analyzed using covariance and multiple linear regression analysis with SAS 8.1.

RESULTSThe levels of NO [(217.05 +/- 153.31) micromol/L] and NOS [(14.09 +/- 7.14) U/ml] in patients were significantly higher than that in the healthy controls [(140.69 +/- 90.96) micromol/L, (7.75 +/- 3.79) U/ml, respectively, P < 0.01]. Smoking and drinking were the independent risk factors for NOS, while sex was the independent risk factor for NO (P < 0.01).

CONCLUSIONSThe levels of plasma NO and NOS are closely related with coronary heart disease.

Adult ; Aged ; Aged, 80 and over ; Case-Control Studies ; Coronary Disease ; blood ; Female ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; blood ; Plasma ; metabolism

Animals ; Female ; Liver ; blood supply ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; Sex Factors

This study was purposed to identify endothelial nitric oxide synthase (eNOS) mRNA in human RBCs during storage and to investigate the relationship of its changing profile and preservation time at 4°C. RT-PCR and gene sequencing were applied to identify eNOS-mRNA in banked RBC. Real time PCR was used to study the relationship of eNOS-mRNA expression and preservation time. The results showed that eNOS mRNA was detected in RBC. Compared with fresh RBC, the content of eNOS mRNA in RBC was 0.868 ± 0.119 stored for 1 week, which was 0.379 ± 0.289, 0.108 ± 0.134, 0.141 ± 0.141, 0.125 ± 0.12 stored for 2, 3, 4 and 5 weeks respectively. It is concluded that eNOS mRNA exists in human RBC and its content is decreasing gradually along with the prolongation of storage time in banked RBC. Stored for 3 weeks, the content of eNOS-mRNA remains to be at lower level of concentration in human RBC.
Blood Donors ; Blood Preservation ; Erythrocytes ; metabolism ; Humans ; Nitric Oxide Synthase Type III ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism

OBJECTIVETo observe the influence of aminoguanidine on cardiac troponin (cTnI) and nitric oxide (NO) levels in serum and myocardium in severely scalded rats.

METHODSSeventy-two Wistar rats were subjected to 30% TBSA full-thickness scald and randomly divided into scald group(S) and aminoguanidine group (A, with intraperitoneal injection of 40 mg/kg aminoguanidine before scald). The venous blood and myocardial tissue of the rats were harvested for the determination of the level of cTnI and nitrite in both serum and myocardium before scald and at 1, 3, 6, 12 and 24 post-burn hours(PBH). Six sham scalded rats served as control group. The changes in the cTnI level and myocardial function were determined among control group, A and S groups at 6PBH.

RESULTSThe serum level of NO in S group [(59.6 +/- 5.4) micromol/L] was obviously higher than that before scald [(24.6 +/- 0.8) micromol/L, P < 0.01], and it peaked at 6 PBH, then decreased obviously at 24 PBH, which was still markedly higher than that in A group (P < 0.01). The changes in NO level in myocardium were similar to the above tendency. Compared with S group, the level of cTnI was significantly increased in A group at each time-point. Compared with A group at 6 PBH, the inhibition of the cardiac function was relatively reduced in S group at 6 PBH.

CONCLUSIONInhibition of NO synthesis by aminoguanidine aggravates cardiac damage and impairment of cardiac function of scalded rats, indicating that NO exerts protective effect on myocardium at early stage after a scald injury.

Animals ; Burns ; metabolism ; Disease Models, Animal ; Myocardium ; metabolism ; Nitric Oxide ; blood ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Troponin T ; blood

Expression of endogenous ouabain in placenta and the concentrations of serum ET-1 and NO were examined in 30 patients with hypertensive disorder complicating pregnancy (HDCP) and 30 healthy pregnant women to investigate the effect of endogenous ouabain on HDCP. Compared with the healthy pregnant group, the expression of endogenous ouabain dramatically increased in the HDCP groups (P<0.01). There was a significantly positive correlation between the expression of endogenous ouabain with ET-1 (r=0.5567, P<0.01), while the correlation of endogenous ouabain and NO was significantly negative (r=-0.6895, P<0.01). As expected, the correlation between ET-1 and NO was negative (r=-0.7796, P<0.01). ET-1 concentrations of maternal and cord sera in HDCP groups were significantly higher in comparison with healthy pregnant group (P<0.01). On the contrast, NO concentrations were much lower in the maternal and cord sera of HDCP groups as compared with healthy pregnant group (P<0.01). Our data suggest that endogenous ouabain is directly involved in the nosogenesis of HDCP, with accompanying decreased NO and the elevated of ET-1.
Case-Control Studies ; Endothelin-1/*blood ; Hypertension, Pregnancy-Induced/*metabolism ; Nitric Oxide/*blood ; Ouabain/*metabolism ; Placenta/*metabolism

OBJECTIVETo study the effect of radiation injury on nitric oxide (NO) concentration in mouse peripheral blood and liver.

METHODSNIH mice were subjected to gamma-ray exposure at 9.0 Gy and transferred immediately in room temperature condition. NO concentrations in the liver and peripheral blood were examined before and at different time points after the exposure.

RESULTSCompared to that before exposure, NO concentration in the peripheral blood and liver significantly increased after gamma-ray exposure. NO concentration in the peripheral blood began to increase 3 h after the exposure, but that in the liver increased till 6 h after the exposure.

CONCLUSIONRadiation can cause the increase of NO concentration in the peripheral blood and liver, but different tissues may exhibit different response intensities to radiation.

Animals ; Gamma Rays ; Liver ; metabolism ; radiation effects ; Male ; Mice ; Nitric Oxide ; blood ; metabolism ; Radiation Injuries, Experimental ; blood ; metabolism ; Time Factors