I034 Serum levels of nitric oxide and urinary excretion of cGMP in amlodipine-treated hypertensive patients

1998 ◽  
Vol 11 (4) ◽  
pp. 176A
Author(s):  
F PUENTESARCINIEGAS
2021 ◽  
Vol 7 (1) ◽  
pp. 44-48
Author(s):  
Olatunbosun Arinola ◽  
Temiloluwa Olaiya ◽  
Victory Edem ◽  
Sheu Rahamon

Background: Asthma is associated with increased production of reactive oxygen and nitrogen species and an alteration in the levels of antioxidants activities in the lung and blood. The increased production of the superoxide anion radicals contributes to airway remodelling and disease severity. Physiologically, the effect of increased free radical generation is eliminated by corresponding activities of a network of antioxidants. Presently, there is the dearth of information on the steady-state concentrations of nitric oxide (NO) and uric acid (UA) in children with asthma. The serum and urinary levels of NO and UA in children with asthma were thus determined in this study. Methodology: Fifty children consisting of 25 children with asthma and 25 age-matched apparently healthy children without asthma were enrolled into this study. Serum and urinary levels of NO and UA were determined using standard methods. Results: Serum levels of NO and UA were significantly higher while the urinary levels of NO and UA were significantly lower in children with asthma compared with the controls. There was no significant correlation between the serum ad urinary levels of NO and UA in children with asthma. Also, gender differences were not observed in the serum and urinary levels of NO and UA in children with asthma. Conclusion: Children with asthma have elevated serum levels of NO and UA accompanied with suboptimal urinary excretion. Therefore, children with asthma might benefit from routine renal function assessment owing to damages that can result from systemic accumulation of UA with concomitant reduction in its urinary excretion.


Author(s):  
Yale B. M. ◽  
Yeldu M. H.

Background: Hypertension is recognized as most common cardiovascular disorder and a leading cause of morbidity and mortality worldwide. Endothelial dysfunction, which is associated with impaired nitric oxide is an important risk factor for both hypertension and cardiovascular diseases. There is abnormal lipid peroxidation which suggested that oxidative stress is important in the pathogenesis of hypertension.  This study assessed serum levels of nitric oxide and malondialdehyde in hypertensive population in Sokoto-Nigeria.Methods: A total of 474 subjects who are within the age range of 25 to 76 years, including 316 hypertensive patients and 158 age- and sex- matched normotensive subjects were included in this study. Clinical and anthropometric parameters, nitric oxide and malondialdehyde were measured using standard techniques.Results: The result indicated that, mean systolic blood pressure (SBP) was significantly (p˂0.001) higher in hypertensive patients (166.00±1.39mmHg) than controls (124.97±0.95 mmHg) similarly the mean BMI was significantly (p˂0.001) higher in hypertensive patients (27.13±0.31 Kg/m2) than controls (23.54±0.12Kg/m2). Mean serum malondialdehyde (MDA) was significantly (p˂0.001) higher in hypertensive patients (3.62±0.07µmol/L) as compared to controls (1.97±0.03µmol/L), while serum nitric oxide (NO) was significantly (p=0.009) lower among hypertensive patients (7.12±0.14µmol/L) than controls (15.26±0.15µmol/L).Conclusions: Hypertension is a complex disorder that is strongly associated with other risk factors for cardiovascular disease. The aetiology of the association between impaired NO bioactivity, increase MDA and hypertension has not been fully elucidated. Further clarification of the role of impaired NO bioactivity and increased MDA level in hypertension could have important implications for the management of hypertension.


2008 ◽  
Vol 54 (2) ◽  
pp. 292-300 ◽  
Author(s):  
Renke Maas ◽  
Edzard Schwedhelm ◽  
Lydia Kahl ◽  
Huige Li ◽  
Ralf Benndorf ◽  
...  

Abstract Background: Endothelial function is impaired in hypercholesterolemia and atherosclerosis. Based on mostly indirect evidence, this impairment is attributed to reduced synthesis or impaired biological activity of endothelium-derived nitric oxide (NO). It was the aim of this study to directly estimate and compare whole-body NO production in normo- and hypercholesterolemia by applying a nonradioactive stable isotope dilution technique in vivo. Methods: We enrolled 12 normocholesterolemic and 24 hypercholesterolemic volunteers who were all clinically healthy. To assess whole-body NO synthesis, we intravenously administered l-[guanidino-(15N2)]-arginine and determined the urinary excretion of 15N-labeled nitrate, the specific end product of NO oxidation in humans, by use of gas chromatography-mass spectrometry. In addition, we measured flow-mediated vasodilation (FMD) of the brachial artery, expression of endothelial NOS (eNOS) in platelets, plasma concentration of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), and urinary excretion of 8-isoprostaglandin F2α (8-iso-PGF2α). Results: After infusion of l-[guanidino-(15N2)]-arginine, cumulative excretion of 15N-labeled-nitrate during 48 h was 40% [95% CI 15%–66%] lower in hypercholesterolemic than normocholesterolemic volunteers [mean 9.2 (SE 0.8) μmol vs 15.4 (2.3) μmol/l, P = 0.003]. FMD was on average 36% [4%–67%] lower in hypercholesterolemic than normocholesterolemic volunteers [6.3 (4.0)% vs 9.4 (4.6)%, P = 0.027]. Normalized expression of NOS protein in platelets was also significantly lower in hypercholesterolemic volunteers, whereas there were no significant differences in plasma ADMA concentration or urinary excretion of 8-iso-PGF2α between the 2 groups. Conclusions: This study provides direct evidence for a decreased whole body NO synthesis rate in healthy people with hypercholesterolemia.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masato Tsutsui ◽  
Yasuko Yatera ◽  
Hiroaki Shimokawa ◽  
Sei Nakata ◽  
Kiyoko Shibata ◽  
...  

We have recently developed mice lacking all three nitric oxide synthase (NOS) isoforms: nNOS, iNOS, and eNOS ( PNAS 2005). In this study, we examined the effects of a high-cholesterol (HC) diet on lipid metabolism and vascular lesion formation in those mice. Experiments were performed in 2-month-old male wild-type (WT) and singly, doubly, and triply NOS −/− mice (n=6–9). They were maintained on either a regular diet or a HC diet for 3 months. The HC feeding significantly increased plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) in all the genotypes studied as compared on the regular diet (all P <0.05). These serum levels of TC and LDL on the HC diet (mg/dl) were both significantly higher in all the singly, doubly, and triply NOS −/− genotypes as compared with the WT genotype (singly nNOS −/− [371±61 and 205±65], iNOS −/− [559±62 and 350±62], eNOS −/− [619±22 and 395±25], doubly n/iNOS −/− [518±77 and 328±72], n/eNOS −/− [635±56 and 458.8±42], e/iNOS −/− [480±38 and 260±40], triply n/i/eNOS −/− [2316±704 and 1588±715], and WT [326±43 and 244±54]) (all P <0.05). Notably, the extent of the dyslipidemia was by far severest in the triply n/i/eNOS −/− genotype among the NOS −/− genotypes, and intriguingly, the serum levels of TC and LDL in the triply n/i/eNOS −/− genotype were equivalent to those in apolipoprotein E −/− mice that exhibit severe hypercholesterolemia. Lipid accumulation in the aorta on the HC diet (lipid area, %, oil red O staining) was also significantly more accelerated in all the NOS −/− genotypes than in the WT genotype (singly nNOS −/− [6.6±1.5], iNOS −/− [6.7±2.2], eNOS −/− [5.5±2.3], doubly n/iNOS −/− [4.7±1.7], n/eNOS −/− [6.4±1.4], i/eNOS −/− [6.8±1.3], triply n/i/eNOS −/− [20.6±1.0], and WT [3.6±1.2]), while the extent of the aortic atherosclerosis was again by far severest in the triply n/i/eNOS −/− genotype (all P <0.05). These results demonstrate that mice deficient in all NOSs manifest severe hypercholesterolemia and lipid-rich atherosclerotic lesion formation in response to a HC diet, indicating a pivotal role of the whole NOS system in preventing those disorders. Our triply NOS −/− mouse is a new experimental model of human hypercholesterolemia and atherosclerosis.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Dongsheng Gu ◽  
Gaoke Feng ◽  
Guanyang Kang ◽  
Xiaoxin Zheng ◽  
Yuying Bi ◽  
...  

Using poly-L-lactic acid for implantable biodegradable scaffold has potential biocompatibility issue due to its acidic degradation byproducts. We have previously reported that the addition of amorphous calcium phosphate improved poly-L-lactic acid coating biocompatibility. In the present study, poly-L-lactic acid and poly-L-lactic acid/amorphous calcium phosphate scaffolds were implanted in pig coronary arteries for 28 days. At the follow-up angiographic evaluation, no case of stent thrombosis was observed, and the arteries that were stented with the copolymer scaffold had significantly less inflammation and nuclear factor-κB expression and a greater degree of reendothelialization. The serum levels of vascular endothelial growth factor and nitric oxide, as well the expression of endothelial nitric oxide synthase and platelet-endothelial cell adhesion molecule-1, were also significantly higher. In conclusion, the addition of amorphous calcium phosphate to biodegradable poly-L-lactic acid scaffold minimizes the inflammatory response, promotes the growth of endothelial cells, and accelerates the reendothelialization of the stented coronary arteries.


2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Yu-Chi Chang ◽  
Bang-Gee Hsu ◽  
Hung-Hsiang Liou ◽  
Chung-Jen Lee ◽  
Ji-Hung Wang

2021 ◽  
Author(s):  
Osman Baştuğ ◽  
Bahadır İnan ◽  
Ahmet Özdemir ◽  
Binnaz Çelik ◽  
Funda Baştuğ ◽  
...  

Abstract Background: Hypocalcemia, hypomagnesemia, and hyperphosphatemia are common electrolyte disturbances in perinatal asphyxia(PA). Different reasons have been proposed for these electrolyte disturbances. This study investigated the effect of the urinary excretion of calcium(Ca), magnesium(Mg), and phosphorus(P) on the serum levels of these substances in babies who were treated using therapeutic hypothermia for hypoxic ischemic encephalopathy(HİE) caused by PA. This study sheds light on the pathophysiology that may cause changes in the serum values of these electrolytes.Method: This study included 21 healthy newborns(control group) and 38 patients(HİE group) who had undergone therapeutic hypothermia due to HİE. Only infants with a gestational age of 36 weeks and above and a birth weight of 2000 g and above were evaluated. The urine and serum Ca, Mg, P, and creatinine levels of all infants were evaluated at 24, 48, and 72 hours.Results: The lower serum Ca value and the higher serum P value of the HİE group were found to be statistically significant compared to the control group. There was no significant difference in serum Mg values between the groups. However, hypomagnesemia was detected in five patients from the HİE group. The urine excretions of these substances, which were checked at different times, were found to be significantly higher in the HİE group compared to the control group.Conclusion: This study determined that the urinary excretion of Ca, Mg, and P has an effect on the serum Ca, Mg, and P levels of infants with HİE.


1997 ◽  
Vol 8 (9) ◽  
pp. 1437-1442
Author(s):  
B Anderstam ◽  
K Katzarski ◽  
J Bergström

Nitric oxide (NO) is involved in blood pressure regulation, and its synthesis is inhibited by methylarginines. It has been hypothesized that one of these, asymmetrical dimethylarginine (ADMA), may contribute to dialysis-associated hypertension because it accumulates in the plasma of hemodialysis (HD) patients in a concentration high enough (4 mumol/L) to inhibit NO synthesis in experimental model systems. A precolumn HPLC technique was used to quantify methylarginines (ADMA and symmetrical dimethylarginine [SDMA]) in plasma from HD patients before and after dialysis, from continuous ambulatory peritoneal dialysis (CAPD) patients, and from healthy subjects. Plasma ADMA concentrations were 0.59 +/- 0.22 (SD) mumol/L in HD patients predialysis (n = 19) and 0.70 +/- 0.27 mumol/L in CAPD patients (n = 11), versus about half of the concentration in control subjects (0.36 +/- 0.08 mumol/L, n = 7). The concentrations of SDMA (not an inhibitor of NO formation) were approximately four to five times the ADMA concentrations in both HD and CAPD patients, in contrast to a ratio of 1:1 in the control subjects. Methylarginine concentrations were reduced by 23% and 40% postdialysis, as calculated from ADMA and SDMA values, respectively. No significant correlations were observed between ADMA concentrations, on the one had, and blood pressure, creatinine and dialysis dose (Kt/V urea), on the other hand. It is concluded that plasma levels of ADMA are considerably lower than those reported earlier in patients treated with HD and also below the levels that hitherto have been thought to have clinical relevance. The role of ADMA in inhibiting NO in dialysis-associated hypertension is questioned.


2011 ◽  
Vol 10 (1) ◽  
pp. 39 ◽  
Author(s):  
Asaf A Qureshi ◽  
Julia C Reis ◽  
Nilofer Qureshi ◽  
Christopher J Papasian ◽  
David C Morrison ◽  
...  

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