Arginase, nitrates, and nitrites in the blood plasma and erythrocytes in hypertension and after therapy with lisinopril and simvastatin

Kaminskii, Yu. G.; Suslikov, A. V.; Tikhonova, Lyudmila A.; Galimova, M. Kh.; Ermakov, G. L.; Tsvetkov, V. D.; Kosenko, Elena

doi:10.1134/s1062359011050074

Cited by 7 publications

(7 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Various studies have demonstrated increase in arginase activity in different clinical conditions, such as hypertension [ 13 , 14 ], type 2 diabetes mellitus [ 15 , 16 ], hypercholesterolemia [ 17 ], aging [ 18 – 20 ], and atherosclerosis [ 21 ], proposing a critical contribution of this enzyme in the pathogenesis of cardiovascular diseases. In this direction, the present review focuses on the role of arginase in atherosclerosis and its implications in endothelial function, aiming to contribute to the pathophysiological discussion of the main regulatory mechanisms of the enzyme.…”

Section: Introductionmentioning

confidence: 99%

Arginase as a Critical Prooxidant Mediator in the Binomial Endothelial Dysfunction-Atherosclerosis

Rabelo

Ferreira

Nunes-Souza

et al. 2015

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Arginase is a metalloenzyme which hydrolyzes L-arginine to L-ornithine and urea. Since its discovery, in the early 1900s, this enzyme has gained increasing attention, as literature reports have progressively pointed to its critical participation in regulating nitric oxide bioavailability. Indeed, accumulating evidence in the following years would picture arginase as a key player in vascular health. Recent studies have highlighted the arginase regulatory role in the progression of atherosclerosis, the latter an essentially prooxidant state. Apart from the fact that arginase has been proven to impair different metabolic pathways, and also as a consequence of this, the repercussions of the actions of such enzyme go further than first thought. In fact, such metalloenzyme exhibits direct implications in multiple cardiometabolic diseases, among which are hypertension, type 2 diabetes, and hypercholesterolemia. Considering the epidemiological repercussions of these clinical conditions, arginase is currently seen under the spotlights of the search for developing specific inhibitors, in order to mitigate its deleterious effects. That said, the present review focuses on the role of arginase in endothelial function and its participation in the establishment of atherosclerotic lesions, discussing the main regulatory mechanisms of the enzyme, also highlighting the potential development of pharmacological strategies in related cardiovascular diseases.

show abstract

Section: Introductionmentioning

confidence: 99%

Arginase as a Critical Prooxidant Mediator in the Binomial Endothelial Dysfunction-Atherosclerosis

Rabelo

Ferreira

Nunes-Souza

et al. 2015

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…18 Kaminskii et al found that hypertensive patients received lisinopril were associated with significant increase in nitrate level. 19 Similarly, Kosenko et al investigated the effect of lisinopril on nitrate level among 29 hypertensive patients in Finland who visited health centers. Of note, NO is a highly unstable free radical and is oxidized rapidly to nitrate in circulating blood.…”

mentioning

confidence: 99%

Relationship of lisinopril with kallikrein-kinin system in hypertensive patients in Erbil city, Iraq

Hamad¹,

Ibrahim

2018

ZJMS

View full text Add to dashboard Cite

in the pathogenesis of hypertension through interaction with the elements of the renin-angiotensin system. This study aimed to examine the effects of lisinopril on mean arterial pressure and biosubstances of Kallikrein-kinin-system (bradykinin), endothelial dysfunction (nitric oxide), and oxidative stress (malondialdehyde). Methods: A clinical trial was conducted in Erbil city from December 1 st , 2015 to August 10 th , 2016. The study included 65 patients with essential hypertension and 25 apparently healthy subjects; their ages were in between 18 and 55 years. The patients were receiving 10 mg lisinopril orally per day for six weeks as a starting dose. Results: At hypertension diagnosis, patients were with lower bradykinin and nitric oxide levels when compared with apparently healthy subjects; however, malondialdehyde level showed no significant difference when compared with of healthy subjects. After six weeks patients treatment, comparing bradykinin, nitric oxide, and malondialdehyde mean levels with their baselines, showed that significantly increased in bradykinin and nitric oxide (P <0.01) and significantly decreased in malondialdehyde (P <0.01). On the other hand, the differences between after treatment and healthy subjects had no significant difference, except bradykinin. Eventually, during treatment, the mean arterial pressure was significantly lowered. Conclusion: in addition to the significant lowering of blood pressure, lisinopril 10 mg daily for six weeks can significantly elevate kallikrein-kinin system and endothelial dysfunction markers, and significantly lowered in oxidative stress marker in hypertensive Kurd patients in Erbil city.

show abstract

“…Thus, a key element of the pathogenesis of ED is the deficit of endogenous NO. Normally functioning endothelium continuously produces NO via endothelial NO synthase (eNOS) from L-arginine [5,6,7,8,9].…”

mentioning

confidence: 99%

“…However, along with deficit of NO production, a decrease in its bioaccessibility has a significant importance in the pathogenesis of ED, which may be due to increase level in plasma asymmetric dimethylarginine (ADMA), an endogenous competitive еNOS inhibitor. Another mechanism of NO reduction is associated with increased production of oxygen free radicals [4, 9,10].…”

mentioning

confidence: 99%

See 1 more Smart Citation

Cardiovascular Effects of an Arginase Ii Selective Inhibitor

Yakushev¹,

Покровский²

2016

RR.P and CP

View full text Add to dashboard Cite

For the first time in vitro experiments there were studied the inhibitory activity and safety of potential molecules arginase II selective inhibitors from the group of norleucine derivatives. Also first the substance under the code ZB49-0010C from the group of norleucine derivatives showed the greatest selectivity and inhibitory activity against arginase II in experiments in vitro. However, this substance in vivo exerts dose-dependent hypotensive action and cardioprotective and endothelial protective effects on the L-NAME induced and homocysteine-induced endothelial dysfunction (ED), which are most pronounced at a dose of 10 mg/kg in intragastric administration. Endothelial protective effect consists of in preventing the increase of coefficient of endothelial dysfunction (CED) and the decrease in the concentration of stable metabolites of nitric oxide in the blood plasma. Cardioprotective effect consists of in preventing the increase of the level of left ventricular pressure during the test for adrenoreactivity and reducing of the cardiac reserve during the overload resistance test, and also in preventing the development of the left ventricular hypertrophy. As part of the study there was investigated the dose-dependent anti-ischemic effect of the arginase II selective inhibitor, substance ZB49-0010C on the chronic limb ischemia in rats, which most pronounced at a dose of 10 mg/kg and consists of in preventing the fall in microcirculatory level on the 29th day of the experiment in the ischemic limb and a protective effect based on the morphological examination of the muscle tissue.

show abstract

Arginase, nitrates, and nitrites in the blood plasma and erythrocytes in hypertension and after therapy with lisinopril and simvastatin

Cited by 7 publications

References 29 publications

Arginase as a Critical Prooxidant Mediator in the Binomial Endothelial Dysfunction-Atherosclerosis

Arginase as a Critical Prooxidant Mediator in the Binomial Endothelial Dysfunction-Atherosclerosis

Relationship of lisinopril with kallikrein-kinin system in hypertensive patients in Erbil city, Iraq

Cardiovascular Effects of an Arginase Ii Selective Inhibitor

Contact Info

Product

Resources

About