Nitric oxide synthase responsible for <scp>l</scp>‐arginine‐induced relaxation of rat aortic rings <i>in vitro</i> may be an inducible type

Moritoki, Hideki; Takeuchi, Shougo; Hisayama, Tetsuhiro; Kondoh, Wataru

doi:10.1111/j.1476-5381.1992.tb12752.x

Cited by 29 publications

(16 citation statements)

References 42 publications

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“…This raises the prospects of the presence of more than one regulating mechanism. The significant reduction of intimal thickness and improvement of endothelial function observed with l-arginine treatment is in harmony with the report of Moritoki et al (31), who showed that l-arginine treatment causes relaxation of rat aortic rings.…”

Section: Aortic Intimal Thickness In Nitroglycerin-treated Rabbitsupporting

confidence: 78%

Investigating the Cardio-Protective Abilities of Supplemental L-Arginine on Parameters of Endothelial Function in a Hypercholesterolemic Animal Model

Maaty

El-Maraghy

Fahim

et al. 2014

J Nutr Sci Vitaminol

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Summary Endothelial dysfunction is now widely recognized as an early marker of cardiovascular disease, making its treatment, or complete avoidance, an emerging, interesting therapeutic target. This study investigated the ability of the highly intriguing amino acid l-arginine to influence endothelial function. Its therapeutic potential is also compared to that of known cardiovascular medications, namely nitroglycerin [a nitric oxide (NO) donor] and enalapril [an angiotensin-converting enzyme (ACE) inhibitor]. Fifty male New Zealand rabbits were included in the study, divided into 5 equal groups: control, hypercholesterolemia (untreated), hypercholesterolemia (1l-arginine), hypercholesterolemia (1enalapril), and hypercholesterolemia (1nitroglycerin). Biochemical investigations included measurement of circulating NOx, malondialdehyde (MDA), and lipid profile markers, as well as dimethylarginine dimethylaminohydrolase (DDAH) and ACE activities. Furthermore, aortic ACE activity and blood platelet aggregation were estimated. A histopathological examination and intimal thickness measurement were also conducted. Compared to the untreated hypercholesterolemic group, all agents were capable of positively influencing MDA levels, platelet aggregation and intimal thickness; however, only the l-arginine group was capable of beneficially and significantly altering both NOx levels and serum and aortic ACE activities. No agents were capable of modulating serum DDAH activity inhibited by hypercholesterolemia. Based on the results of this study, l-arginine appears to be a novel cardio-protective agent, illustrated by its ability to ameliorate the deleterious effects of hypercholesterolemia on endothelial function, in a manner comparable to, and sometimes more potent than, commonly used cardiovascular medications.

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Section: Aortic Intimal Thickness In Nitroglycerin-treated Rabbitsupporting

confidence: 78%

Investigating the Cardio-Protective Abilities of Supplemental L-Arginine on Parameters of Endothelial Function in a Hypercholesterolemic Animal Model

Maaty

El-Maraghy

Fahim

et al. 2014

J Nutr Sci Vitaminol

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“…Initial efforts to determine regional NO biosynthesis by determining tissue nitrite/nitrate and cGMP levels in slices of dissected renal zones, isolated glomeruli, and various cell cultures systems. These studies indicated that tissues of both the renal cortex and medulla were indeed capable of generating NO in abundant amounts (6,10,13,25,36,69,93,108).…”

Section: Localization Of No Production Within Vascular and Tubular Stmentioning

confidence: 97%

Role of renal NO production in the regulation of medullary blood flow

Cowley

Mori

Mattson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

176

202

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. Role of renal NO production in the regulation of medullary blood flow. Am J Physiol Regul Integr Comp Physiol 284: R1355-R1369, 2003 10.1152/ajpregu.00701.2002The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced production of NO within the renal medulla on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure is described. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormoneinduced reduction of medullary blood flow and tissue oxygen levels. When NO synthase (NOS) activity is reduced within the renal medulla, either pharmacologically or genetically [Dahl salt-sensitive (S) rats], a super sensitivity to vasoconstrictors develops with ensuing hypertension. Reduced NO production may also result from reduced cellular uptake of L-arginine in the medullary tissue, resulting in hypertension. It is concluded that NO production in the renal medulla plays a very important role in sodium and water homeostasis and the long-term control of arterial pressure. renal medulla; Dahl salt-sensitive rats; hypertension; L-arginine THE RENAL MEDULLARY CIRCULATION is now recognized to be of importance for reasons that extend far beyond providing the economy of countercurrent exchange to concentrate large volumes of filtrate to produce small volumes of concentrated urine. It is now recognized that medullary blood flow (MBF) can play an important role in determining long-term levels of arterial pressure and that 15-30% reductions of blood flow to the renal medulla in the face of imperceptibly small changes of total renal blood flow can lead to the development of hypertension (16,21). Evidence is reviewed showing that nitric oxide (NO) plays a unique role in the acute and chronic regulation of renal MBF, sodium homeostasis, and arterial pressure. More specifically, the role of NO in the regulation of MBF, in linking tubular metabolic needs with delivery of nutrients and as a counterregulatory system to protect the medulla from the consequences of underperfusion, are the focus of this review. The influence of NO on the renal cortex and such issues that relate to pressure-natriuresis, autoregulation of total renal blood flow, tubuloglomerular feedback, and glomerular filtration rate (GFR) regulation are important subjects of renal function that either have been reviewed by others (2,29,43,55,96) or are beyond the scope of this relatively brief review.

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“…Angiograms were then obtained periodically (1, 2, 3, 4, 5, 6, 7 hours) after LPS solution (0.5 rag/2 ml saline) or saline was injected into the cistema magna through a 22 G spinal needle. In some experiments, L-arginine (100 gmol), N~-monomethyl-L-arginine (L-NMMA, 10 gmol), vasopressin (10 nmol) or bradykinin (10 nmol) in 2.0 ml of saline were injected by the same route 6 hours after LPS injection, when submaximal dilation of the basilar artery had been obtained, and angiography was then performed over the next hour (5,10,15,20,25,30,45, 60 rain).…”

Section: Angiographymentioning

confidence: 99%

“…The expanding family of nitric oxide synthase isoforms generally divide into two categories: constitutive forms regulated by Ca 2+ and calmodulin in vascular endothelium or neuronal cells, and cytokine-inducible forms, that are less sensitive to Ca 2 § but are induced in various cell types including vascular smooth muscle cells, macrophages, neutrophils, and liver cells, under pathological conditions [14,20].…”

Section: Introductionmentioning

confidence: 99%

Vasodilation by intrathecal lipopolysaccharide of the cerebral arteries after subarachnoid haemorrhage in dogs

et al. 1996

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To investigate the influence of inducible nitric oxide synthase on cerebral arteries after subarachnoid haemorrhage (SAH) in vivo, lipopolysaccharide (LPS), a major inducer of inducible nitric oxide synthase, was injected intracisternally into control and SAH model dogs. Intracisternal injection of LPS (0.5 mg) produced a long-lasting, submaximal vasodilation of the basilar artery of control dogs on angiography. This effect became significant at 4 hours after LPS injection and plateaued after 6 hours. This vasodilation was reduced by N(G)-monomethyl-L-arginine. Vasopressin slightly suppressed the vasodilation, while bradykinin increased it. The concentration of L-arginine in CSF decreased after LPS injection, while that of L-citrulline increased. In cytokines, the concentration of tumour necrosis factor-alpha; (TNF-alpha;) in CSF increased transiently at 4 hours after LPS injection, while interleukin-1 beta, interleukin-6, interferon-gamma, did not change. These data suggest that vasodilation by LPS is mainly due to nitric oxide predominantly synthesized by an inducible nitric oxide synthase, proximally induced by TNF-alpha. Our data make it unlikely that SAH itself induces the inducible nitric oxide synthase in vascular tissue, since isolated endothelium-denuded basilar artery from SAH model dogs did not respond to L-arginine. In SAH model dogs, the degree of vasodilation by LPS differed with the severity of vasospasm. Vasodilation was much greater in mild than in severe vasospasm in dogs, and was increased by superoxide dismutase. These findings suggest that the induction of inducible nitric oxide synthase or its activity may be less effective in severe vasospasm.

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Nitric oxide synthase responsible for l‐arginine‐induced relaxation of rat aortic rings in vitro may be an inducible type

Cited by 29 publications

References 42 publications

Investigating the Cardio-Protective Abilities of Supplemental L-Arginine on Parameters of Endothelial Function in a Hypercholesterolemic Animal Model

Investigating the Cardio-Protective Abilities of Supplemental L-Arginine on Parameters of Endothelial Function in a Hypercholesterolemic Animal Model

Role of renal NO production in the regulation of medullary blood flow

Vasodilation by intrathecal lipopolysaccharide of the cerebral arteries after subarachnoid haemorrhage in dogs

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