Up‐regulation of endothelial nitric oxide synthase expression by cyclic guanosine 3′,5′‐monophosphate

Ravichandran, Lingamanaidu V.; Johns, Roger A.

doi:10.1016/0014-5793(95)01134-z

Cited by 28 publications

(9 citation statements)

References 36 publications

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“…In bovine main pulmonary artery endothelium, eNOS expression is increased by exogenous cGMP, and a cGMP-dependent positive-feedback control of eNOS has been proposed. 44 Our results show that increased eNOS expression was paralleled by reduced intracellular cGMP levels. We hypothesize that eNOS gene expression could be regulated by a negative-, rather than a positive-, feedback control mechanism in HUVECs.…”

Section: Casanello Et Al Iugr Inhibits Endothelial L-arginine/no Pathwaysupporting

confidence: 53%

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y ⁺ /hCAT-1 and y ⁺ /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Casanello

Sobrevía

2002

Circulation Research

109

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Section: Casanello Et Al Iugr Inhibits Endothelial L-arginine/no Pathwaysupporting

confidence: 53%

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y ⁺ /hCAT-1 and y ⁺ /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Casanello

Sobrevía

2002

Circulation Research

109

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“…[38][39][40] Certainly, Yamamoto et al 38 and Marumo et al 39 showed that activation of cGMP-protein kinase by ANP via cGMP upregulates cytokine-induced iNOS expression after 24-hour incubation in the cells mentioned above. However, on the basis of the present results, this mechanism should be ruled out, because de novo synthesis of the enzyme is unlikely to occur within this brief experimental period.…”

Section: Table 3 Effects Of Anp On Nadph-d Activitymentioning

confidence: 99%

Atrial Natriuretic Peptide Modifies Arterial Blood Pressure Through Nitric Oxide Pathway in Rats

et al. 2000

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Abstract-The aim of the present study was to determine the relationship between the hypotensive effect of the atrial natriuretic peptide (ANP) and the nitric oxide (NO) pathway. N G -nitro-L-arginine methyl ester bolus (L-NAME, 1 mg/kg) reverted the decrease in mean arterial pressure induced by ANP administration (5 g/kg bolus and 0.2 g ⅐ kg Ϫ1 ⅐ min Ϫ1 infusion), and the injection of L-NAME before peptide administration suppressed the ANP hypotensive response. To confirm these findings, a histochemical reaction was used to determine NADPH-diaphorase activity (a NO synthase marker) in the endothelium and smooth muscle of aorta and arterioles of the small and large intestine. ANP increased aorta and arteriole endothelium staining after both in vivo administration and in vitro tissue incubation. In both cases, L-NAME prevented the ANP effect on NADPH-diaphorase activity. Tissues incubated with 8-bromoguanosine 3Ј, 5Ј-cyclic monophosphate mimicked ANP action. In addition, ANP administration increased urinary excretion of NO x end products. These findings indicate that ANP increases NO synthesis capability and NO production and suggest that the cGMP pathway may be involved. In conclusion, the NO pathway could be an intercellular messenger in the ANP endothelium-dependent vasorelaxation mechanism. (Hypertension. 2000;35:1119-1123.) Key Words: natriuretic peptides Ⅲ nitric oxide Ⅲ arterial pressure Ⅲ NADPH diaphorase Ⅲ cyclic GMP Ⅲ vasodilation A trial natriuretic peptide (ANP) and nitric oxide (NO), a free radical in the form of a highly diffusible gas, are vasoactive substances that induce hypotension through their vasorelaxant effects. 1 -3 Several factors, such as an increase in intracellular cGMP levels, a decrease in cytosolic Ca 2ϩ levels, and the activation of calcium-gated potassium channels, are involved in the cellular vasorelaxation mechanism. 4,5 An increase in cGMP results in the activation of cGMPdependent protein kinases and the phosphorylation of proteins involved in the dephosphorylation of myosin light chains, which is a precondition for smooth muscle relaxation. 6 Both ANP and NO induce an increase in intracellular cGMP levels, but they do so through different pathways. The cellular effects of ANP are mainly mediated by the guanylyl cyclase-coupled natriuretic receptors, natriuretic peptide receptor (NPR)-A and NPR-B. 7,8 These receptors are expressed on the surface of different types of cells, including renal endothelial cells, both arterial and venous smooth muscle and endothelial cells, etc. 6 These receptors present an intracellular protein kinaselike domain (KLD), a domain with an autoinhibitory function that mediates adenine nucleotide effects on the guanylyl cyclase domain. On binding of ANP to the extracellular domain of the receptor, a conformational change would ensue, allowing binding of ATP to the KLD. This, in turn, would lead to a further conformational change, freeing the guanylyl cyclase domain from the inhibitory constraint of the KLD and enabling cGMP production. 9 NO is produced ...

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“…20 Furthermore, an upregulated eNOS was found in cultured endothelial cells incubated for 48 hours with 8-bromocGMP. 21 Another candidate that contributes to the upregulation of eNOS expression induced by endogenous kinins might be cAMP. Increased endothelial cAMP is induced by forskolin and amplified by activation of a cAMP-dependent protein kinase, the bradykinin-induced synthesis of cGMP.…”

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confidence: 99%

Late Treatment With Ramipril Increases Survival in Old Spontaneously Hypertensive Rats

et al. 1999

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Abstract-Spontaneously hypertensive rats (SHR) begin to die from cardiovascular complications at Ϸ15 months of age.We tested whether chronic ACE-inhibitor treatment would extend the lifespan of such old animals. We also studied cardiac hypertrophy and function, endothelial function and expression, and activity of NO synthase (eNOS). One hundred 15-month-old SHR were randomized into 3 groups, control (nϭ10), placebo-treated (nϭ45), and ramipriltreated with an antihypertensive dose of 1 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 in drinking water (nϭ45). Ex vivo experiments were performed after 15 months (control) and 21 months, when Ϸ80% of the placebo group had died. Late treatment with ramipril significantly extended lifespan of the animals from 21 to 30 months. Fully established cardiac hypertrophy, observed in placebo-treated animals and in controls, was significantly reversed by ramipril treatment. In isolated working hearts, a significantly improved function associated with increased cardiac eNOS expression was seen versus placebo and control hearts. Endothelial dysfunction in isolated aortic rings from control and placebo-treated SHR was significantly improved by ACE inhibition and associated with enhanced NO release. Late treatment of SHR with the ACE inhibitor ramipril extended lifespan from 21 to 30 months, which is comparable to the lifespan of untreated normotensive Wistar-Kyoto rats. This lifespan extension, probably due to blood pressure reduction, correlated with increased eNOS expression and activity followed by a regression of left ventricular hypertrophy and cardiac and vascular dysfunction.

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Up‐regulation of endothelial nitric oxide synthase expression by cyclic guanosine 3′,5′‐monophosphate

Cited by 28 publications

References 36 publications

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y ⁺ /hCAT-1 and y ⁺ /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y ⁺ /hCAT-1 and y ⁺ /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Atrial Natriuretic Peptide Modifies Arterial Blood Pressure Through Nitric Oxide Pathway in Rats

Late Treatment With Ramipril Increases Survival in Old Spontaneously Hypertensive Rats

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Up‐regulation of endothelial nitric oxide synthase expression by cyclic guanosine 3′,5′‐monophosphate

Cited by 28 publications

References 36 publications

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y + /hCAT-1 and y + /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y + /hCAT-1 and y + /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Atrial Natriuretic Peptide Modifies Arterial Blood Pressure Through Nitric Oxide Pathway in Rats

Late Treatment With Ramipril Increases Survival in Old Spontaneously Hypertensive Rats

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Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y ⁺ /hCAT-1 and y ⁺ /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells

Intrauterine Growth Retardation Is Associated With Reduced Activity and Expression of the Cationic Amino Acid Transport Systems y ⁺ /hCAT-1 and y ⁺ /hCAT-2B and Lower Activity of Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells