Role of Nitric Oxide in Short-term and Prolonged Effects of Angiotensin II on Renal Hemodynamics

In these studies we investigated if losartan, an AT1- receptor blocker has any beneficial effect on NO production from the bovine aortic preparations in vitro while under stimulation from angiotensin II. Experiments were performed on intact specimens of bovine thoracic aorta, incubated in Dulbeco's MOD medium in a metabolic shaker for 24 hours under 95 % O2 and 5 % CO2 at a temperature of 37°C. We found that angiotensin II 1nM−10 μM does not exert any statistically significant action on NO production. On the contrary, angiotensin II 10nM increases the production of NO by 58.14 % (from 12.16 + 2.9 μm/l to 19.23 + 4.2 μm/l in the presence of losartan 1nM (P<0.05). Nitric oxide levels depend on both rate production and rate catabolism or chemical inactivation. Such an equilibrium is vital for the normal function of many systems including the cardiovascular one. The above results demonstrate that the blockade of AT1-receptors favors the biosynthesis of NO and indicate the protective role of losartan on the vascular wall.

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Role of endothelium-derived nitric oxide in control of renal microvasculature in aging male rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.5.r1126 ◽

1993 ◽

Vol 265 (5) ◽

pp. R1126-R1131 ◽

Cited By ~ 5

Author(s):

J. F. Reckelhoff ◽

R. D. Manning

Keyword(s):

Nitric Oxide ◽

Oral Treatment ◽

Renal Hemodynamics ◽

Male Rats ◽

Glomerular Capillary ◽

Old Rats ◽

Renal Microvasculature ◽

Glomerular Hemodynamics ◽

Renal Vascular

The objective of this study was to evaluate the role of nitric oxide (NO) in the regulation of whole kidney and glomerular hemodynamics during aging. After 2 wk of oral treatment with N-nitro-L-arginine methyl ester (L-NAME; 4.5 mg.kg body wt-1.day-1) to inhibit NO synthesis, male rats, aged 3-5, 13-15, and 21-24 mo, were studied by micropuncture. Blood pressure increased by 50% in old (21-24 mo) rats with L-NAME but only 20-30% in the two younger groups. With L-NAME, renal vascular resistance increased fivefold in old rats but only twofold in younger groups. Glomerular capillary pressure increased 20-30% in younger L-NAME rats and 60% in older rats. Afferent and efferent resistances increased dramatically, and the glomerular capillary ultrafiltration coefficient decreased in all L-NAME-treated rats but most strikingly in the 21- to 24-mo-old group. Acute infusion of L-arginine significantly attenuated the effects of NO synthase inhibition on arterial pressure and renal hemodynamics in both young and old rats. This study confirms that NO synthesis blockade has a greater effect on renal hemodynamics in aging rats and implies that NO may play a progressively more important role in controlling renal function with advancing age.

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Apoptotic cascade initiated by angiotensin II in neonatal cardiomyocytes: role of DNA damage

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00408.2003 ◽

2003 ◽

Vol 285 (6) ◽

pp. H2364-H2372 ◽

Cited By ~ 51

Author(s):

Valentina Grishko ◽

Viktor Pastukh ◽

Viktoriya Solodushko ◽

Mark Gillespie ◽

Junichi Azuma ◽

...

Keyword(s):

Nitric Oxide ◽

Dna Damage ◽

Angiotensin Ii ◽

Nadph Oxidase ◽

Ventricular Remodeling ◽

Oxidase Inhibitor ◽

Neonatal Cardiomyocytes ◽

Diphenylene Iodonium ◽

Nitric Oxide Inhibitor

Angiotensin II contributes to ventricular remodeling by promoting both cardiac hypertrophy and apoptosis; however, the mechanism underlying the latter phenomenon is poorly understood. One possibility that has been advanced is that angiotensin II activates NADPH oxidase, generating free radicals that trigger apoptosis. In apparent support of this notion, it was found that angiotensin II-mediated apoptosis in the cardiomyocyte is blocked by the NADPH oxidase inhibitor diphenylene iodonium. However, three lines of evidence suggest that peroxynitrite, rather than superoxide, is responsible for angiotensin II-mediated DNA damage and apoptosis. First, the inducible nitric oxide inhibitor aminoguanidine prevents angiotensin II-induced DNA damage and apoptosis. Second, based on ligation-mediated PCR, the pattern of angiotensin II-induced DNA damage resembles peroxynitritemediated damage rather than damage caused by either superoxide or nitric oxide. Third, angiotensin II activates p53 through the phosphorylation of Ser15 and Ser20, residues that are commonly phosphorylated in response to DNA damage. It is proposed that angiotensin II promotes the oxidation of DNA, which in turn activates p53 to mediate apoptosis.

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Role of AT1 receptors in the renal papillary effects of acute and chronic nitric oxide inhibition

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.3.r760 ◽

1998 ◽

Vol 274 (3) ◽

pp. R760-R766 ◽

Cited By ~ 8

Author(s):

M. Clara Ortíz ◽

Lourdes A. Fortepiani ◽

Francisco M. Ruiz-Marcos ◽

Noemí M. Atucha ◽

Joaquín García-Estañ

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Angiotensin Ii ◽

Chronic Administration ◽

Acute Administration ◽

Synthesis Inhibitor ◽

Renal Vasoconstriction ◽

Oxide Inhibition ◽

Stimulation Of

Nitric oxide (NO) is a vasodilator substance controlling renal papillary blood flow (PBF) in the rat. In this study we have evaluated the role of AT1 angiotensin II receptors as modulators of the whole kidney and papillary vasoconstrictor effects induced by the acute or chronic inhibition of NO synthesis. Experiments have been performed in anesthetized, euvolemic Munich-Wistar rats prepared for the study of renal blood flow (RBF) and PBF. In normal rats, acute administration of the NO synthesis inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) increased mean arterial pressure (MAP) and decreased RBF and PBF. Either acute or chronic treatment with the AT1 receptor blocker losartan did not modify the decreases in RBF or PBF secondary to l-NAME. In animals made hypertensive by chronic inhibition of NO, basal MAP was higher, whereas RBF and PBF were lower than in the controls. In these animals, acute or chronic administration of losartan decreased MAP and increased both RBF and PBF significantly. These results indicate that, under normal conditions, the decreases in RBF or PBF induced by the acute inhibition of NO synthesis are not modulated by AT1-receptor stimulation. However, the arterial hypertension, renal vasoconstriction, and reduced PBF present in chronic NO-deficient hypertensive rats is partially due to the effects of angiotensin II, via stimulation of AT1-receptors.

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Short-term angiotensin II treatment regulates cardiac nanomechanics via microtubule modifications

Nanoscale ◽

10.1039/d0nr02474k ◽

2020 ◽

Vol 12 (30) ◽

pp. 16315-16329

Author(s):

Pamela Swiatlowska ◽

Jose L. Sanchez-Alonso ◽

Catherine Mansfield ◽

Denis Scaini ◽

Yuri Korchev ◽

...

Keyword(s):

Angiotensin Ii ◽

Young’S Modulus ◽

Young's Modulus ◽

Short Term ◽

Nanoscale Level

MechanoSICM is used to understand the role of angiotensin II on transverse Young's modulus at the nanoscale level.

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Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats.

Hypertension ◽

10.1161/01.hyp.21.4.476 ◽

1993 ◽

Vol 21 (4) ◽

pp. 476-484 ◽

Cited By ~ 80

Author(s):

H Kumagai ◽

D B Averill ◽

M C Khosla ◽

C M Ferrario

Keyword(s):

Nitric Oxide ◽

Angiotensin Ii ◽

Sympathetic Nerve ◽

Spontaneously Hypertensive Rats ◽

Sympathetic Nerve Activity ◽

Hypertensive Rats ◽

Nerve Activity ◽

Spontaneously Hypertensive

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Stroma-free hemoglobin increases blood pressure and GFR in the hypotensive rat: role of nitric oxide

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.5.2348 ◽

1994 ◽

Vol 77 (5) ◽

pp. 2348-2354 ◽

Cited By ~ 64

Author(s):

A. Thompson ◽

A. E. McGarry ◽

C. R. Valeri ◽

W. Lieberthal

Keyword(s):

Nitric Oxide ◽

Intravascular Volume ◽

Oncotic Pressure ◽

Free Hemoglobin ◽

Albumin Solution ◽

Short Term ◽

Marked Contrast ◽

Hemorrhagic Hypotension ◽

No Inhibition

The short-term systemic and renal hemodynamic effects of two stroma-free hemoglobin (SFH) solutions, one unmodified and the other modified by cross-linking, were examined in anesthetized rats after hemorrhagic hypotension. Both forms of SFH increased mean arterial pressure (MAP) and glomerular filtration rate (GFR) to baseline (prehemorrhage) values. The increase in MAP induced by unmodified SFH was greater than the increase in MAP caused by an albumin solution isoncotic to the unmodified SFH solution. Similarly, the increase in MAP caused by the modified SFH was also substantially greater than that induced by an albumin solution of comparable oncotic pressure to the modified SFH solution. Both unmodified and modified SFH increased GFR. As with MAP, the increase in GFR induced by both SFH solutions was greater than that associated with the oncotically matched albumin solutions. In separate experiments, the effects of nitric oxide (NO) inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) on MAP after hemorrhagic hypotension and subsequent infusion of unmodified SFH or albumin were also examined. In the albumin-infused rats, L-NAME increased MAP. In marked contrast, NO inhibition with L-NAME had no further effect on MAP when infused after SFH. We conclude that both unmodified and modified SFH solutions acutely improve MAP and GFR by the combined effects of intravascular volume expansion resulting from the colloid effect of the protein and by inactivation of NO.

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