Biosynthesis and homeostatic roles of nitric oxide in the normal kidney

Kone, Bruce C.; Baylis, Chris

doi:10.1152/ajprenal.1997.272.5.f561

Cited by 255 publications

(275 citation statements)

References 142 publications

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“…In that respect, rats that received NTG displayed attenuated renal vasoconstrictive response to pneumoperitoneum, whereas rats pretreated with L-NAME displayed a higher sensitivity to this surgical procedure, suggesting a greater dependence of the kidney on NO as a beneficial counterregulatory system during pneumoperitoneum. This conclusion is compatible with the notion that NO plays a prominent role in the control of renal hemodynamics and tubular function (28,29). NO is constitutively produced from its precursor, L-arginine, by the enzyme endothelial NO synthase and acts on adjacent smooth muscle cells to exert vasodilatory tone on the renal microvasculature, primarily the afferent arteriole.…”

Section: Discussionsupporting

confidence: 88%

“…These results are at odds with those reported that administration of Ro 61-0612, a mixed ET A and ET B blocker, attenuated the fall in GFR and oliguria during pneumoperitoneum (1,39). It should be emphasized that these authors applied similar IAP and drug infusion protocol; however, the pneumoperitoneum was established for Because endothelium-derived NO is important in the regulation of RBF and kidney function (28,29), we tested the hypothesis of whether altered activity of the NO system may be involved in the pathogenesis of the reduced RBF and kidney function characterizing pneumoperitoneum. Indeed, the most prominent finding in the present study was the effects of NO modulations on the adverse renal effects of elevated IAP.…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, several studies have demonstrated that medullary NO plays a pivotal role in the regulation of renal medullary hemodynamics and excretory function (27,28,30). Previously, our laboratory (14,18) and others (48) have shown that the renal vasodilatory actions of ET B , as well as its stimulatory effects on water and sodium excretion, are mediated through generation of NO.…”

mentioning

confidence: 95%

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Adverse effects of pneumoperitoneum on renal function: involvement of the endothelin and nitric oxide systems

Abassi

Bishara²,

Karram³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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The mechanism underlying this phenomenon is largely unknown. This study was designed to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO) systems in IAP-induced renal dysfunction. Rats were subjected to IAP of 14 mmHg for 1 h, followed by a deflation for 60 min (recovery). Four additional groups were pretreated with 1) ABT-627, an ET A antagonist; 2) A-192621, an ETB antagonist; 3) nitroglycerine; and 4) N G -nitro-L-arginine methyl ester, a NO synthase inhibitor, before IAP. Urine flow rate (V), absolute Na ϩ excretion (UNaV), glomerular filtration rate (GFR), and renal plasma flow (RPF) were determined. Significant reductions in kidney function and hemodynamics were observed when IAP was applied. V decreased from 8.1 Ϯ 1.0 to 5.8 Ϯ 0.5 l/min, UNaV from 1.08 Ϯ 0.31 to 0.43 Ϯ 0.10 eq/min, GFR from 1.84 Ϯ 0.12 to 1.05 Ϯ 0.06 ml/min (Ϫ46.9 Ϯ 2.7% from baseline), and RPF from 8.62 Ϯ 0.87 to 3.82 Ϯ 0.16 ml/min (Ϫ54 Ϯ 3.5% from baseline). When the animals were pretreated with either ABT-627 or A-192621, given alone or combined, the adverse effects of IAP on GFR, RPF, V, and UNaV were significantly augmented. When the animals were pretreated with nitroglycerine, the adverse effects of pneumoperitoneum on GFR and RPF were substantially improved. In contrast, pretreatment with N G -nitro-L-arginine methyl ester remarkably aggravated pneumoperitoneum-induced renal dysfunction. In conclusion, decreased renal excretory function and hypofiltration are induced by increased IAP. These effects are related to impairment of renal hemodynamics and could be partially ameliorated by pretreatment with nitroglycerine and aggravated by NO and ET blockade.rat; intra-abdominal pressure PNEUMOPERITONEUM AT PRESSURE above 10 mmHg during laparoscopic surgery has been shown to produce transient oliguria and reduced glomerular filtration rate (GFR) and renal blood flow (RBF) (3,9,16,33,34). Despite much research in this field, the systemic physiological consequences of CO 2 pneumoperitoneum and the mechanisms underlying its adverse effects on renal hemodynamics and excretory function are not fully understood (9). However, there is compelling experimental evidence that the adverse renal effects induced by pneumoperitoneum are affected by the level of intra-abdominal pressure (IAP), volume status, degree of hypercarbia, positioning, and individual hemodynamic and renal reserves (9, 10). Additional factors that may affect renal function during pneumoperitoneum include direct compression of the renal parenchyma and renal vein (4, 17), increased resistance in the renal vasculature (47), and release of vasoconstrictors, such as vasopressin, angiotensin II, catecholamines, and endothelin (ET)-1 (1, 13). The latter is a very potent natural mammalian vasoconstrictor agent (25), acting on the cardiovascular and renal systems and other target organs by binding to two major types of receptors, ET A and ET B (2,25,36). High abundance of ET A receptors has been detected in the aorta, heart, and kidney, whereas ET B receptors are expre...

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

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Adverse effects of pneumoperitoneum on renal function: involvement of the endothelin and nitric oxide systems

Abassi

Bishara²,

Karram³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…iNOS (NOS-2) is an isoform of nitric oxide synthase found in renal tubules, vascular smooth muscle, fibroblasts, and macrophages (13). Its gene expression is increased after ischemic ARF, and persistent high concentrations of NO result.…”

mentioning

confidence: 99%

Docosahexaenoic Acid Ameliorates Murine Ischemic Acute Renal Failure and Prevents Increases in mRNA Abundance for both TNF-α and Inducible Nitric Oxide Synthase

Kielar¹,

Jeyarajah²,

Zhou³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. This study demonstrates that intraperitoneal injections of DHA (all cis 4,7,10,13,16,19 docosahexaenoic acid C22: n-3) bound to bovine serum albumin ameliorate murine acute renal failure (ARF) induced by temporary occlusion of the renal artery. Three micromoles of DHA decreased serum creatinine (Scr) from 2.3 mg/dl to 1.1 mg/dl 24 h after reperfusion (n ϭ 15; P Ͻ 0.05). Scr of the treated animals were significantly lower than controls throughout a 7-d time course. Although lower doses of DHA were less effective, higher doses were not more effective. Ribonuclease (RNase) protection assays showed that ischemia increased mRNA abundance for TNF-␣ and inducible nitric oxide synthase (iNOS) at 24 h. This increase was prevented by DHA administration. Because TNF-␣ and iNOS contribute to renal ischemic injury, their inhibition may contribute to DHA's salutary effect. In addition, the data may have therapeutic implications, because the DHA improves ARF even when administered at 4 h after reperfusion.

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“…NOS2 is expressed in the endothelium of glomerular capillaries and afferent and efferent arterioles, renal arteries, and descending vasa recta, as well as in proximal tubule and medullary thick ascending limb. NOS3 is also expressed in tubules, including S3 segments of the proximal tubule, medullary thick ascending limb, and collecting duct, in addition to arcuate arteries and vasa recta bundles (Kone, BC, 1997). Both in vivo and in vitro studies have provided conflicting results regarding NOS expression and NO production in diabetes.…”

Section: Nitric Oxidementioning

confidence: 99%