Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

Gomez, Sabas I.; Strick, D. M.; Romero, J. Carlos

doi:10.1590/s0100-879x2008000200014

Cited by 5 publications

(2 citation statements)

References 24 publications

(44 reference statements)

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“…97 Inhibition of cyclooxygenase enzymes within the kidney is thought to decrease the production of vasodilatory prostanoids, which normally help to maintain renal blood flow in the face of vasoconstrictors. 112 In particular, both cortical and medullary blood flow can be reduced by the administration of NSAIDs, 85 and NSAID-induced nephropathy is characterized by papillary necrosis and interstitial nephritis. Acute tubular injury from NSAID-induced nephropathy is similar to that seen in cats with an experimental ischemic insult of the kidney (Figs.…”

Section: Potential Causes Of Renal Hypoxia In Catsmentioning

confidence: 99%

Chronic Kidney Disease in Aged Cats

et al. 2016

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Chronic kidney disease (CKD) is the most common metabolic disease of domesticated cats, with most affected cats being geriatric (>12 years of age). The prevalence of CKD in cats exceeds that observed in dogs, and the frequency of the diagnosis of CKD in cats has increased in recent decades. Typical histologic features include interstitial inflammation, tubular atrophy, and fibrosis with secondary glomerulosclerosis. In contrast to people and dogs, primary glomerulopathies with marked proteinuria are remarkably rare findings in cats. Although a variety of primary renal diseases have been implicated, the disease is idiopathic in most cats. Tubulointerstitial changes, including fibrosis, are present in the early stages of feline CKD and become more severe in advanced disease. A variety of factors-including aging, ischemia, comorbid conditions, phosphorus overload, and routine vaccinations-have been implicated as factors that could contribute to the initiation of this disease in affected cats. Factors that are related to progression of established CKD, which occurs in some but not all cats, include dietary phosphorus intake, magnitude of proteinuria, and anemia. Renal fibrosis, a common histologic feature of aged feline kidneys, interferes with the normal relationship between peritubular capillaries and renal tubules. Experimentally, renal ischemia results in morphologic changes similar to those observed in spontaneous CKD. Renal hypoxia, perhaps episodic, may play a role in the initiation and progression of this disease.

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Section: Potential Causes Of Renal Hypoxia In Catsmentioning

confidence: 99%

Chronic Kidney Disease in Aged Cats

et al. 2016

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“…Urinary PGE2 excretion rate is considered to reflect largely the intrarenal PGE2 production by RMICs [78]. PGE2 induce a significant vasodilation of the vasa recta by activation of EP2 and EP4 receptors, resulting in an increase in medullary blood [122][123][124].…”

Section: Inner Medullary Interstitial Cells and Medullary Blood Flowmentioning

confidence: 99%

Vaptans or voluntary increased hydration to protect the kidney: how do they compare?

Bankir

Guerrot

Bichet

2021

Nephrology Dialysis Transplantation

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The adverse effects of vasopressin (AVP) in diverse forms of chronic kidney disease have been well described. They depend on the antidiuretic action of AVP mediated by V2 receptors (V2R). Treatment with tolvaptan, a selective V2R antagonist, is now largely used for the treatment of patients with ADPKD. Another way to reduce the adverse effects of AVP is to reduce endogenous AVP secretion by voluntary increase in fluid intake. These two approaches differ in several ways, including the level of thirst and AVP. With voluntary increased drinking plasma osmolality will decline and so will AVP secretion. Thus, not only will V2R-mediated effects be reduced, but also those mediated by V1a (V1aR) and V1b receptors. In contrast, selective V2R antagonism will induce a loss of fluid that will stimulate AVP secretion and thus, increase AVP's influence on V1a and V1b receptors. V1aR are expressed in the luminal side of the collecting duct and in inner medullary interstitial cells, and their activation induces the production of prostaglandins, mostly PGE2. Intrarenal PGE2 have been shown to reduce sodium and water reabsorption in the collecting duct and to increase blood flow in the renal medulla, both effects contributing to increase sodium and water excretion and reduce urine concentrating activity. Conversely, non-steroidal anti-inflammatory drugs have been shown to induce a significant water and sodium retention and potentiate the antidiuretic effects of AVP. Thus, during V2R antagonism, V1aR-mediated actions may be responsible for part of the diuresis observed with this drug. These V1aR-dependent effects do not take place with voluntary increase in fluid intake. In summary, while both strategies may have beneficial effects, the information reviewed here lead us to assume that the pharmacological V2R antagonism, with resulting stimulation of V1aR and increased PGE2 production, may provide greater benefit than voluntary HWI. The influence of tolvaptan on PGE2 excretion rate and the possibility to use somewhat lower tolvaptan doses than presently prescribed remain to be evaluated.

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Role of nitric oxide and prostaglandin in the maintenance of cortical and renal medullary blood flow

Cited by 5 publications

References 24 publications

Chronic Kidney Disease in Aged Cats

Chronic Kidney Disease in Aged Cats

Vaptans or voluntary increased hydration to protect the kidney: how do they compare?

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