Relationship of renal prostaglandins to three diuretics

Favre, L.; Vallotton, Michel B.

doi:10.1016/0262-1746(84)90115-x

Cited by 14 publications

(8 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nevertheless, the present results showing a significant increase of PRC in both A1AR +/+ and A1AR −/− mice suggest that CA inhibitors may stimulate renin secretion. An increase in plasma renin activity and urinary aldosterone concentration following the administration of acetazolamide has been observed in humans [4]. The increase in renin secretion may be caused by extracellular volume depletion, and by the acidification resulting from CA inhibition.…”

Section: Discussionmentioning

confidence: 98%

Effect of carbonic anhydrase inhibition on GFR and renal hemodynamics in adenosine-1 receptor-deficient mice

Hashimoto

Huang

Castrop

et al. 2004

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

The reduction of glomerular filtration rate (GFR) caused by inhibitors of carbonic anhydrase (CA) is thought to be initiated by activation of the tubuloglomerular feedback (TGF) mechanism. We determined the effect of the CA inhibitor benzolamide (Bz) on renal hemodynamics in adenosine-1 receptor (A1AR) knockout mice that have been shown previously to lack a TGF response. In A1AR(+/+) mice, Bz (150 microg plus 2 microg/min) reduced RBF by 19.8% (from 829+/-42 to 666+/-44 microl/min; n=7), and GFR by 19.8% (from 396+/-43 to 324+/-46 microl/min; n=9, P=0.001). In A1AR(-/-) mice, RBF fell by 15.9 % (from 809+/-24 to 680+/-40 microl/min; n=7), and GFR by 21.1% (from 358+/-27 to 287+/-32 microl/min; n=10, P=0.0003; NS compared with A1AR(+/+)). The absence of TGF responses both before and during Bz infusion in A1AR(-/-) mice was confirmed by micropuncture. Following angiotensin II-receptor blockade with candesartan, Bz did not alter RBF (1.4+/-0.2 vs. 1.4+/-0.15 ml/min in A1AR(+/+), and 1.4+/-0.22 vs. 1.39+/-0.2 ml/min in A1AR(-/-); n=5/genotype) while GFR changed by -8.9 % in A1AR(+/+) mice ( n=7), and by -1% in A1AR(-/-) mice ( n=9; NS compared with A1AR(+/+)). Bz caused a significant rise of plasma renin concentration in both A1AR(+/+) and A1AR(-/-) mice. Our data show that the absence of a functional TGF mechanism does not prevent the reduction in GFR or RBF caused by CA inhibition. Acute angiotensin II receptor blockade, on the other hand, diminishes the effect of CA inhibition on GFR and RBF. The causes for the GFR reduction appear to be complex and include an effect of the renin-angiotensin system.

show abstract

Section: Discussionmentioning

confidence: 98%

Effect of carbonic anhydrase inhibition on GFR and renal hemodynamics in adenosine-1 receptor-deficient mice

Hashimoto

Huang

Castrop

et al. 2004

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

show abstract

“…We illustrated Figure 2 as an example of the association between interaction mechanisms and pharmacological/chemical subgroups, and Figure 3A shows another example of the associations. D00386 (Triamterene) interacts 8 different drugs, of which 6 drugs are classified "Acetic acid derivatives" subgroup, and these interactions cause acute renal failure [9,10]. Figure 3B illustrates the case of D00089 (Oxytocin), and these interactions result in the enhancement effect of both drugs and lead to serious events [11].…”

Section: Discussionmentioning

confidence: 99%

Network Analysis of Adverse Drug Interactions

Takarabe

Okuda

Itoh

et al. 2008

Genome Informatics 2008

View full text Add to dashboard Cite

Harmful cffects associated with use of drugs are caused as a result of their side effects and combined use of different drugs. These drug interactions result in increased or decreased drug effects, or produce other new unwanted effects and are serious problems for medical institutions and pharmaceutical companies. In this study, we created a drug-drug interaction network from drug package inserts and characterized drug interactions. The known information about the potential risk of drug interactions is described in drug package inserts. Japanese drug package inserts are stored in the JAPIC (Japan Pharmaceutical Information Center) database and GenomeNet provides the GenomeNet pharmaceutical products database, which integrate the JAPIC and KEGG databases. We cxtracted drug interaction data from GenomeNet, where interactions are classified according to risks, contraindications or cautions for coadministration, and some entries include information about cnzymes metabolizing the drugs. We defined drug target and drug-metabolizing enzymes as interaction factors using information on them in KEGG DRUG, and classified drugs into pharmacological/chemical subgroups. In the resulting drug-drug interaction network, the drugs that are associated with the same interaction factors are closely interconnected. Mechanisms of these interactions were then identified by each interaction factor. To characterize other interactions without interaction factors, we used the A TC classification system and found an association between interaction mechanisms and pharmacological/chemical subgroups.

show abstract

“…Although there have been no prospective controlled studies comparing the relative nephrotoxicity of the po tassium-sparing diuretics, a large body of evidence is available which supports the concept of intrinsic nephro toxicity for TA [3, 21, 30, 52-62, 64, 68] which, in turn, relates to its negative effect on cardiac output [67], renal hemodynamics [30,58) and renal prostaglandin produc tion [54,[69][70][71]. The latter assumes added significance when NSAIDs are coadministered with TA since their combined negative effects on renal function appear syn ergistic [52][53][54].…”

Section: Hemodynamic Volumementioning

confidence: 99%

“…The administration of TA to either normal volunteers or essential hypertensives was shown to predictably sti mulate both plasma renin activity [18,19,54,70,71] and urinary prostaglandin excretion [54,[69][70][71], The latter is likely to reflect an adaptive mechanism to preserve renal blood flow in light of the rise in renal vascular [30,58] and peripheral resistance [67] which follows the administra tion of TA. This increase in renal prostaglandin produc tion, although conferring some protection from the pot entially harmful renal vasoconstrictive effects of TA, is abolished when and if TA is administered in combination with NSAIDs [52][53][54][55].…”

Section: Hemodynamic Volumementioning

confidence: 99%

“…The observed decline in renal function was generally abrupt and distinguished by oligoanuria and slow resolution [52][53][54][55]. The proliferation of such cases then provided the impetus for a number of investi gators to further explore the effects of TA on the reninangiotensin-aldosterone [19,54] and renal prostaglandin systems [69][70][71] as potential mediators/modifiers of this phenomenon.…”

Section: Hemodynamic Volumementioning

confidence: 99%

See 1 more Smart Citation

Triamterene and the Kidney

Sica¹,

Gehr²

1989

Nephron

View full text Add to dashboard Cite

Triamterene (TA) is a mild ‘potassium-sparing’ diuretic usually employed in combination with other more potent diuretics in the treatment of hypertension. TA pharmacokinetics and pharmacodynamics in normal volunteers, elderly subjects and in patients with renal and hepatic dysfunction are reviewed. A variety of adverse renal effects, such as abnormalities in urinary sediment, nephrolithiasis, interstitial nephritis and acute renal failure, has been reported to occur and is also reviewed. Of particular concern with the increased availability of ‘over-the-counter’ nonsteroidal anti-inflammatory medications (NSAID) is the adverse interaction between TA and NSAID which may culminate in acute renal failure. Although a rare occurrence, the clinician should be aware of potential adverse reactions associated with the use of TA.

show abstract

Relationship of renal prostaglandins to three diuretics

Cited by 14 publications

References 6 publications

Effect of carbonic anhydrase inhibition on GFR and renal hemodynamics in adenosine-1 receptor-deficient mice

Effect of carbonic anhydrase inhibition on GFR and renal hemodynamics in adenosine-1 receptor-deficient mice

Network Analysis of Adverse Drug Interactions

Triamterene and the Kidney

Contact Info

Product

Resources

About