Iodinated contrast media inhibit oxygen consumption in freshly isolated proximal tubular cells from elderly humans and diabetic rats: Influence of nitric oxide
2016 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 121, no 1, 12-16 p.Article in journal (Refereed) PublishedText
Objectives Mechanisms underlying contrast medium (CM)-induced nephropathy remain elusive, but recent attention has been directed to oxygen availability. The purpose of this study was to evaluate the effect of the low-osmolar CM iopromide and the iso-osmolar CM iodixanol on oxygen consumption (QO(2)) in freshly isolated proximal tubular cells (PTC) from kidneys ablated from elderly humans undergoing nephrectomy for renal carcinomas and from normoglycemic or streptozotocin-diabetic rats. Materials PTC were isolated from human kidneys, or kidneys of normoglycemic or streptozotocin-diabetic rats. QO(2) was measured with Clark-type microelectrodes in a gas-tight chamber with and without each CM (10 mg I/mL medium). L-NAME was used to inhibit nitric oxide (NO) production caused by nitric oxide synthase. Results Both CM reduced QO(2) in human PTC (about -35%) which was prevented by L-NAME. PTC from normoglycemic rats were unaffected by iopromide, whereas iodixanol decreased QO(2) (-34%). Both CM decreased QO(2) in PTC from diabetic rats (-38% and -36%, respectively). L-NAME only prevented the effect of iopromide in the diabetic rat PTC. Conclusions These observations demonstrate that CM can induce NO release from isolated PTC in vitro, which affects QO(2). Our results suggest that the induction of NO release and subsequent effect on the cellular oxygen metabolism are dependent on several factors, including CM type and pre-existing risk factors for the development of CM-induced nephropathy.
Place, publisher, year, edition, pages
TAYLOR & FRANCIS LTD , 2016. Vol. 121, no 1, 12-16 p.
human; Contrast media; nitric oxide; oxygen consumption; proximal tubule; rat
IdentifiersURN: urn:nbn:se:liu:diva-127063DOI: 10.3109/03009734.2016.1144664ISI: 000372123700002PubMedID: 26933994OAI: oai:DiVA.org:liu-127063DiVA: diva2:919368
Funding Agencies|Swedish Research Council Medicine and Health; Swedish Diabetes Foundation; Swedish Medical Association2016-04-132016-04-132016-04-13