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Effect of nitric oxide on renal autoregulation during hypothermia in the rat.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology. Karolinska Univ Hosp, Dept Pediat Perioperat Med & Intens Care, ECMO Ctr Karolinska, S-17176 Stockholm, Sweden.; Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden .
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2017 (English)In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 469, no 5-6, p. 669-680Article in journal (Refereed) Published
Abstract [en]

Hypothermia-induced reduction of metabolic rate is accompanied by depression of both glomerular perfusion and filtration. The present study investigated whether these changes are linked to changes in renal autoregulation and nitric oxide (NO) signalling. During hypothermia, renal blood flow (RBF) and glomerular filtration rate (GFR) were reduced and urine production was increased, and this was linked with reduced plasma cGMP levels and increased renal vascular resistance. Although stimulation of NO production decreased vascular resistance, blood pressure and urine flow, intravenous infusion of the NO precursor L-arginine or the NO donor sodium nitroprusside did not alter RBF or GFR. In contrast, inhibition of NO synthesis by N(w)-nitro-L-arginine led to a further decline in both parameters. Functional renal autoregulation was apparent at both temperatures. Below the autoregulatory range, RBF in both cases increased in proportion to the perfusion ±pressure, although, the slope of the first ascending limb of the pressure-flow relationship was lower during hypothermia. The main difference was rather that the curves obtained during hypothermia levelled off already at a RBF of 3.9 ± 0.3 mL/min then remained stable throughout the autoregulatory pressure range, compared to 7.6 ± 0.3 mL/min during normothermia. This was found to be due to a threefold increase in, primarily, the afferent arteriolar resistance from 2.6 to 7.5 mmHg min mL(-1). Infusion of sodium nitroprusside did not significantly affect RBF during hypothermia, although a small increase at pressures below the autoregulatory range was observed. In conclusion, cold-induced rise in renal vascular resistance results from afferent arteriolar vasoconstriction by the autoregulatory mechanism, setting RBF and GFR in proportion to the metabolic rate, which cannot be explained by reduced NO production alone.

Place, publisher, year, edition, pages
2017. Vol. 469, no 5-6, p. 669-680
Keywords [en]
Autoregulation, GFR, Hypothermia, Nitric oxide, Renal blood flow, Vascular resistance
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-317887DOI: 10.1007/s00424-017-1967-1ISI: 000401865900008PubMedID: 28315005OAI: oai:DiVA.org:uu-317887DiVA, id: diva2:1083469
Funder
Swedish Research Council, K97-04X-11557-02B, 2016-01381Swedish Heart Lung Foundation, 20140448Available from: 2017-03-21 Created: 2017-03-21 Last updated: 2017-08-07Bibliographically approved

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