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Aldosterone Blockade Reduces Low Salt‐induced Renal Oxygen Consumption
Author(s) -
Patinha Daniela,
Pihl Liselotte,
Fasching Angelica,
Palm Fredrik
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1218.4
Subject(s) - aldosterone , chemistry , medicine , endocrinology , renal blood flow , angiotensin ii , renal function , kidney , renin–angiotensin system , oxidative stress , mineralocorticoid receptor , blood pressure
Low salt (LS) diet activates the renin‐angiotensin system, in order to maintain volume homeostasis, which increases active electrolyte transport and thus kidney oxygen consumption (QO 2 ). However, the role of aldosterone in low salt‐induced QO 2 and tissue hypoxia is presently unknown. Male Sprague Dawley rats were fed normal (NS, 0.4%) or low (LS, 0.01%) salt diet during two weeks. Thereafter, catheters were placed in the carotid artery and femoral vein for blood pressure measurement and infusion of 3 H‐inulinin thiobutabarbital‐anesthetized animals. The left kidney was immobilized. Measurements were obtained before and after intravenous administration of the aldosterone antagonist canrenoic acid (20 mg/kg). QO 2 was estimated from the arterio‐venous difference in oxygen content multiplied by renal blood flow (RBF; Transonic flow probe). Renal cortical and medullary partial pressures of oxygen (PO 2 ) were measured using Clark‐type electrodes. Mean arterial blood pressure, glomerular filtration rate and RBF were similar in both groups. LS rats had lower fractional excretion of Na + (FE Na ) and less efficient Na + transport (T Na ), defined as T Na /QO 2 together with increased QO 2 and markers of oxidative stress compared to NS. LS intake also reduced cortical PO 2 and increased medullary PO 2 . Acute aldosterone inhibition doubled FE Na , normalized QO 2 and reduced oxidative stress only in LS. In conclusion, LS‐induced QO 2 and oxidative stress are caused by increased intrarenal aldosterone signaling. However, if the beneficial effects of aldosterone blockade for long‐term kidney function in chronic kidney disease are due to normalized oxygen metabolism remains to be determined. Support or Funding Information This work was supported by the Swedish Heart and Lung Foundation and the Swedish Research Council.