W.A.B. Howells, C.L. Chapman, S.M. Holt, C.T. O’Connell, S.C. Brazelton, H.M. Medved, E.L. Reed, K. Wiedenfeld Needham, J.R. Halliwill, FACSM, C.T. Minson, FACSM

University of Oregon, Eugene, OR

Oral protein consumption increases circulating amino acids that increase renal perfusion. Prolonged water deprivation evokes marked reductions in renal blood flow. Reduced renal perfusion during hypohydration is the primary mechanism of acute kidney injury of pre-renal etiology. It is not known whether the renal hemodynamic response to oral protein consumption is modified during prolonged hypohydration. This knowledge gap has implications for oral rehydration strategies following prolonged hypohydration. PURPOSE: To test the hypothesis that increases in segmental artery blood velocity following oral protein loading are attenuated during prolonged mild hypohydration compared to when euhydrated. METHODS: In a block-randomized crossover design, twenty-two healthy adults [11 males, 11 females; age: 21(3) years] completed 24 hours of fluid deprivation to induce hypohydration (HYPO) or 24 hours normal fluid consumption (EUHY). Protocols were separated by ³72 hours. Baseline measurements were obtained at the end of each 24-hour protocol. Participants then ingested a whey protein shake (1.0 g protein and 10 ml water per kg of body mass). Body fluid losses were estimated via the change in body mass over 24 hours (∆BM). Blood pressure (electrosphygmomanometer) and segmental artery blood velocity in the right kidney (Doppler ultrasound) were measured at baseline and 150-minutes post-protein. Segmental artery vascular conductance was calculated as blood velocity divided by mean arterial pressure. Data are presented as the change from baseline (∆) as mean with 95% confidence intervals. RESULTS: Reductions in ∆BM were greater in HYPO vs. EUHY [-2.5% (-2.9, -2.1) vs. 0.0% (-0.4, 0.4), P

Supported by NIH R01HL144128 and F32HL164021.

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