Purpose: GLP-1 receptor agonism has shown beneficial cardiovascular effects which could include the kidneys. In the human kidney, the high GLP-1 extraction and its natriuretic effect depend on the GLP-1 receptor and is accompanied by suppression of angiotensin II, independent of changes in renal plasma flow. Preclinical data showed that angiotensin II constricts the vasa recta and lowers medullary perfusion. The current randomized, controlled study was designed to test the hypothesis that GLP-1 increases renal medullary perfusion in healthy humans.
Methods: Healthy male participants (n=10, 27 ± 4 years) ingested a fixed sodium intake for 4 days and were examined twice during a 1-hour infusion of either GLP-1 (1.5 pmol/kg/min) or placebo together with infusion of 0.9% NaCl (750 mL/h) . Interleaved measurements of renal artery flow, oxygenation (R2*) , and perfusion were acquired in the renal cortex and medulla during infusions, using magnetic resonance imaging.
Results: GLP-1 infusion increased medullary perfusion (32 ± 7%, p<0.001) and cortical perfusion (13 ± 4%, p<0.001) compared to placebo. Here, NaCl infusion decreased medullary perfusion (-5 ± 2%, p=0.007) while cortical perfusion remained unchanged. R2* values increased by 3 ± 2% (p=0.025) in the medulla and 4 ± 1% (p=0.008) in the cortex during placebo, indicative of decreased oxygenation but remained unchanged during GLP-1. Renal arterial blood flow was not altered significantly by either intervention.
Conclusions: GLP-1 increases predominantly medullary but also cortical perfusion in healthy human kidneys and maintains oxygenation during NaCl-loading. In perspective, GLP-1 may exert protective effects against renal hypoperfusion and ischemia.
B. Haddock: n/a. B. L. Jensen: None. A. Asmar: None.