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Acute intrarenal angiotensin (1‐7) infusion decreases diabetes‐induced glomerular hyperfiltration but increases kidney oxygen consumption in the rat
Author(s) -
Persson Patrik,
Fasching Angelica,
Palm Fredrik
Publication year - 2019
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.13254
Subject(s) - glomerular hyperfiltration , diabetes mellitus , medicine , endocrinology , oxygen , angiotensin ii , kidney , renal function , renin–angiotensin system , consumption (sociology) , urology , chemistry , diabetic nephropathy , blood pressure , social science , organic chemistry , sociology
Aim Common kidney alterations early after the onset of insulinopenic diabetes include glomerular hyperfiltration, increased oxygen consumption and tissue hypoxia. Increased activity of the renin‐angiotensin‐aldosterone system (RAAS) has been implicated in most of these early alterations. The RAAS peptide angiotensin (1‐7) has the potential to modulate RAAS‐mediated alterations in kidney function. Thus, the aim of the present study was to determine the acute effects of angiotensin (1‐7) in the kidney of insulinopenic type 1 diabetic rat and the results compared to that of normoglycaemic controls. Methods Renal haemodynamics and oxygen homeostasis were measured 3 weeks after administration of streptozotocin before and after acute intrarenal infusion of angiotensin (1‐7) at a dose of 400 ng min −1 . Results Arterial pressure and renal blood flow were similar between groups and not affected by exogenous angiotensin (1‐7). Diabetics presented with glomerular hyperfiltration, increased urinary sodium excretion and elevated kidney oxygen consumption. Angiotensin (1‐7) infusion normalized glomerular filtration, increased urinary sodium excretion, decreased proximal tubular reabsorption, and elevated kidney oxygen consumption even further. The latter resulting in tubular electrolyte transport inefficiency. Angiotensin (1‐7) did not affect tissue oxygen tension and had no significant effects in controls on any of the measured parameters. Conclusion Diabetes results in increased responsiveness to elevated levels of angiotensin (1‐7) which is manifested as inhibition of tubular sodium transport and normalization of glomerular filtration. Furthermore, elevated angiotensin (1‐7) levels increase kidney oxygen consumption in the diabetic kidney even further which affects tubular electrolyte transport efficiency negatively.