Abstract
Background: Acute renal failure (ARF) following renal ischemia-reperfusion (I/R) injury is considered a relevant risk factor for cardiac damage, but the underlying mechanisms, particularly those triggered at cardiomyocyte level, are unknown. Methods: We examined intracellular Ca2+ dynamics in adult ventricular cardiomyocytes isolated from C57BL/6 mice 7 or 15 days following unilateral renal I/R. Results: After 7 days of I/R, the cell contraction was significantly lower in cardiomyocytes compared to sham-treated mice. It was accompanied by a significant decrease in both systolic Ca2+ transients and sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) activity measured as Ca2+ transients decay. Moreover, the incidence of pro-arrhythmic events, measured as the number of Ca2+ sparks, waves or automatic Ca2+ transients, was greater in cardiomyocytes from mice 7 days after I/R than from sham-treated mice. Ca2+ mishandling related to systolic Ca2+ transients and contraction were recovered to sham values 15 days after I/R, but Ca2+ sparks frequency and arrhythmic events remained elevated. Conclusions: Renal I/R injury causes a cardiomyocyte Ca2+ cycle dysfunction at medium (contraction-relaxation dysfunction) and long term (Ca2+ leak), after 7 and 15 days of renal reperfusion, respectively.
Highlights
Acute renal failure (ARF) caused by renal ischemia-reperfusion (I/R) injury is a complex clinical entity related to a variety of clinical and surgical settings, including sepsis and kidney transplantation [1–3], and is characterized by the suspension of blood flow to the kidney followed by restoration of perfusion and re-oxygenation
We employed an experimental model of ARF to comprehensively analyze the cardiac consequences of acute unilateral renal ischemia and reperfusion (I/R) through the occlusion of the left renal pedicle
We show that ARF induces intracellular Ca2+ mishandling, man‐
Summary
Acute renal failure (ARF) caused by renal ischemia-reperfusion (I/R) injury is a complex clinical entity related to a variety of clinical and surgical settings, including sepsis and kidney transplantation [1–3], and is characterized by the suspension of blood flow to the kidney followed by restoration of perfusion and re-oxygenation. The complex physiological relationship that exists between the kidneys and the heart has long been appreciated, and damage to one organ may induce damage to the other, which has been termed the cardiorenal syndrome This coexistence of cardiac and renal dysfunction has been classified into 5 types of cardiorenal syndrome based on the initial injured organ and the range of the conditions (acute or chronic) [8]. Results: After 7 days of I/R, the cell contraction was significantly lower in cardiomyocytes compared to sham-treated mice. It was accompanied by a significant decrease in both systolic Ca2+ transients and sarco/endoplasmic reticulum Ca2+ -ATPase (SERCA2a ) activity measured as Ca2+ transients decay.
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