Constructing a continuous hemodiafiltration-type circulatory model of acute kidney injury in pigs.

Introduction: Animal-model experimental systems capable of reflecting the effects of devices for continuous renal replacement therapy (CRRT) on living organisms are limited; thus, aimed to construct an animal model of AKI-CRRT using pigs.

Methods: Pigs were subjected to renal artery ischemia-reperfusion injury (IRI) and then to a maximum of 24 h of continuous hemodiafiltration (CHDF)-type CRRT.

Results: Post-IRI, pigs' creatinine levels rose threefold, and they exhibited 24 h of anuria and clear aggravation of oxidative stress, demonstrating successful induction of AKI for CRRT.

Synapsin I is phosphorylated at Ser603 by p21-activated kinases (PAKs) in vitro and in PC12 cells stimulated with bradykinin.

The function of synapsin I is regulated by phosphorylation of the molecule at multiple sites; among them, the Ser(603) residue (site 3) is considered to be a pivotal site targeted by Ca(2+)/calmodulin-dependent kinase II (CaMKII). Although phosphorylation of the Ser(603) residue responds to several kinds of stimuli, it is unlikely that many or all of the stimuli activate the CaMKII-involved pathway. Among the several stimulants tested in PC12 cells, bradykinin evoked the phosphorylation of Ser(603) without inducing the autophosphorylation of CaMKII, which was determined using phosphorylation site-specific antibodies against phospho-Ser(603)-synapsin I (pS603-Syn I-Ab) and phospho-Thr(286/287)-CaMKII.