Mechanism of inhibition of tubuloglomerular feedback by CO and cGMP.

ABSTRACT: Tubuloglomerular feedback (TGF) is a mechanism that senses NaCl in the macula densa (MD) and causes constriction of the afferent arteriole. CO, either endogenous or exogenous, inhibits TGF at least in part via cGMP. We hypothesize that CO in the MD, acting via both cGMP-dependent and -independent mechanisms, attenuates TGF by acting downstream from depolarization and calcium entry into the MD cells. In vitro, microdissected rabbit afferent arterioles and their MD were simultaneously perfused and TGF was measured as the decrease in afferent arteriole diameter. MD depolarization was induced with ionophores, while adding the CO-releasing molecule-3 to the MD perfusate at nontoxic concentrations. CO-releasing molecule-3 blunted depolarization-induced TGF at 50 μmol/L, from 3.6±0.4 to 2.5±0.4 µ

SUBMITTER: Ren Y 

PROVIDER: S-EPMC3821182 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature