Role of connexins in microvascular dysfunction during XXXX .

@entity32 @entity16899 @entity295 @entity43173 @entity19 @entity842 @entity563 @entity35 @entity16898 @entity669
In arterioles, a locally initiated diameter change can propagate rapidly along the vessel length (arteriolar conducted response), thus contributing to arteriolar hemodynamic resistance. The response is underpinned by electrical coupling along the arteriolar endothelial layer. Connexins (Cx; constituents of gap junctions) are required for this coupling. This review addresses the effect of @entity32 ( @entity295 ) on arteriolar conduction and interendothelial electrical coupling. Lipopolysaccharide (LPS; an initiating factor in @entity295 ) and polymicrobial @entity295 (24 h model) attenuate conducted vasoconstriction in @entity19 . In cultured microvascular endothelial cells harvested from @entity35 and @entity19 skeletal muscle, LPS reduces both conducted hyperpolarization-depolarization along capillary-like structures and electrical coupling along confluent cell monolayers. LPS also @entity669 -phosphorylates @entity16899 and @entity563 -dephosphorylates @entity16898 . Since LPS-reduced coupling is @entity16898 - but not @entity16899 -dependent, only @entity16898 dephosphorylation may be consequential. @entity842 (NO) overproduction is critical in advanced @entity295 , since the removal of this overproduction prevents the attenuated conduction. Consistently, (i) exogenous NO in cultured cells reduces coupling in a @entity43173 -dependent manner, and (ii) the septic microvasculature in vivo shows no @entity16898 phenotype. A complex role emerges for endothelial connexins in @entity295 . Initially, LPS may reduce interendothelial coupling and arteriolar conduction by targeting @entity16898 , whereas NO overproduction in advanced @entity295 reduces coupling and conduction by targeting @entity43173 instead.
