Lipopolysaccharide (LPS) enhancement of outward current in lung pericytes.
Patch clamp methods were used to study the effect of lipopolysaccharide (LPS), an endotoxin produced by gram-negative bacteria, on voltage-dependent outward current of lung pericytes. Pericytes are located in capillary walls and may mediate pathological changes in microvascular hemodynamics and permeability that accompany endotoxin-mediated pulmonary edema. Previous studies have shown that LPS reduces lung pericyte contractility. Lung pericytes exhibited a voltage-dependent outward current, presumed to be K+ current, and this current increased in magnitude in response to LPS. Cells incubated for 48 hr without LPS (control) had an average peak current at 50 mV of 101 pA (n = 5 cells), whereas cells incubated with 100 mg/ml LPS had an average peak current of 927 pA (n = 9 cells, P<0.01 compared to control). When held at 50 mV for 50 msec, net outward current decreased in control cells by 10.7% and in LPS-treated cells by 2.6% (P<0.05). The increased activation of outward current in LPS-treated cells may be due to a previously inactive potassium channel and may mediate LPS-induced relaxation of the lung pericyte.
Herskovic
J J
JJ
Department of Physiology, Wayne State University, Detroit, MI, 48201, USA.
Speyer
C L
CL
Simples
J E
JE
Steffes
C P
CP
Ram
J L
JL
D000818:Animals; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000098:blood supply* / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D023421:Models, Animal; D020286:Pericytes / Q000187:drug effects* / Q000502:physiology*; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley
D008070:Lipopolysaccharides; D024642:Potassium Channels, Voltage-Gated