AJP - Heart and Circulatory Physiology, Vol 239, Issue 2 199-H205, Copyright © 1980 by American Physiological Society
Mechanisms of ouabain-induced arterial muscle contraction
N. Toda
Ouabain caused dose-related contractions in helically cut strips of
cerebral, mesenteric, renal, and femoral arteries isolated from dogs and
monkeys; the contractions were elicited at lower concentrations in cerebral
than in the peripheral arteries. Contractions induced by ouabain were
abolished by exposure of cerebral arteries to Ca2+-free media. Contractions
induced by Ca2+ in Ca2+-free media were potentiated by ouabain.
Substitution of LiCl for NaCl and reduction of [K+]0 suppressed the
contractile response of cerebral arteries to ouabain. Pretreatment of dogs
with reserpine abolished the response of peripheral arteries to ouabain but
not the cerebroarterial response. Phentolamine also abolished the response
of peripheral arteries. Once oubain-induced contractions were stabilized,
the alpha-antagonist caused a marked relaxation in peripheral but not in
cerebral arteries. Ouabain-induced contractions appear to be mediated by an
increase in the Ca2+ influx that results mainly from an inhibition of the
electrogenic Na+ pump in low concentrations (cerebral arteries) and from a
release of norepinephrine from nerves in high concentrations (mesenteric,
renal, and femoral arteries).
