Why the study?
Does excess potassium alter the contractile response to prostaglandin F2α in isolated dog arteries?
Does excess potassium alter the contractile response to prostaglandin F2α in isolated dog arteries?
Contractions caused by PGF2α in dog arteries at specific concentrations may not be associated with membrane depolarization, as they are not attenuated by excess potassium.
May indicate depolarization-independent PGF2α contraction in canine arteries; leaves open relevance to human vessels or in vivo settings.
Concentration-response curve for prostaglandin (PG) F2α in helical strips of dog cerebral, coronary and mesenteric arteries were compared in control media and in those in which all the NaCI was replaced with isomolar KCI. Contractile responses to PGF2α in concentrations up to 2×10−6 M in cerebral arteries, to 10−5 M in coronary arteries and to 5×10−7 M in mesenteric arteries were not attenuated by excess K+. Contractions caused by PGF2α, at least at these concentrations or lower, may not be associated with membrane depolarization.
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Toda et al. (1988) studied this question.
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