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Hair Loss Study Abstract: Potassium channel conductance as a control mechanism in hair follicles.
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Title
Potassium channel conductance as a control mechanism in hair follicles.
Author
Buhl AE, Conrad SJ, Waldon DJ, Brunden MN
Address
Dermatology Research, Upjohn Company, Kalamazoo, MI 49001.
Source
J Invest Dermatol, 101: 1 Suppl, 1993 Jul, 148S-152S
Abstract
The opening of intracellular potassium channels is a common mechanism of action for a
set of anti-hypertensive drugs that includes the hair-growth-inducing agent minoxidil.
Recent work suggests potassium channel openers (PCOs) also influence hair growth.
Correlative studies demonstrate that a series of PCOs including minoxidil, pinacidil,
P-1075, an active pinacidil analog, RP-49,356, cromakalim, and nicorandil maintain hair
growth in cultured vibrissa follicles. Studies using balding stumptail macaques verify
that minoxidil, P-1075, and cromakalim but not RP-49,356 stimulate hair growth. The
definition of potassium channels and documentation of drug effects on these channels is
classically done using electrophysiologic techniques. Such studies require the
identification and isolation of target cells. Both these are among the unsolved problems
in the area of hair biology. Estimating K+ flux using 86Rb+ as a K+ tracer is an accepted
method of assessing potassium channel conductance in other organ systems. Both pinacidil
and RP-49,356 induce measurable Rb+ flux in isolated vibrissa follicles and a hair
epithelial cell line whereas neither minoxidil nor minoxidil sulfate had measurable
effects. Potassium channels have been studied successfully in other organ systems using
specific pharmacologic blockers for the various channel subtypes. Blockers including
glyburide, tetraethylammonium, and procaine failed to inhibit minoxidil stimulation of
cultured follicles. The current explosion of knowledge on potassium channel biology,
cloning of channels, and continued progress in hair biology promise to clarify the role of
K+ ions in the control of hair follicles.
Language of Publication
English
Unique Identifier
93315888
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