Electromechanical coupling and the conducted vasomotor response
.
Xia, J., and Brian R. Duling.
Department of Molecular Physiology and Biological Physics, School
of Medicine, University of Virginia, Charlottesville, VA 22908
APStracts 2:0175H, 1995.
Conducted vasomotor responses are viewed as one of the mechanisms for
functional integration of the components of the microvascular tree.
It is hypothesized that the conducted vasomotor response is the
result of an electrical current and its passive, electrotonic spread
along the length of a microvessel. We tested this hypothesis in
isolated, unpressurized arterioles from the hamster cheek pouch using
conventional intracellular membrane potential recording techniques.
KCl or phenylephrine (PE) were applied through a glass pipette placed
close to the arteriole, either by pressure pulse ejection or by
ionophoresis respectively. Cell membrane potentials were recorded
using glass microelectrodes filled with 2 M KCl. The mean resting
membrane potential (RMP) was 67 +/- 1 mV (n = 30). KCl and PE pulse
-stimulation both induced transient depolarizations at the site of
stimulation (local) that could also be recorded with decreasing
amplitude over several hundred [mu]m from the local site. In addition
to the electrical responses following KCl and PE stimulations,
transient vasomotor responses were also evoked at both local and
conducted (560 [mu]m) sites. It was noted, however, that the
conducted vasomotor response could not be induced until the conducted
electrical response exceeded a threshold of -45 mV for a minimum
amount of time. The relationship between the amplitude of diameter
change, expressed as a percentage of resting diameter, and the
amplitude-time area of depolarization above -45 mV was examined for
both KCl and PE at the local and 560 [mu]m sites. This relationship
was the same for KCl at the local site, and at 560 [mu]m site, as
well as for PE at 560 [mu]m site. All of these responses were
significantly different from that for PE at the local site.
Nifedipine (1[mu]M) did not change the electrical response of either
the local or 560 [mu]m site, but greatly reduced the local and
conducted mechanical responses to both KCl and PE. Our results
indicate that the conducted component of the vasomotor responses to
both KCl and PE are the result of the generation and subsequent
conduction of electrical signals along the vessel, but that the
corresponding mechanical response occurs only when the electrical
response exceeds a threshold level. We found no evidence for a
nonelectrical factor (i.e. pharmacomechanical coupling) in the
conducted vasomotor response to PE, even though it is clearly present
in the local response.
Received 19 January 1995; accepted in final form 13 April 1995.
APS Manuscript Number H51-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 9 May 1995.