Chronic [alpha]1 adrenergic blockade stimulates terminal and arcade
arteriolar development.
Price, Richard J., and Thomas C. Skalak.
Department of Biomedical Engineering, University of Virginia,
Charlottesville, VA 22908
APStracts 3:0097H, 1996.
The arteriolar network undergoes structural adaptation in several
physiological and pathological conditions including exercise,
maturation, hypertension, and reduced tissue perfusion due to
arterial ligation. Although many physical and biochemical stimuli for
arteriolar adaptation have been proposed, the individual
contributions of these specific stimuli have yet to be elucidated.
The objective of this investigation was to test the hypothesis that
hemodynamic stress is an important determinant of growth and
remodeling in the arteriolar network. An immunofluorescence dual
-labeling technique for the smooth muscle (SM) contractile proteins SM
[alpha]-actin and SM myosin heavy chain (MHC) was used to assess
terminal and arcade arteriolar remodeling in the rat gracilis muscle
arteriolar network in response to chronic vasodilation, a stimulus
that elevates circumferential wall stress levels in the arterioles
and capillaries. SM [alpha]-actin, a marker of SM from the earliest
stages of differentiation, was used to delineate the terminal and
arcade arterioles. SM-MHC, a marker of SM in later stages of
differentiation, was used to assess the relative maturity state of SM
in terminal arteriolar endings. The mean percentage of SM-MHC
negative terminal arteriolar endings per muscle, a measure of
terminal arteriolar development, increased from 37.6% to 56.0% after
1 week of prazosin treatment and from 36.3% to 57.6% after 2 weeks of
treatment. The mean number of AA segments with diameters less than 15
[mu]m increased more than threefold from 1.25 to 5.25 after 2 weeks,
consistent with the formation of new AA segments by the anastomoses
of small diameter terminal arterioles. Because arteriolar remodeling
proceeded in a network pattern that has been shown to be consistent
with a circumferential wall stress-growth rule, and inconsistent with
a wall shear stress-growth rule, the experimental results suggest
that circumferential wall stress is a stimulus for arteriolar network
remodeling.
Received 12 October 1995; accepted in final form 1 February 1996.
APS Manuscript Number H956-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96