Hypertension, Vol 22, 913-921, Copyright © 1993 by American Heart Association
A Huang, D Sun and A Koller
To elucidate the underlying reason or reasons for the increased peripheral
resistance in hypertension, we investigated the pressure- diameter
relation--the myogenic response--of isolated, cannulated arterioles
(approximately 50 microns) of cremaster muscle of 12-week- old Wistar-Kyoto
(WKY) rats, spontaneously hypertensive rats (SHR), and normal Wistar (NW)
rats. All arterioles constricted in response to step increases in perfusion
pressure from 20 to 160 mm Hg. This constriction was, however,
significantly enhanced from 60 to 160 mm Hg in arterioles of SHR compared
with NW or WKY rats. For example, at 80 and 140 mm Hg, respectively, the
normalized diameter (expressed as a percentage of the corresponding passive
diameter of arterioles of SHR) was 11.8% and 27.6% (P < .05) less
compared with those of WKY rats. Endothelium removal eliminated the
enhanced pressure-induced tone in SHR. Similarly, indomethacin (10(-5)
mol/L, sufficient to block prostaglandin synthesis) or SQ 29,548 (10(-6)
mol/L), a thromboxane A2- prostaglandin H2 receptor blocker that inhibited
vasoconstriction to the thromboxane agonist U46619, attenuated the enhanced
pressure- diameter curve and reversed the blunted dilation to arachidonic
acid in SHR. In contrast, the thromboxane A2 synthesis inhibitor CGS 13,080
(5 x 10(-6) mol/L) did not affect the increased pressure-induced tone or
the reduced dilation to arachidonic acid in SHR. Thus, the present findings
suggest that in early hypertension pressure-induced arteriolar constriction
is increased. This seems to be due to an enhanced production of
endothelium-derived constrictor factors, primarily prostaglandin H2.
ARTICLES
Endothelial dysfunction augments myogenic arteriolar constriction in hypertension
Department of Physiology, New York Medical College, Valhalla 10595.
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