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Department of Physiology, New York Medical College, Valhalla, New York 10595
Previous studies show that
agonist-induced, nitric oxide (NO)-mediated arteriolar dilations are
greater in female than in male rats. Thus we hypothesized that
flow-dependent arteriolar dilation, which is in part mediated by NO, is
also greater in females than in males. Gracilis muscle arterioles from
12-wk-old female and male Wistar rats were isolated, cannulated, and
pressurized. At 80 mmHg of perfusion pressure, the active diameter and
passive diameter (PD) of arterioles of female and male rats were 58.3 ± 3.4 and 53.2 ± 2.6 µm as well as 103.6 ± 4.0 and 115.3 ± 4.8 µm, respectively. Dilations to step increases in
perfusate flow from 0 to 25 µl/min were significantly greater in
arterioles of female rats and ovariectomized rats with estrogen
replacement (OVE) than in male and ovariectomized female (OV) rats
(98.6 ± 0.6 and 97.4 ± 1.1% vs. 72.6 ± 3.3 and 72.5 ± 3.6% of PD at 25 µl/min). Calculation of wall shear stress (WSS)
revealed that the maintained WSS was significantly lower in arterioles
of female than in those of male rats (~20 vs. ~35
dyn/cm2). After indomethacin
pretreatment,
N
-nitro-L-arginine
methyl ester (L-NAME;
10
4 M) eliminated
flow-dependent dilation in arterioles of male and OV rats but only
attenuated (by ~50%) the responses in arterioles of female and OVE
rats. In vessels of these latter two groups of rats, the remaining
flow-induced dilation was completely eliminated by administration of
105 M Hb or
103 M
L-NAME. The greater flow/shear
stress-induced dilation of arterioles of female rats indicates a gender
difference in the regulation of WSS, which is likely to be due to the
greater release of NO in female vessels requiring the chronic presence
of estrogen. These findings suggest an important role for estrogen in
the regulation of peripheral resistance in females.
microvessels; arterioles; endothelium; peripheral resistance
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