Kathleen S. Curtis, J. Thomas Cunningham, and Cheryl M. Heesch
Am. J. Physiol. 277 (1999)
Am. J. Physiol. 277 (1999)
Pregnancy in humans and other
animals may cause changes in baroreflex function. Specifically, the ability to
increase sympathetic nerve activity (SNA) in response to a hypotensive
challenge appears to be decreased during pregnancy. This could be due to the
fact that the control of sympathetic outflow is altered by hormonal changes
associated with pregnancy. 3a-OH-DHP (reproductive
hormone) has been shown to increase the activity of inhibitory GABAergic pathways
that play an important role in the baroreflex. When 3a-OH-DHP was injected into the RVLM of non-pregnant rats, they
showed inability to increase SNA during hypotensive challenges, similar to what
is seen in pregnant rats. This attenuated increase in SNA in response to a
hypotensive challenge during pregnancy may indicate that there are differences
in the central processing of information related to control of sympathetic outflow.
This study examined Fos immunoreactivity
in pregnant rats after acute decreases in blood pressure to determine whether
the activation of brain stem areas known to be involved in the central control
of SNA is altered by pregnancy. Immunolabeling for dopamine b-hydroxylase (DBH) was also performed to
determine whether pregnancy differentially affected the activity of
catecholamine-containing neurons in response to acute decreases in blood pressure.
To test these points pregnant and virgin rats were injected with either hydralazine
(HDZ; induces hypotension) or an isotonic saline vehicle (VEH; control) and
compared.
Among other things, this study
found that Fos expression in the RVLM of HDZ-treated pregnant rats was less
than that of HDZ-treated virgin female rats, and the difference was specific to
noncatecholaminergic neurons (DBH negative). Additional experiments are
necessary to determine the phenotype and projections of the neurons affected by
pregnancy. The attenuated SNA in HDZ-treated pregnant rats could be attributed
to reproductive hormones augmenting GABAergic inhibitory pathways, or attenuating
ANG II-mediated excitatory pathways.
- Ben Huber
- Ben Huber
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