By Ling Xu and Alan F. Sved
Angiotensin II (ANG II) levels have two competing influences
on sympathetic outflow. ANG II seems to increase SNA. However, it also acts as
a vasoconstrictor to increases MAP, which in turn stimulates baroreceptors,
thereby inhibiting SNA. This makes it hard to determine the direct actions of
ANG II. In order to determine what it directly effects, this experiment
administered ANG II to sinoaortic-denervated rats (no baroreflex).
Baseline MAP was higher in SAD than control rats. In control
rats, infusion of ANG II rapidly increased MAP, which was accompanied by
bradychardia and sympathoinhibition. Over time, HR and LSNA slowly returned to
normal by the end of the infusion period. In contrast, denervated rats had a
larger initial increase in MAP upon ANG II injection. However, the increase in
MAP was accompanied by increased HR and LSNA, rather than the decrease seen in the
control group. This indicates that ANG II can produce rapid sympathoexcitation.
There are several sites at which ANG II could act to increase SNA and HR. It
has been shown to act directly on the heart in high concentrations.
Alternatively, in might increase HR by increasing sympathetic neural activity
to the heart and/or decreasing parasympathetic neural activity to the heart.
ANG II may act on areas of the CNS lacking a blood brain barrier, such as the
area postrema. I will expand on its effects on the CNS in future blog posts.
No comments:
Post a Comment