<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Previous studies have demonstrated that insulin and
IGF-1 both increase lumbar sympathetic nerve activity
(LSNA) and decrease mean arterial pressure
(MAP). We hypothesized that the peripheral responses
to insulin and IGF-1 are mediated, at least
in part, <italic>via</italic> the central nervous system. In this study
we determined the effects of the peripheral administration
of both insulin and IGF-1 on cardiovascular
dynamics and LSNA following removal of the area
postrema (APX), a major site of blood-brain communication.
Insulin infusion in normal rats decreased
MAP but increased HR and LSNA. When
insulin was infused in APX rats it also decreased the
MAP but the MAP recovered rapidly and plateaued
at a level equivalent to normals after 40 min. Insulin
significantly increased the HR and LSNA in the
APX rats compared to normals. However, when hypoglycemia
was prevented by glucose infusion,
the HR and LSNA responses to insulin in the APX
rats were similar to normals. IGF-1 also decreased
MAP and to a greater extent in the APX rats
compared to normals but the increased LSNA in
APX rats was equivalent to normals. The APX rats
when compared to normals had a greater sensitivity
to insulin-induced hypoglycemia while IGF-1 decreased
the plasma glucose to a lesser degree in APX
rats. We conclude that insulin and IGF-1 entry into
the CNS at least <italic>via</italic> the area postrema does not
contribute significantly to the hypotensive response
and that the greater depressor response to IGF-1 is
likely due to enhanced vascular sensitivity in APX
rats. The increased HR and LSNA following insulin
were likely mediated by an increased reflexive
response to hypoglycemia.</p>
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Int J Exp Diabetes Res. 2000; 1(1):59-67