AJP - Regulatory, Integrative and Comparative Physiology, Vol 244, Issue 2 285-R291, Copyright © 1983 by American Physiological Society
Angiotensin II and bradykinin: interactions between two centrally active peptides
R. E. Lewis, W. E. Hoffman and M. I. Phillips
Two neuropeptides, bradykinin (BK) and angiotensin II (ANG II), produce an
increase in blood pressure when injected into the brain ventricles. This
study is an example of central peptide-peptide interaction and was carried
out to determine if BK and ANG II share a common mechanism in the brain to
control blood pressure and drinking in rats. Prior injection of saralasin
[10 micrograms intraventricularly (ivt)] was found to enhance the pressor
response to ivt BK (5 micrograms) by 44%. The same dose of saralasin
attenuated the pressor response to ivt ANG II (200 ng) by 55%. 50 ng ANG II
and 5 micrograms BK given together ivt did not significantly alter blood
pressure or urine conductance compared to 50 ng ANG II alone. Drinking to
ivt infusions of ANG II (14 ng/min) was significantly attenuated when
combined with BK (0.7 micrograms or 2.8 micrograms/min). Pretreatment with
10 micrograms indomethacin ivt diminished the pressor response to 5
micrograms ivt BK. Prostaglandin E2 (1.4 micrograms/min), but not
prostaglandin A2, inhibited drinking to 14 ng/min ivt infusions of ANG II.
The results suggest that ANG II and BK share an interrelationship with
respect to their central actions: ANG II inhibits the BK pressor response
and BK acts to inhibit drinking induced by ANG II. Prostaglandins of the E
series may mediate these central actions of bradykinins.
