Angiotensin II and bradykinin: Interactions between two centrally active peptides

R. E. Lewis, W. E. Hoffman, M. I. Phillips

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

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 μg intraventricularly (ivt)] was found to enhance the pressor response to ivt BK (5 μg) 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 μg 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 μg or 2.8 μg/min). Pretreatment with 10 μg indomethacin ivt diminished the pressor response to 5 μg ivt BK. Prostaglandin E2 (1.4 μg/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.

Original languageEnglish (US)
Pages (from-to)R285-R291
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume13
Issue number2
DOIs
StatePublished - 1983

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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