Angiotensin III-induced modulation of neurogenic responses in the rabbit vas deferens and portal vein

George J. Trachte, Edmund J. Sybertz, Marshall Michener, S. Bruce Binder, Michael J. Peach

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

The effects of prostaglandin synthesis inhibitors on the presynaptic actions of angiotensin (ang) II and III were examined in isolated rabbit vasa deferentia and portal veins. Ang II caused dose-dependent potentiation of low frequency, nerve stimulation in vasa deferentia and portal vein. Indomethacin (26 μM) enhanced the electrically-induced contractions in the vasa deferentia only but did not alter the potency of ang II in either preparation. In contrast, ang II decreased contractions in vasa deferentia induced by nerve stimulation by up to 36% (10-6 M) and potentiated these contractions at concentrations higher than 10-6 M. The inhibitory action of ang III on vasa deferentia was converted to potentiation by pretreatment with indomethacin or mepacrine. Exogenous PGE2 blocked low frequency nerve stimulation and not responses to norepinephrine. This prostaglandin appeared to mimic ang III in the vas deferens. No effects of ang III were observed if the contractions were induced by exogenous alpha adrenergic agonists. [Sar1, Ala8] and II antagonized all responses to the angiotensins, whereas [Sar1, Cys-CH38] ang II selectively antagonized the angiotensin-induced potentiation. Responses in field-stimulated portal veins were potentiated by ang III and this response was unaffected by indomethacin. This investigation strongly suggests the existence of at least two ang receptors in the vas deferens and demonstrates for the first time selective responses to the octa- and heptapeptides in the same effector organ.

Original languageEnglish (US)
Pages (from-to)327-333
Number of pages7
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Volume326
Issue number4
DOIs
StatePublished - Dec 1984

Keywords

  • Adrenergic transmission
  • Angiotensin II
  • Angiotensin III
  • Presynaptic modulation
  • Prostaglandins

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