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PERTUSSIS TOXIN ATTENUATES ANGIOTENSIN II BUT NOT β‐ADRENOCEPTOR FACILITATION OF NORADRENALINE RELEASE FROM RAT KIDNEY CORTEX
Author(s) -
Murphy Timothy V.,
Majewski Henryk
Publication year - 1990
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1990.tb01352.x
Subject(s) - isoprenaline , pertussis toxin , endocrinology , medicine , stimulation , angiotensin ii , chemistry , receptor , agonist , angiotensin receptor , muscarinic acetylcholine receptor , renin–angiotensin system , g protein , biology , blood pressure
SUMMARY 1. Angiotensin II (AII; 0.01 and 0.1 μmol/L), angiotensin I (AI, 0.1 μmol/L) and the β‐adrenoceptor agonist isoprenaline (0.1 μmol/L) all facilitated the stimulation‐induced outflow of radioactivity from slices of rat kidney cortex incubated in [ 3 H]‐noradrenaline. 2. Treatment of rats with pertussis toxin (25 and 50 μg/kg i.v.) to inactivate G‐proteins attenuated the facilitation caused by AII and AI, but not that caused by isoprenaline. 3. The hypothesis that isoprenaline enhances noradrenaline release by generating AII to activate facilitatory prejunctional AII receptors is not supported by the present study. The hypothesis predicts that pertussis toxin, by inactivating the G‐proteins associated with AII receptors, should have inhibited the facilitatory effect of isoprenaline. This did not occur.