Premium
FACILITATION OF NORADRENALINE RELEASE BY ISOPRENALINE IN RAT ISOLATED ATRIA DOES NOT INVOLVE ANGIOTENSIN II FORMATION
Author(s) -
Mian M. A.,
Majewski H.,
Rand M. J.
Publication year - 1989
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.1440-1681.1989.tb02401.x
Subject(s) - isoprenaline , saralasin , angiotensin ii , medicine , endocrinology , chemistry , stimulation , renin–angiotensin system , captopril , norepinephrine , dopamine , receptor , blood pressure
SUMMARY 1. Rat isolated atria were incubated with 3 H‐noradrenaline and the intramural sympathetic nerves were stimulated at 2 Hz for 60 s. The stimulation‐induced (SI) efflux of radioactivity was used as an index of release of transmitter noradrenaline. 2. Isoprenaline (0.1 μmol/L) alone did not increase noradrenaline release. Cocaine (30 μmol/L) produced a 73% increase in the stimulation‐induced release of noradrenaline. In the presence of cocaine, isoprenaline enhanced noradrenaline release by 22%. 3. In the presence of cocaine, both angiotensin I (0.3 μmol/L) and angiotensin II (0.3. μmol/L) produced almost two‐fold enhancements in the SI release of noradrenaline. 4. Captopril (5 μmol/L) blocked the facilitatory effect of angiotensin I on nor‐adrenaline release but did not alter that of isoprenaline. 5. Saralasin (0.1 μmol/L) reduced the facilitatory effect of angiotensin II on noradrenaline release but did not alter that of isoprenaline. 6. The findings indicate that the facilitation of noradrenaline release by isoprenaline in rat atria is not mediated by local formation of angiotensin II.