-transparent.png){kind=logo}
Trifluoperazine (5-200 microM) stimulated the release of 3H-NE from isolated whole pineal glands in a dose dependent manner. Trifluoperazine-induced release was not dependent on extracellular Ca++, whereas 60 mM K+-evoked release was attenuated in the presence of EGTA and zero Ca++ Krebs. 60 mM K+ and 50 microM trifluoperazine produced an additive effect on 3H-NE release. Clonidine (5 microM) significantly reduced trifluoperazine-induced release by approximately 50% in the presence of Ca++, and in its absence, clonidine significantly attenuated the trifluoperazine response by 42%. Thus trifluoperazine may be acting upon the alpha 2 receptor or intracellular stores of Ca++. These intracellular interactions remain for further study.
K A Yurko, and
L F Quenzer
January 1987,
Advances in experimental medicine and biology,
K A Yurko, and
L F Quenzer
July 1987,
The Journal of endocrinology,
K A Yurko, and
L F Quenzer
May 1969,
European journal of pharmacology,
K A Yurko, and
L F Quenzer
September 1985,
Brain research,
K A Yurko, and
L F Quenzer
May 1989,
Zhongguo yao li xue bao = Acta pharmacologica Sinica,
K A Yurko, and
L F Quenzer
April 1970,
The Journal of pharmacology and experimental therapeutics,
K A Yurko, and
L F Quenzer
July 1988,
Neuroendocrinology,
K A Yurko, and
L F Quenzer
May 1974,
Life sciences,
K A Yurko, and
L F Quenzer
August 1982,
Japanese journal of pharmacology,
K A Yurko, and
L F Quenzer
June 1989,
Molecular and cellular endocrinology,
