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Effects of Norepinephrine on Cyclic Nucleotide Levels in Dog Thyroid Slices^*

YUJI AIYOSHI, KAMEJIRO YAMASHITA, SONO YAMASHITA and ETSURO OGATA

Department of Medicine, University ofTsukuba Ibaraki, 300–31, Japan
The Section of Surgery, (Y.A.), Central Hospital of Ibaraki, Tomobe, Nishi-Ibaraki, 309–17, Japan

Abstract

In vitro effects of norepinephrine on cyclic nucleotide levels were studied in dog thyroid slices incubated in Krebs-Ringer bicarbonate buffer. Norepinephrine (1-100 HM) caused a rise in cAMP levels. By using the maximal dose of norepinephrine (100 /XM) the cAMP concentration reached a peak (about 200% of the basal) within 1 min and declined thereafter, returning to the basal level within 10 min. cGMP concentrations were increased by norepinephrine at concentrations higher than 10µM. The maximal dose of norepinephrine (100 µM) caused a gradual increase in cGMP levels, reaching a peak of about 300% of the basal after 30 min.

A β-adrenergic blocking agent, propranolol (100 µM), prevented the effect of norepinephrine on cAMP levels, but not on cGMP levels. Phentolamine, an aadrenergic blocking agent, had little or no effect on norepinephrine stimulation of cAMP levels, although it caused a marked inhibition of the norepinephrine stimulation of cGMP levels. Slices incubated with norepinephrine exhibited a diminished responsiveness of the cAMP system when they were later reexposed to this catecholamine. Exclusion of Ca⁺⁺ from the buffer had no effect on the basal levels of cAMP and cGMP. Effects of norepinephrine on the cGMP levels were attenuated by removing Ca⁺⁺ from the buffer, whereas those effects on the cAMP were not influenced by this procedure.

These findings indicate that in the dog thyroid gland, norepinephrine activates the cAMP system via β-adrenergic receptors and the cGMP system via a-adrenergic receptors. Contrary to cGMP, stimulation of cAMP was not Ca⁺⁺-dependent. (Endocrinology 102: 1527, 1978)

Footnotes

^* This study was supported in part by grants from the University of Tsukuba project and from the Ministry of Welfare of Japan.

To whom all correspondence and requests for reprints should be addressed: Department of Medicine, University of Tsukuba, Ibaraki, 300–31, Japan.

Received April 11, 1977.