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By J.H.U. Brown, James Francis Dickson

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T h u s r a t h e r t h a n being a C R F , vasopressin could be viewed as a C R F releasing factor. T h e subsequent experiments of Hedge and Smelik (1969) confirmed and extended these results. These workers showed t h a t vasopressin was effective in producing only a t r a n sient stimulus to A C T H release when the production of C R F had been inhibited by prior t r e a t m e n t with dexamethasone. Furthermore, when a first stimulus was applied to release previously stored and synthesized C R F , then subsequent t r e a t m e n t with vasopressin was ineffective.

If the melatonin-adrenergic mechanism is involved in the mediation of the circadian r h y t h m , the findings of Krieger and Rizzo (1969) with reserpine m a y be explained by a concurrent action on two opposing parts of the system. At present, the hypothesis t h a t multiple indole-active sites are involved in the driving of the circadian r h y t h m seems attractive, although neuroanatomical findings indicate a dominance of the anterior hypothalamic p a t h w a y . I n any event, the circadian r h y t h m must be included in any comprehensive model of adrenocortical control.

W u r t m a n (1967) found t h a t the r h y t h m of H I O M T depended exclusively upon light (which suppresses it) through a path which coursed from the retina to the brainstem to the cervical sympathetic nerves to the pineal. Recently, R a l p h and associates (1971) have questioned W u r t m a n ' s finding of total light dependence. R a l p h et al. found t h a t a r h y t h m of pineal melatonin persists after blinding or in darkness, although persistent light leads to persistent suppression of melatonin.

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