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Endocrinology, Vol 105, 1093-1099, Copyright © 1979 by Endocrine Society
ARTICLES |
WJ De Greef and JD Neill
Tonic hypothalamic inhibition of PRL release is partially explainable by dopamine secretion into hypophysial portal blood. However, the probable existence of other PRL-inhibiting factors as well as PRL- releasing factors opens to question the role of dopamine in the dynamic regulation of PRL secretion. We investigated this question in the present study by measuring dopamine concentrations in hypophysial stalk blood of the rat during the surgess of PRL secretion induced by cervical stimulation. Urethane anesthesia, necessary for the surgery attendant to stalk blood collection, did not suppress the surge of PRL secretion induced by cervical stimulation 16-24 h previously. Increases in plasma PRL levels during such surges were 4- to 5-fold above baseline. Dopamine concentrations in hypophysial stalk plasma were 36% lower in cervically stimulated than in control rats during the diurnal and nocturnal PRL surges. However, dopamine levels were not different during the interval between the surges, a time at which PRL levels are similar in stimulated and control rats. To determine if the observed 36% decrease in dopamine levels might account for the associated 4- to 5-fold rise in PRL levels during surges, we treated rats with alpha- methyl-p-tyrosine to block endogenous dopamine secretion and then infused dopamine at various rates to achieve plasma dopamine concentrations throughout the physiological range. These dopamine levels significantly but incompletely suppressed PRL levels, and a 36% decrease in administered dopamine was associated with only an approximate 1.5-fold increase in plasma PRL levels. Thus, it is unlikely that changes in dopamine secretion alone can account for the increased release of PRL engendered by cervical stimulation.
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