Endocrine Abstracts (2004) 7 P143

Pregnancy-induced plasticity in rat pituitary: a morphological and endocrine study of somatotroph and lactotroph function

MM El-Kasti1, HC Christian2, I Huerta2, N Hill3, DR Matthews3 & T Wells1

1School of Biosciences, Cardiff University, Cardiff, UK; 2Department of Anatomy & Human Genetics, Oxford University, Oxford, UK; 3Oxford Centre for Diabetes, Endocrinology & Metabolism, Oxford University, Oxford, UK.

Pregnancy is associated with increased circulating growth hormone (GH), which is thought to originate from the placenta in humans, but from the pituitary in rats. In this study we investigated the changes in somatotroph and lactotroph populations, and quantified spontaneous and secretagogue-induced GH and prolactin (PRL) secretion during pregnancy in rats.

Using electron microscopy and immunogold labelling, somatotroph and lactotroph populations were quantified in virgin (V) and 1-, 2- and 3-week pregnant Sprague-Dawley rats. During pregnancy, the proportion of type I lactotrophs increased progressively [16.0±1.5% (V; n=3) vs. 26.0±1.2% (3-week; n=3); p<0.05], somatotrophs and type II lactotrophs remained unchanged, and somatomammotrophs were reduced [1.0±0.0% (V) vs 0.2±0.1% (3-week); p<0.01]. These cellular changes were not observed following pseudopregnancy.

Spontaneous GH secretion was measured in conscious pregnant rats. Total secretory output was progressively elevated during pregnancy [AUC: 142.9±25.3ng/ml.min (V; n=6) vs 339.3±39.2ng/ml.min (3-week; n=6); p<0.01]. Although Fourier analysis demonstrated that GH pulse frequency was unchanged, distribution analysis1 revealed a progressive elevation in baseline secretion [OC5: 1.2±0.6ng/ml (V) vs 16.0±4.8ng/ml (3-week); p<0.01], without significant alteration in pulse height (OC95). In contrast, there were no consistent changes in spontaneous PRL secretion.

Circulating GH and PRL responses and somatotroph and lactotroph sensitivity to secretagogue treatment (iv injections of rat ghrelin, rat GRF, TRH, or sulpiride) were determined in chronically cannulated pregnant rats. Although ghrelin failed to elicit PRL secretion at any stage of pregnancy, the robust stimulation of GH secretion remained unaltered.

These findings confirm that the pregnancy-induced increase in circulating GH in rats is due to an elevation in baseline secretion. Although the increase in type I lactotrophs and reduction in somatomammotrophs are dependent upon the presence of the placenta, these additional lactotrophs do not appear to affect PRL secretion during pregnancy.

1. Matthews DR et al, (1991) Clin Endocrinol 35: 245-252.

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