Effect of thyroid status on the prolactin-releasing action of vasoactive intestinal peptide in humans: comparison with the action of thyrotropin-releasing hormone.

Abstract

Recent studies have shown that primary hypothyroidism induced in the rat was able to stimulate the biosynthesis of vasoactive intestinal peptide (VIP) in the anterior pituitary (AP). Since the AP VIP is known to stimulate prolactin (PRL) secretion through a paracrine and/or autocrine mechanism, it is interesting to hypothesize that hyperprolactinemia seen in hypothyroid patients may at least in part be due to a paracrine effect of elevated VIP on AP PRL secretion. Prompted by this information, we in the present study examined the effect of VIP load on PRL secretion in patients with primary hyperthyroidism or hypothyroidism, and compared the data with those from thyrotropin-releasing hormone (TRH) load performed in the same patients. Eight female patients with Graves' disease and 8 females with chronic thyroiditis received intravenous bolus injections of VIP (100 micrograms) and TRH (500 micrograms) 2-3 days apart from each other, during both the dysthyroid and euthyroid (attained by medical treatment) states. Compared to the data in the euthyroid state of the respective group, hyperthyroidism was associated with a lower basal PRL level and a lower PRL responsiveness (estimated by net percent increase in PRL) to TRH, whereas hypothyroidism was associated with higher values of these parameters. With respect to VIP, although the peptide was able to significantly stimulate PRL secretion during both the dysthyroid and euthyroid states of hyper- and hypothyroid patients, PRL responsiveness to VIP was essentially the same regardless of thyroid status.(ABSTRACT TRUNCATED AT 250 WORDS)