Factors modulating the secretion of thyrotropin and other hormones of the thyroid axis.

Abstract

The first portion of this paper is devoted to an overview of the normal function of the hypothalamo-pituitary-thyroid axis. This section emphasizes areas of current research interest and it identifies several sites and mechanisms that are potentially important interfaces with toxins or toxic mechanisms. We then describe an in vitro technique for the continuous superfusion of enzymatically dispersed pituitary cells; this approach is particularly valuable in studying the dynamics of the TSH responses to the factors known (or suspected) to regulate TSH secretion in vivo. Using this technique, we have found that 10(-5)M prostaglandin (PG)I2 stimulates TSH secretion without altering the response to TRH (10(-8)M), and that this stimulation is not due to its rapid conversion to 6-keto PGF1 alpha. In contrast PGs of the E series (PGE1 and PGE2, 10(-5)M) increase responsiveness to TRH but have no effect alone. We found no effects of any of the other prostanoids tested (PGs A2, B2, F1 alpha, F2 alpha, thromboxanes A2 and B2, and the endoperoxide analog, U-44069. Somatostain (10(-9)M inhibits TRH-induced TSH secretion, but does not alter the responsiveness to PGI2. These findings suggest that somatostatin blocks TSH secretion at a point that is functionally prior to the involvement of the PGs, and perhaps does so by blocking synthesis or limiting availability of selected PGs.

Assessment of Pentachlorophenol Toxicity in Newborn Calves: Clinicopathology and Tissue Residues

“…Since the free hormone acts in a negative feedback fashion on the hypothalamopituitary axis to regulate T4 biosynthesis via thyroid stimulating hormone secretion, decreased TBG would cause a concomitant decrease in T4 levels. Triiodothyronine is derived in large part from peripheral (extrathyroidally) deiodination of T4 (Hedge et al, 1981). Although TBG was not measured, total protein, albumin and globulin concentrations decreased 23%, 18% and 30%, respectively, in the 10 mg/kg tPCP calves (table 6).…”

“…The mechanism(s) of action underlying these effects has not been definitively elucidated. Moreover, given the interactive nature of the hypothalamopituitarythyroid axis, there are numerous steps where toxicants can possibly act (Hedge et al, 1981;Thomas and Bell, 1984). First, as noted by Bastomsky (1977) in TCDD-or PCB-treated rats, induction of hepatic glucuronyl transferase increased the conjugation and biliary excretion of I"4, thereby lowering blood levels of the hormone.…”

Hipertensão arterial pulmonar e doenças da tireoide

“…(29) In addition, one group of authors demonstrated that PGI 2 stimulates TSH secretion. (30) The enzyme responsible for NO formation, NO synthase, is a potent endothelium-derived vasodilator. There is an association between PAH and decreased levels of this enzyme.…”