naloxone and Hypothyroidism

The role of endogenous opiate peptides in puerperal hyperprolactinaemia, and in the control of TSH in hypothyroidism, has been investigated. Although exogenous opioids raise prolactin and TSH levels, 16 mg naloxone administered to women on days 2-4 of the puerperium produced no significant change in serum prolactin and the same dose of naloxone had no significant effect on serum TSH in six primary hypothyroid patients. There is little evidence that endogenous opioid peptides are major modulators of prolactin or TSH in man under these conditions.

Topics: Endorphins; Female; Humans; Hypothyroidism; Naloxone; Postpartum Period; Pregnancy; Prolactin; Thyrotropin

Male golden Syrian hamsters made hypothyroid by 5 wk of propylthiouracil (PTU) treatment and control hamsters given tap water were studied. Both groups of nine animals demonstrated increased oxygen consumption after SC naloxone administration relative to saline treatment. Naloxone stimulated ventilation and ventilation in response to hypoxic (10% O2) and hyperoxic, hypercapnic (7% CO2 in oxygen) challenges in control hamsters. Relative to their responses to saline, PTU-treated hamsters exhibited no stimulation of ventilation nor of ventilation in response to the gas challenges after naloxone treatment. These results suggest that (a) the stimulation of oxygen consumption by naloxone does not directly increase ventilation; and (b) thyroid hormone status in the hamster affects opioid modulation of ventilation.

Topics: Animals; Carbon Dioxide; Cricetinae; Hypothyroidism; Injections, Subcutaneous; Male; Mesocricetus; Naloxone; Oxygen; Propylthiouracil; Receptors, Opioid; Respiration; Thyroid Hormones

The effects of morphine (10 mg i.v.), an opioid agonist, and of naloxone (10 mg i.v.), an opioid antagonist, on serum levels of TSH and PRL were studied in 7 hypothyroid patients and in 5 normal volunteers. Morphine administration induced a prompt, significant increase in serum TSH and PRL in all subjects. The degree of PRL release after morphine was similar in the two groups, while, as regards TSH, the increase was more evident in hypothyroid subjects. Pretreatment with naloxone (4 mg i.v. 5 min before morphine administration) blocked these effects in all subjects. In contrast, naloxone alone was not able to affect significantly TSH and PRL secretion. Moreover, in 5 other euthyroid volunteers, morphine significantly enhanced the response of TSH and PRL to TRH stimulation (200 micrograms i.v.). These data demonstrate that morphine exerts a stimulatory action on TSH and PRL secretion: the possible mode of action of this drug and the physiologic significance of these findings are discussed.

Topics: Adult; Aged; Female; Humans; Hypothyroidism; Male; Middle Aged; Morphine; Naloxone; Prolactin; Thyrotropin; Thyrotropin-Releasing Hormone

This study assessed the effect of the opiate antagonist naloxone on anterior pituitary hormone release in normal subjects and patients with disturbances of the gonadotropic axis. Intravenous bolus injections of naloxone resulted in a rise of plasma LH, but had no significant effect on plasma levels of FSH or PRL. It also failed to alter the LH, FSH, or TSH response to LRF and TRH, although it did augment the PRL response to TRH. Slow iv infusion of naloxone resulted in increased plasma LH and FSH concentrations in both normal subjects and patients with hyperprolactinemia. The rise of LH correlated with the mean basal LH concentrations; a low basal level only responded to naloxone with a small increase in circulating LH concentration and vice versa. This relationship of the response of LH to the resting levels also held in several other pathological states in which there were marked differences of androgen and estrogen status as well as up to a 100-fold variation in basal LH concentrations. It is concluded that LH is under inhibitory opioid control both in normal subjects and in widely differing pathological states of the gonadotropic axis.

Topics: Adenoma; Adult; Craniopharyngioma; Female; Follicle Stimulating Hormone; Humans; Hypothyroidism; Luteinizing Hormone; Male; Naloxone; Pituitary Neoplasms; Polycystic Ovary Syndrome; Prolactin