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Thyrotropin-releasing hormone (TRH) is engaged in the modulation of the hypothalamo-neurohypophysial system activity. Effects of repeated intravenously injections of TRH in a dose of 100 ng/100 g b.w. on vasopressin (VP) and oxytocin (OT) biosynthesis and release from the hypothalamo-neurohypophysial system was investigated in rats in different age (1-, 3- or 7-months of the life). To estimate the biosynthesis rate of both neurohormones the colchicine procedure was used (the dose of 5 microg/5 microl icv 20 hours before the decapitation). It has been observed that vasopressin synthesis in the hypothalamus increased gradually with maturation of rats, while OT biosynthesis decreased in the same animals. Hypothalamic biosynthesis rate of VP and OT is most effective in youngest rats and declines during the adolescence of animals. Thyrotropin-releasing hormone directly affects VP-ergic and OT-ergic hypothalamic neurons activity and both neurohormones biosynthesis process. This effect, however, is opposed: TRH acts as a stimulator of vasopressin biosynthesis most of all in young male rats and as an inhibitor for oxytocin biosynthesis especially in mature animals.

A thorough presentation of the influence of thyroliberin (TRH) on vasopressin and oxytocin release from the hypothalamo-neurohypophysial system is presented. Thyroliberin affects in different ways both neurohormone secretion in females during lactation according to the water-electrolyte metabolism in the course of the circadian rhythm of vasopressin and oxytocin release as well as during in vitro incubation of isolated neurointermediate lobe or hypothalamo-neurohypohysial explants. The results showed that: TRH acts as a stimulator of oxytocin release into the blood by equilibrated water-electrolyte metabolism, TRH acts in the central nervous system as an inhibitory neuromodulator of vasopressin and oxytocin release from the hypothalamo-neurohypophysial system under in vitro conditions, by osmotic stimulation, as well as in females during lactation, TRH inhibits AVP release in acute bleeding-provoked hypovolemia and alters the circadian rhythm of vasopressin and oxytocin release. It is assumed that this neuropeptide can interact with the mechanisms engaged in vasopressin and oxytocin release and can disturb these mechanisms, especially under conditions of augmented demand of the organism for these neurohormones.

Since the thyrotropin-releasing hormone (TRH) can modulate the processes of vasopressin (AVP) and oxytocin (OT) biosynthesis and release mainly at the hypothalamo-neurohypophysial level, the present experiments were undertaken to estimate whether TRH, administered intravenously in different doses, modifies these mechanisms under conditions of osmotic stimulation, brought about by dehydration. AVP and OT contents in the hypothalamus and neurohypophysis as well as plasma levels of AVP, OT, free thyroxine (FT4) and free triiodothyronine (FT3) were studied after intravenously TRH treatment in euhydrated and dehydrated for two days male rats. Under conditions of equilibrated water metabolism TRH diminished significantly the hypothalamic and neurohypophysial AVP and OT content but was without the effect on plasma oxytocin level; however, TRH in a dose of 100 ng/100 g b.w. raised plasma AVP level. TRH, injected i.v. to dehydrated animals, resulted in a diminution of AVP content in the hypothalamus but did not affect the hypothalamic OT stores. After osmotic stimulation, neurohypophysial AVP and OT release was significantly restricted in TRH-treated rats. Under the same conditions, injections of TRH were followed by a significant decrease of plasma OT level. I.v. injected TRH enhanced somewhat FT3 concentration in blood plasma of euhydrated animals but diminished FT4 plasma level during dehydration. Data from the present study suggest that TRH displays different character of action on vasopressin and oxytocin secretion in relation to the actual state of water metabolism.

The effect of thyrotropin-releasing hormone (TRH; 200 ng i.c.v.) on oxytocin (OT), vasopressin (AVP) and prolactin (PRL) release was estimated in female Wistar rats during midlactation. The hypothalamo-neurohypophysial radioimmunoassayed OT and AVP storage as well as blood plasma level of both neurohypophysial hormones and PRL in females suckled or not suckled have been studied. I.c.v. administration of TRH increased AVP content both in the hypothalamus and neurohypophysis of suckled females; however, plasma AVP level did not change. TRH increased the hypothalamic as well as neurohypophysial OT content during suckling. Simultaneously, TRH inhibited OT release into the blood plasma. On the contrary, in not suckled females TRH increased OT plasma concentration. I.c.v. TRH raised the PRL concentration in plasma of lactating but, at the moment, not suckled females. On the contrary, i.c.v. TRH injection into females just suckled was followed by a decrease in PRL plasma level. TRH probably acts in the central nervous system as an inhibitory neuromodulating factor for the vasopressin release. Also, it cannot be excluded that TRH--otherwise known to enhance the PRL release--suppresses the oxytocin-prolactin positive feedback mechanism when activated temporarily by suckling.

Incubation of hypothalamo-neurohypophysial explants in Locke's solution containing 28 nM/L thyrotropin-releasing hormone (TRH) resulted in an inhibition of vasopressin and oxytocin secretion during depolarization due to excess potassium. These data suggest the involvement of TRH in the regulatory mechanisms of vasopressin and oxytocin release; the inhibitory effect of TRH cannot be excluded.

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly decreased hypothalamic oxytocin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats drinking tap water, neurohypophysial oxytocin content decreased. Plasma oxytocin concentration was distinctly elevated under TRH treatment in rats euhydrated but, on the contrary, decreased in salt-loaded rats as compared with animals similarly drinking hypertonic saline but not TRH-treated. The present data suggest that TRH may be involved in some regulatory processes related to oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.

Rats euhydrated and dehydrated during two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. A single dose of TRH injected to euhydrated animals increased the hypothalamic vasopressin content but did not affect significantly the content of vasopressin in the neurohypophysis as well as that of oxytocin both in the hypothalamus and neurohypophysis. In rats deprived of water for two days TRH completely prevented the decrease of neurohypophysial oxytocin due to stimulation of osmoreceptor origin. Similarly, TRH restrained both the hypothalamic and the neurohypophysial vasopressin and oxytocin depletion in rats dehydrated for four days.

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.) for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic vasopressin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats given hypertonic saline, neurohypophysial vasopressin content increased. Plasma vasopressin concentration was distinctly diminished under TRH treatment, the respective difference being significant, however, barely in salt-loaded rats. The present data suggest that TRH may be involved in some regulatory processes related to vasopressin biosynthesis and release from the rat hypothalamo-neurohypophysial system.

Rats drinking and libitum tap water or hypertonic (i.e., 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), during three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic oxytocin content in both euhydrated (i.e., given tap water ad libitum) and salt-loaded rats and vasopressin content only in euhydrated rats. Similarly, neurohypophysial vasopressin and oxytocin content significantly increased in animals drinking tap water or 2% sodium chloride during treatment with TRH. The present data suggest that TRH may be involved in some regulatory processes to vasopressin and oxytocin biosynthesis and release from the rat hypothalamo-neurohypophysial system.

Rats euhydrated and dehydrated for two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride.) A single dose of TRH administered to euhydrated animals was followed by a significant increase of the vasopressin content in the neurohypophysis and hypothalamus as well as of the hypothalamic oxytocin content. On the contrary, a single dose of TRH decreased the oxytocin content in the neurohypophysis. Under conditions of dehydration TRH distinctly restrained the decrease of vasopressin and oxytocin in the hypothalamus. In animals dehydrated for two or four days the decrease of oxytocin in the neurohypophysis, brought about by stimulation of osmoreceptors, was distinctly more marked under treatment with TRH. On the contrary, the depletion of neurohypophysial vasopressin was significantly less apparent under such conditions. 28 nmol/L TRH markedly increased vasopressin release but inhibited that of oxytocin from the neurointermediate lobes incubated in vitro both under basal conditions as well as during stimulation with excess (56 mmol) potassium.