Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present investigations was to examine the effects of the states of hypothyroidism or hyperthyroidism on vasopressin (AVP) and oxytocin (OT) release under conditions of equilibrated water metabolism as well as of osmotic stimulation, brought about by the dehydration or hypertonic saline administration. The euhydrated and simultaneously hypothyroid rats showed decreased hypothalamic AVP and OT content and somewhat higher but not significant neurohypophysial AVP content. In these animals the raised OT (but not AVP) plasma level has been observed. In hyperthyroid rats drinking tap water ad libitum the neurohypophysial AVP and OT content significantly diminished; plasma OT concentration (but not AVP) was then elevated. The state of osmotic stimulation was the reason of different response of the hypothalamo-neurohypohysial system function in hypo- or hyperthyroid rats. Significant decreases of neurohypophysial AVP and OT content were found in both hypothyroid dehydrated as well as hypothyroid hypertonic saline-treatment rats as compared with hypothyroid euhydrated ones. On the contrary, in the state of hyperthyroidism AVP content in the neurohypophysis distinctly raised in dehydrated and salt-loaded rats; in these last neurohypophysial OT content increased as well. Plasma OT (but not AVP) distinctly diminished in hyperthyroid and simultaneously dehydrated or hypertonic saline injected rats in relation to hyperthyroid control subgroup. Data from the present study suggest that: 1). altered thyroid gland function affects vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in the state of equilibrated water metabolism; 2). the state of hypo- or hyperthyroidism modifies the response of AVP-ergic and OT-ergic neurons upon the osmoreceptors/osmodetectors stimulation. It may be supposed that OT-ergic neurons display greater than AVP-ergic neurons sensitivity upon the thyroid hormone influence.
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PMID:Vasopressin and oxytocin release and the thyroid function. 1521 63

Oxytocin knockout (OT KO) mice acutely consume inappropriate amounts of sodium following overnight water deprivation suggesting that oxytocinergic neurons inhibit excessive sodium ingestion (Amico JA, Morris M, Vollmer RR. Mice deficient in oxytocin manifest increased saline consumption following overnight fluid deprivation. Am J Physiol - Regul Integr Comp Physiol 2001; 281:R1368-R1373). This study sought to determine whether oxytocin (OT) provides long-term regulation of voluntary sodium ingestion. Wild-type (WT) and oxytocin knockout male mice were provided choices between diets or drinking solutions that differed in their sodium content. Mice were given access for 1 week to two diets, one containing low sodium (0.01% sodium chloride [NaCl]) content and a second containing a normal sodium (1.0% NaCl) content. During the second week, the animals were given a choice between a low sodium diet and a high sodium (8.0% NaCl) diet. In the second week, mice consumed 4 times more sodium; however, there were no differences between WT and OT KO mice. In a second experiment, mice had access to a two-bottle choice of tap water and a 0.5 M NaCl solution made palatable by the addition of a 4.1% Intralipid emulsion. Both genotypes consumed large, but equivalent, volumes of the Intralipid/sodium solution. The ingestion of this sodium-rich solution stimulated thirst and enhanced the intake of water. Thus, the availability of palatable sodium-rich food or solutions can lead to excessive voluntary sodium ingestion. Compared with oxytocin knockout mice, enhanced voluntary ingestion of sodium-rich solid and liquid diets proceeded unimpeded in WT mice. Therefore, OT pathways may not be essential for regulating solute intake in this setting.
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PMID:Voluntary sodium ingestion in wild-type and oxytocin knockout mice. 2278 7


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