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)

We examined the effect of neurohypophysectomy with and without vasopressin replacement on the ACTH response to hypotension and ovine CRF infusion and on the adrenocortical response to ACTH and angiotensin II infusion in conscious dogs. Nitroprusside hypotension (decrease in mean arterial pressure of 25 mm Hg) in the intact state resulted in large increases in plasma arginine vasopressin (pAVP; from 2.6 +/- 0.3 to 296 +/- 63 pg/ml) and ACTH (from 35 +/- 6 to 395 +/- 92 pg/ml). Neurohypophysectomy resulted in greatly attenuated pAVP (8.4 +/- 1.6 pg/ml) and ACTH (80 +/- 10 pg/ml) responses to hypotension which were not normalized by physiological low dose vasopressin replacement (6-18 pg/kg.min continuously, iv, for 2 weeks). However, acute administration of vasopressin (4-6 ng/kg.min) simultaneously with hypotension in the neurohypophysectomized (neurohypox) dog, which produced pAVP levels equivalent to the hypotensive response to intact dogs, almost completely normalized the ACTH response to hypotension (to 248 +/- 74 pg/ml). The ACTH response to 20 ng/kg.min ovine CRF, iv (from 43 +/- 8 to 268 +/- 77 pg/ml), was not attenuated by neurohypophysectomy. The cortisol responses to infusion of 0.5 and 2 ng/kg.min ACTH-(1-24), iv, were essentially normal in neurohypox dogs. However, the ACTH and aldosterone responses to 5 ng/kg.min angiotensin II infusion iv were attenuated in neurohypox dogs off AVP replacement. Histological examination revealed normal adrenal glands and anterior pituitaries in neurohypox dogs. Immunocytochemical staining for vasopressin and neurophysin revealed normal cell bodies in the paraventricular and supraoptic nuclei of the hypothalami from neurohypox dogs. However, median eminence staining for AVP and neurophysin was greatly diminished in neurohypox dogs. In summary, neurohypophysectomy 1) attenuated the ACTH response to hypotension and angiotensin II, but not to CRF, and 2) attenuated the aldosterone response to high dose angiotensin II. Furthermore, the deficit in ACTH secretion was almost completely normalized by increasing plasma AVP levels to those observed in the intact dogs. We conclude that an action of circulating pAVP increases ACTH secretion by a direct effect at the pituitary and by activating afferent input to the hypothalamus.
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PMID:Control of adrenocorticotropin secretion and adrenocortical sensitivity in neurohypophysectomized conscious dogs: effects of acute and chronic vasopressin replacement. 283 Oct 29

Nitroprusside-induced hypotension evokes ACTH secretion which is primarily mediated by enhanced secretion of immunoreactive corticotropin-releasing factor (irCRF) into the hypophysial-portal circulation. Portal plasma concentrations of neither arginine vasopressin nor oxytocin are significantly altered in this paradigm. Application of a delayed feedback signal, in the form of a 2-h systemic corticosterone infusion in urethane-anesthetized rats with pharmacological blockade of glucocorticoid synthesis, is without effect on the resting secretion of arginine vasopressin and oxytocin at any corticosterone feedback dose tested. Resting irCRF levels are suppressed only at the highest corticosterone infusion rate, which resulted in systemic corticosterone levels of 40 micrograms/dl. Suppression of irCRF secretion in response to nitroprusside-induced hypotension is observed and occurs at a plasma corticosterone level between 8-12 micrograms/dl. These studies provide further evidence for a strong central component of the delayed feedback process which is mediated by modulation of irCRF release.
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PMID:Inhibition of immunoreactive corticotropin-releasing factor secretion into the hypophysial-portal circulation by delayed glucocorticoid feedback. 301 67

Extracellular recordings were carried out in the paraventricular nucleus of halothane-anesthetized male rats. Responses of neurons identified by antidromic criteria with projections to the nucleus tractus solitarius or to the ventral lateral medulla were compared to those of neurohypophysial neurons following alterations in blood pressure and osmolarity, hemorrhage and after intravenous injection of cholecystokinin. Neurohypophysial neurons displayed the well-described responses to blood pressure for putative vasopressin neurons and increases in excitability after cholecystokinin for putative oxytocin neurons. Twenty per cent of the ventral lateral medulla-projecting neurons were responsive to cardiovascular perturbations, with these displaying reduced activity after either decreases or increases in blood pressure. None of nine neurons projecting to the ventral lateral medulla responded to i.v. cholecystokinin. Two of 20 nucleus tractus solitarius-projecting neurons showed reduced activity after cholecystokinin and none increased their firing rate. Nitroprusside-induced hypotension was associated with reduced activity in 10% of this population. Three neurons displayed axon projections to both pituitary and medulla; two of these which projected to the nucleus tractus solitarius were activated by cholecystokinin. We conclude that some of the paraventricular nucleus neurons projecting to the medulla respond to recognized cardiovascular stimuli for neurohypophysial neurons, but neurons in these populations are generally unresponsive to cholecystokinin. The former group of neurons may act to coordinate autonomic and endocrine responses to cardiovascular perturbation; however, there may be other stimuli, such as cholecystokinin, which act only on one of the populations of paraventricular nucleus neurons. Furthermore, many neurons in the descending pathways may respond to stimuli not presently associated with activation of magnocellular neurons.
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PMID:Responses of electrophysiologically identified rat paraventricular neurons to cholecystokinin and other stimuli. 760 84