Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data are presented to show that vasoactive intestinal peptide (VIP) is synthesized and secreted by the hypothalamus and anterior pituitary and that it participates in the regulation of pituitary functions. Immunoreactive VIP in the hypothalamus and pituitary is increased following estrogen treatment and adrenalectomy and is reduced in hyperprolactinemic states. The level of VIP mRNA in the hypothalamus is increased during lactation and sexual maturation, while that in the anterior pituitary shows a sexual dimorphism and is increased with estrogen treatment and hypothyroidism. All these findings suggest a physiological regulation of hypothalamic and pituitary VIP gene expression in relation to its potential role as a neuroendocrine hormone. Furthermore, VIP stimulates prolactin (PRL) release at concentrations attainable in the hypophyseal-portal blood. Passive immunoneutralization studies with anti-VIP antisera suggest that endogenous VIP acts at multiple loci in the hypothalamic-pituitary axis to regulate PRL secretion, interacting possibly with other regulators of PRL secretion such as estrogen, serotonin, cholecystokinin, prostaglandins, galanin and oxytocin. Regarding other pituitary functions, although VIP has been shown to release growth hormone, ACTH, and vasopressin in vivo and in vitro, the physiological significance of these findings remains to be determined.
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PMID:Vasoactive intestinal peptide in the hypothalamus and pituitary. 190 91

Pseudohypoparathyroidism is a complex disorder of renal resistance to parathyroid hormone the mechanism of which is unclear. It is often associated with skeletal abnormalities and there may also be other hormonal defects. This is an extensive endocrinological investigation of five of six affected members in two generations of one family. The phenotypic variability of the syndrome is explored: four members had hypothyroidism; two had abnormal gonadal function; all five had abnormal prolactin response to TRH; one had abnormal hepatic response to glucagon infusion. All had normal hypothalamic-pituitary-adrenal axes, renal responsiveness to vasopressin and growth hormone responses to a variety of stimuli. Special note is made of oral pathology, and evidence of platelet aggregation abnormalities is presented which has not previously been described in the syndrome.
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PMID:Pseudohypoparathyroidism: its phenotypic variability and associated disorders in a large family. 204 19

We monitored the plasma and urine osmolalities, fractional excretion of sodium, fractional excretion of chloride, plasma levels of antidiuretic hormone (ADH, AVP), aldosterone and atrial natriuretic peptide (ANP) before and after acute water ingestion in 12 patients with overt hypothyroidism. The ability of the patients to dilute and concentrate urine was found impaired and the ability of excretion of water load decreased and delayed. Acute water load test was proved to be effective in evaluating the urinary excreting function for the patients. We hypothesize that inappropriate secretion of anti-diuretic hormone and elevated plasma ANP may be homeostatic factors for abnormal urinary excretion in patients with hypothyroidism.
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PMID:Effect of acute water loading on plasma levels of antidiuretic hormone AVP aldosterone, ANP fractional excretion of sodium and plasma and urine osmolalities in myxedema. 214 45

In 2 boys, aged 3 and 13 years, suffering from severe growth failure, endocrine evaluation showed growth hormone deficiency and central hypothyroidism without diabetes insipidus. Magnetic resonance imaging demonstrated a transection of the pituitary stalk, and the presence of an ectopic neurohypophyseal nodule.
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PMID:[Growth hormone deficiency by transection of the pituitary stalk. Value of magnetic resonance imaging. Report of 2 cases]. 217 18

The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism, in 6 with Addison's disease, and in 21 with central diabetes insipidus (CDI). In the latter disease the effect of histamine stimulus was also evaluated. Plasma AVP was measured by radioimmunoassay (RIA). Patients with primary hypothyroidism were classified into subgroups with elevated or normal basal levels of plasma AVP. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels. Patients with Addison's disease exhibited an increased basal level of plasma AVP and a decreased osmotic threshold. CDI patients according to their AVP responses on osmotic stimulus fell into two groups: CDI I gave no response at all, while CDI II responded subnormally. CDI II exhibited blunted AVP release to histamine. The AVP reactions of the CDI I patients fell into two subgroups: CDI I/A had undetectable plasma AVP, whereas histamine evoked AVP release in CDI I/B. Patients with CDI II suffer from a partial CDI, while those with CDI I/A represent a complete form of the disease and CDI I/B presumably have an osmoreceptor failure.
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PMID:[Regulation of vasopressin release in primary hypothyroidism and Addison's disease as well as in central diabetes insipidus]. 219 35

We studied osmoregulation of plasma vasopressin (AVP) in eight patients with untreated myxedema due to primary hypothyroidism. All patients had severe thyroid hormone deficiency due to chronic thyroiditis and had been receiving no medication at the time of this study. AVP release was defined by 5% hypertonic saline infusion test in all patients, and urinary diluting capacity was estimated by the iv water-loading tests in five patients. Plasma AVP was measured by sensitive and specific RIA. The mean basal plasma AVP level in the patients (0.5 +/- 0.1 pmol/L) was significantly lower (P less than 0.01) than that in normal adults (2.5 +/- 0.5 pmol/L). During hypertonic saline infusion, the rise in plasma AVP was normal or subnormal in all patients. In two patients who showed mild to moderate hyponatremia in the basal state and mild urinary diluting defect during water loading, plasma AVP was appropriately suppressed in each case. These results indicate that inappropriate elevation of plasma AVP is not common in myxedema, and that impaired water excretion is due mainly to AVP-independent mechanisms.
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PMID:Osmoregulation of plasma vasopressin in myxedema. 229 64

The authors report two cases of pseudotumor cerebri in patients taking lithium for treatment of bipolar disorder. Pseudotumor cerebri is a poorly understood syndrome characterized by chronic headaches, bilateral papilledema, and increased intracranial pressure without localized neurologic signs or symptoms, intracranial mass, or hydrocephalus. Ventriculography, computed tomography, and nuclear magnetic resonance imaging reveal normal or small ventricles. Multiple etiologies may include Vitamin A toxicity, obesity, head trauma, hypothyroidism or hyperthyroidism, prolonged steroid therapy or its withdrawal, Addison's disease, Cushing's disease, pituitary insufficiency, and lithium therapy. Patients treated with lithium whose antidiuretic hormone-cyclic adenosine monophosphate mechanism is disturbed are most likely to develop pseudotumor cerebri via disregulation of sodium balance, thyroid-stimulating hormone production, and glucose metabolism. The authors recommend careful medical monitoring to avoid iatrogenic effects of lithium, including pseudotumor cerebri.
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PMID:Pseudotumor cerebri associated with lithium therapy in two patients. 203 32

To determine whether hypothyroidism alters responsiveness to centrally infused thyrotropin-releasing hormone (TRH), blood pressure and sympathetic nerve responses to various stimuli were recorded in urethane-anesthetized rats. Four weeks after thyroidectomy or treatment with propylthiouracil, pressor responses elicited by intracerebroventricular- (ICV)-infused TRH or by electrical stimulation of the posterior or ventromedial hypothalamus were always accompanied by increased sympathetic nerve activity in all rats. When serum thyroxine levels were lowered in hypothyroid rats, pressor responses to most stimuli, including intravenous injections of norepinephrine, angiotensin, and vasopressin, were inhibited, indicating that peripheral pressor responsiveness had been reduced. For centrally acting stimuli, pressor inhibition was also considered partly caused by a selective decrease in sympathetic vasomotor tone because sympathetic excitation was reduced only during ICV infusions of TRH, but not during posterior hypothalamic stimulation. On the other hand, there was no obvious explanation why both pressor and sympathetic responses to ventromedial hypothalamic stimulation were spared from inhibition. Because sympathetic nerve responses to ICV-infused TRH were reduced by thyroid suppression, these results imply that sympathetic activation by TRH in intact rats is mediated, at least in part, indirectly by way of TRH stimulation of thyroid activity.
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PMID:Selective suppression of pressor and sympathetic responses to centrally infused TRH in hypothyroid rats. 245 34

Binding sites of vasopressin (VP) have been characterized in the hippocampal synaptic plasma membranes of developing normal and hypothyroid rats using a highly specific tritiated VP antagonist, d(CH2)5Tyr(Me)VP (V1 type). This antagonist bound to an apparently homogeneous population of specific sites with an affinity ten times higher than that of VP itself. The total amount of synaptosomal protein in 15-day-old normal rats represented about 50% of the adult value, but the density of binding sites was already maximal and remained constant thereafter, supporting the concept of an early development of an extrahypophyseal vasopressinergic hippocampal system. Thyroid deficiency specifically reduced the amount of synaptosomal protein. However, the binding site density in the synaptsomal fraction appeared to be relatively well preserved from hypothyroidism, although there was a transient decrease in the apparent affinity of the ligand. These data suggest that thyroid hormones are slightly involved in the early development of high-affinity VP receptors.
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PMID:Effects of hypothyroidism on high-affinity vasopressin binding sites in developing hippocampal synaptosomes. 252 17

Pituitary function and short-term clinical effects after transsphenoidal hypophysectomy were investigated in clinically normal dogs. In study I, 8 dogs were given polyionic fluids IV during the first 12 hours after surgery. In study II, 4 dogs were given polyionic fluids IV and glucocorticoid supplementation for 7 days. Pituitary function was assessed by evaluating basal ACTH concentrations and results of a growth hormone stimulation test before and 1 and 12 weeks after hypophysectomy, an ACTH stimulation test, a thyrotropin-releasing hormone-stimulation test, and a modified water deprivation/vasopressin response test before and 1, 4, 8, and 12 weeks after hypophysectomy. Gross and histologic evaluations of the surgery site, thyroid and adrenal glands, and skin were done at 12 weeks after surgery. Four dogs from study I died within 27 hours after hypophysectomy. Postmortem examinations of these dogs revealed liver and lung congestion compatible with circulatory collapse. None of the dogs in study II died. For the surviving dogs in both studies, diabetes insipidus developed immediately after hypophysectomy and resolved within 2 weeks. Hypernatremia also developed immediately after hypophysectomy and resolved by 1 week. Production of ACTH was evident at 1 and 12 weeks after hypophysectomy in all dogs, and results of ACTH stimulation tests after surgery were not notably different from results obtained before surgery. Results of thyrotropin-releasing hormone stimulation and growth hormone-stimulation tests supported the diagnosis of hypothyroidism and hyposomatotropism attributable to hypophysectomy. Histologic examination revealed thyroid atrophy, epidermal and dermal atrophy, and normal adrenal glands in all dogs and remnants of the hypophysis in 2 dogs from study I.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transsphenoidal hypophysectomy in the clinically normal dog. 284 9


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