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)

Hypothalamic pituitary function and growth hormone releasing hormone (GHRH) loading tests in two children with septo-optic dysplasia (SOD) revealed isolated GH deficiency in one and deficiencies of growth hormone, adrenocorticotropic hormone and antidiuretic hormone in the other. Secretion of GH was elicited in the first patient by single i.v. bolus administration of GHRH and after repetitive i.v. infusions of GHRH in the second. With these results we confirmed that the hypopituitarism in our patients with SOD was of hypothalamic origin. Both patients also had infantile spasms.
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PMID:Growth hormone deficiency of hypothalamic origin in septo-optic dysplasia. 207 74

The effects of cortisol, its steric analog 11-epicortisol, and lysine vasopressin (LVP) on DNA and RNA synthesis in isolated adrenocorticotropic hormone-secreting human pituitary tumor cells obtained by transsphenoidal surgery were studied using [3H]thymidine incorporation in DNA and [3H]uridine in RNA. Cortisol suppressed RNA and, to a greater extent, DNA synthesis in these cells. This could explain the slow growth of pituitary tumors in patients with Cushing's disease and the rapid growth of Nelson's pituitary tumors after bilateral adrenalectomy. 11-Epicortisol also suppressed RNA synthesis, but it had a stimulatory effect on DNA synthesis, which indicates a high specificity of glucocorticoid receptors. When applied together with cortisol, 11-epicortisol antagonized the suppressive effects of cortisol on DNA synthesis. Although LVP stimulated RNA synthesis, it suppressed DNA synthesis in most of the tumor cells.
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PMID:The effects of cortisol, 11-epicortisol, and lysine vasopressin on DNA and RNA synthesis in isolated human adrenocorticotropic hormone-secreting pituitary tumor cells. 215 95

The patterns of catecholamines (adrenaline and noradrenaline), peptide hormones (adrenocorticotropic hormone, antidiuretic hormone, beta-endorphin, growth hormone and prolactin), hydrocortisone (cortisol) and those of immunoglobulins (IgA, IgG and IgM) and total and differential leucocyte counts in the peripheral blood were investigated during and for 6 days after thyroid surgery in 20 patients (F/M: 18/2) performed under acupuncture anaesthesia, supplemented by small doses of pethidine (mean: 45.0 mg, s.d. 8.9). Throughout surgery the patients remained conscious. During surgery a significant increase in the level of catecholamines and the above-mentioned circulating hormones and a decrease of immunoglobulins were observed, whereas the leucocyte and differential counts demonstrated leucocytosis due to lymphocytosis, a decreased percentage of eosinophils and a remarkably reduced percentage of neutrophils. In the postoperative phase, levels of noradrenaline and beta-endorphin remained elevated, whereas the other circulating hormones gradually returned to normal values. Immunoglobulin levels and eosinophil counts returned to the preinduction values within 24 h, and those of neutrophil and lymphocyte counts within 2 days. Changes in number of monocytes and basophils could not be detected peri- and postoperatively.
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PMID:The patterns of stress response in patients undergoing thyroid surgery under acupuncture anaesthesia in China. 217 67

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.
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PMID:[Hyponatremia in isolated deficiency of adrenocorticotropic hormone: role of a decrease in aldosterone secretion independent of antidiuretic hormone excess]. 217 15

An immunocytochemical analysis with 33 antisera was undertaken to investigate the localization of 25 different neurotransmitter-related antigens in the hypothalamic suprachiasmatic nucleus in the rat. To obtain estimates of relative densities of immunoreactive axons a stereological approach was used involving counting of intersections of immunoreactive axons with a superimposed semi-circle test grid. All neurotransmitter-related antigens found in perikarya within the suprachiasmatic nucleus, including those stained with antisera against bombesin, gastrin-releasing peptide, neurophysin, vasopressin, somatostatin, gamma-aminobutyrate, glutamate decarboxylase and vasoactive intestinal polypeptide were also found in axons within the nucleus. A greater number of these immunoreactive axons was found within the nucleus than in the adjacent anterior hypothalamus. The size of all immunoreactive axons in the suprachiasmatic nucleus was consistently small; immunoreactive axons were found ramifying widely in the nucleus, often ending with terminal boutons near perikarya immunoreactive for the same antigen. All neurotransmitter-related substances found in perikarya of the suprachiasmatic nucleus were also found in axons crossing over the midline to innervate the contralateral nucleus, providing an anatomical substrate for a high degree of communication between the paired nuclei. Axons immunoreactive for other putative transmitters including serotonin arising outside the nucleus were also found in high densities within the nucleus and crossing over the midline between the nuclei. Immunoreactivity for some transmitters was found in axons of similar densities within and outside the nucleus, including antisera against tyrosine hydroxylase; a small number of dopamine beta-hydroxylase and a few phenylethanolamine N-methyltransferase-immunoreactive axons were found in the SCN, suggesting that dopamine, norepinephrine and epinephrine may occur in a limited number of axons in the nucleus. Small numbers of axons immunoreactive with antisera raised against cholecystokinin, prolactin, substance P, thyrotropin-releasing hormone and choline acetyltransferase were found within the suprachiasmatic nucleus. Axons immunoreactive for luteinizing hormone-releasing hormone, adrenocorticotropic hormone, alpha-melanocyte-stimulating hormone and neurotensin were rarely found within the suprachiasmatic nucleus; axons immunoreactive for luteinizing hormone-releasing hormone, adrenocorticotropic hormone, cholecystokinin and tyrosine hydroxylase were found in both horizontal and coronal sections in the area between the left and right suprachiasmatic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitters of the hypothalamic suprachiasmatic nucleus: immunocytochemical analysis of 25 neuronal antigens. 241 88

The medial preoptic nucleus (MPN) is a sexually dimorphic complex with three major subdivisions. The cell-dense central (MPNc) and medial (MPNm) subdivisions are larger in male rats, while the cell-sparse lateral subdivision (MPNl) occupies a majority of the nucleus in females. In the present study we evaluated the distribution of possible monoaminergic and peptidergic cells and fibers within the MPN, as well as in adjacent regions of the medial preoptic area of the adult male rat. For this, we used an indirect immunohistochemical method with antisera to serotonin (5HT), dopamine beta-hydroxylase (DBH), tyrosine hydroxylase (TH), neuropeptide Y (NPY), cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT), corticotropin-releasing factor (CRF), luteotropin-releasing hormone (LRH), somatostatin (SS), thyrotropin-releasing hormone (TRH), oxytocin (OXY), vasopressin (VAS), adrenocorticotropic hormone (1-24; ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), leucine-enkephalin (L-ENK), and calcitonin gene-related peptide (CGRP). The results suggest that cell bodies and/or fibers crossreacting with all of these putative neurotransmitters are differentially distributed within the MPN. Within the MPNm, the densest plexuses of fibers were stained with antisera to SP and NPY, while moderate densities of fibers were stained with anti-DBH, SS, CCK, CGRP, ACTH, and alpha-MSH, and only a few fibers were stained with anti-5HT, TH, NT, VAS, and L-ENK. Moderate numbers of SP- and L-ENK-immunoreactive cell bodies, and a few SS-, NT-, CRF-, and TRH-stained cell bodies were also found within the MPNm. The MPNc contained a dense plexus of CCK-immunoreactive fibers, as well as a few CRF-immunoreactive fibers. Both fiber types were localized almost exclusively to this subdivision, while most of the others studied here appeared to avoid it selectively. This suggests that there are relatively few inputs to the MPNc, and that they tend to avoid other parts of the nucleus, although moderate densities of DBH- and NPY-immunoreactive fibers were found in both the MPNm and MPNc. The MPNc contained several CCK-immunoreactive cell bodies as well as a moderate number of TRH-stained cell bodies. Both cell types were nearly completely localized to the MPNc. The major inputs to the MPNl studied here appear to be stained with antisera to 5HT and L-ENK, although moderate numbers of NT- and CRF- immunoreactive fibers were also found in this part of the nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter specificity of cells and fibers in the medial preoptic nucleus: an immunohistochemical study in the rat. 242 28

The effects of human alpha-natriuretic peptide (alpha-ANP) were investigated in seven patients with severe congestive heart failure by incremental bolus injections and by a continuous infusion for 30 min. alpha-ANP was measured in plasma before and after administration. We found a significant inverse correlation between basal levels of alpha-ANP and cardiac output. The administration of alpha-ANP resulted in a fall of peripheral vascular resistance, an increase in cardiac output, a relatively small decrease in blood pressure, and almost no change in pulmonary arterial pressure. alpha-ANP inhibits aldosterone and cortisol secretion and enhances diuresis and urinary sodium and potassium excretion. Plasma adrenocorticotropic hormone was reduced in two of the patients after the continuous infusion. Plasma renin concentration, norepinephrine, vasopressin, and plasma levels of 6-keto prostaglandin F1-alpha and prostaglandin E2 were unchanged. A small but significant decrease of serum potassium was observed.
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PMID:Human atrial natriuretic peptide: plasma levels, hemodynamic, hormonal, and renal effects in patients with severe congestive heart failure. 243 34

Male Wistar rats were anaesthetized, injected intracisternally (i.c.) with saline or colchicine and were decapitated at various time intervals. Trunk blood was collected for the determination of immunoreactive adrenocorticotropic hormone (ACTHi) by radioimmunoassay (RIA) and of corticosterone by a fluorometric assay. Changes in corticotropin-releasing factor (CRF) content of the median eminence (ME) were assessed by quantitative immunocytochemistry (QICC) on cryostat sections of ME preparations or by RIA of CRF in ME-extracts. Administration of colchicine resulted in a long-lasting and dose-dependent stimulation of ACTHi secretion. At a dose of 25 micrograms, high plasma ACTHi levels were found for up to 24 h. A dose of 5 micrograms per rat, that has been reported to effectively block vasopressin transport in paraventricular-neurohypophyseal neurons, resulted in a small elevation of plasma ACTHi. In intact rats, i.c. administration of saline of saline containing 5 micrograms of colchicine had no effect on the CRF content in the ME. In contrast, colchicine caused a depletion of the CRF stores in the ME of 1-week adrenalectomized (ADX) rats. The disappearance rate was 9.2%/h as measured by RIA and 11.2%/h as measured by QICC. When plasma corticosterone and ACTHi were normalized by giving ADX rats corticosterone in drinking water, the colchicine-induced depletion of the CRF stores was fully prevented. We conclude that the rate of decline of CRF in the ME of rats treated with a non-toxic dose of colchicine to block axonal transport is positively correlated to the secretory activity of CRF neurons of the paraventricular-infundibular system.
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PMID:Effect of axonal transport blockade on corticotropin-releasing factor immunoreactivity in the median eminence of intact and adrenalectomized rats: relationship between depletion rate and secretory activity. 245 50

In this study in conscious rats, we tested the hypothesis that substance P, a central pressor peptide and a potential transmitter substance of pain pathways, could be involved in the cardiovascular defense reaction that is typically associated with unpleasant sensory stimuli. The hemodynamic responses to centrally administered substance P were pharmacologically characterized. The increases in blood pressure and heart rate after intracerebroventricular injections of substance P were accompanied by mesenteric and renal vasoconstriction and hind limb vasodilation (pulsed-Doppler flow probes). The pressor and vasoconstrictor responses were attenuated by peripheral alpha 1-adrenoceptor blockade with prazosin but were not influenced by blockade of vascular vasopressin receptors with d(CH2)5Tyr(Me) arginine vasopressin (AVP). Cardiac beta 1-adrenoceptor blockade with metoprolol abolished the tachycardic and reduced the pressor responses. Substance P-induced hind limb vasodilation was not sensitive to intravenous atropine but was largely prevented by peripheral beta 2-adrenoceptor blockade with ICI 118,551. Thus, the substance P-induced pressor effects are mediated by alpha 1-adrenergic sympathetic vasoconstriction and beta 1-adrenergic cardiac stimulation, whereas the hind limb vasodilation is mainly due to beta 2-adrenergic stimulation. Substance P dose-dependently (0.01-10 micrograms i.c.v.) released oxytocin but not vasopressin or adrenocorticotropic hormone (ACTH) from the pituitary gland. High doses reduced basal ACTH levels. Together with the hemodynamic responses, a behavioral arousal reaction was observed, which included increased locomotion, grooming, scratching, and skin biting. Our results demonstrate that a neuropeptide can induce classic cardiovascular defense reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substance P induces a cardiovascular defense reaction in the rat: pharmacological characterization. 245 61

Hemorrhage stimulates endocrine and cardiovascular reflex responses that are appropriate for returning blood volume and pressure to prehemorrhage levels. Fetal sheep respond to hemorrhage with increases in plasma adrenocorticotropic hormone (ACTH), cortisol, and vasopressin concentrations and plasma renin activity, but little is known about the afferent limb of the reflex(es) controlling these responses. Fetal sheep between 128 and 133 days' gestation were chronically prepared with vascular catheters. Five fetal sheep were subjected to bilateral section of the cervical vagosympathetic trunks; six fetal sheep were not vagotomized. Four to six days after surgery, the fetuses were subjected to withdrawal of 10 ml of blood every 10 minutes for 2 hours (130 ml total). Vagotomized fetal sheep responded to the hemorrhage with a greater decrease in central venous pressure than the intact fetuses and a slower restitution of fluid to the vascular space (estimated to be 17% of the hemorrhage volume in 2 hours) than the intact fetuses (estimated to be 28% of the hemorrhage volume in 2 hours). Both groups of fetuses, however, responded to the hemorrhage with increases in fetal plasma ACTH, cortisol, and vasopressin concentrations and plasma renin activity that were not significantly different. A posteriori analysis of the data by correlation analysis revealed that the fetal ACTH, vasopressin, and renin responses to the hemorrhage were more highly correlated to the changes in fetal arterial pH than to changes in fetal mean arterial pressure or central venous pressure. The results suggest that the ACTH, vasopressin, and renin responses to hemorrhage in the fetus be mediated by chemoreceptors, not by cardiovascular mechanoreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of vagosympathetic fibers in the control of adrenocorticotropic hormone, vasopressin, and renin responses to hemorrhage in fetal sheep. 253 57


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