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)

The effect of parathyroid hormone (PTH)-like peptide PTH-related protein (PTHrP)(1-34) from a human cancer cell line on renal electrolyte transport was compared with human PTH(1-34) in a thyroparathyroidectomized anesthetized rat model. Comparing submaximal, maximal and supramaximal phosphaturic concentrations of hPTH with the same PTHrP concentrations, no significant difference could be demonstrated in the urinary excretion of calcium, magnesium, inorganic phosphate or cAMP. Even the small (30.3%) and brief (45 min) reduction in fractional water excretion with the maximal (1 nM/kg/h) hPTH concentration was approximated by PTHrP. It is concluded that the structural homology between hPTH and PTHrP allows a similar action on renal electrolyte transport, including the partial agonist effect of higher concentrations of PTH on vasopressin-induced water transport.
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PMID:Synthetic human parathyroid hormone-related protein and rat renal electrolyte transport. 166 7

The humoral hypercalcemia of malignancy factor (also called PTH-related protein or PTHrp) has been shown to produce effects similar to PTH in the kidney, bone, and cardiovascular system. Binding of PTHrp and PTH has been characterized in renal and osseous tissues, but not in vascular tissue. We have attempted to characterize the interaction of both human PTHrp and rat PTH to renal microvessels as a model of vascular smooth muscle and in a renal tubule preparation from the same rabbit kidneys. Previous studies have shown the microvessel and tubule preparations to be distinct based upon morphological examination, differential enzyme markers, calcitonin and vasopressin-sensitive adenylate cyclase distribution, and different characteristics of guanine nucleotide and of oxidized PTH activation of the adenylate cyclases associated with the preparations. Human PTHrp and rat PTH were iodinated by standard techniques and purified by HPLC. Both ligands bound to microvessels and tubules in a saturable, specific manner, Maximal specific binding of either ligand was 65-75% in microvessels and 80-90% in renal tubules. The time courses of binding of both ligands were identical with steady state achieved within 20 min in the smooth muscle of microvessels and 15 min in the tubules at 22 C. In equilibrium competition binding experiments, bound 125I-PTHrp was displaced by both PTHrp and PTH in microvessels and tubules. Rat PTH displayed slightly higher affinity in microvessels and tubules than PTHrp. Identical results were obtained with 125I-PTH as ligand. Specificity of binding of PTHrp and PTH to both microvessels and tubules was excellent, with competition observed between the radioactive ligand and bovine and rat PTH, PTHrp, and the antagonists, [Nle8,18, Tyr34]bovine PTH and [Nle8,18, Tyr34]bovine PTH but not with several other peptides of unrelated structure. The only major difference in binding between microvessels and tubules was a smaller number of binding sites in microvessels compared to tubules. These results indicate that vascular tissue contains receptor sites for PTH and PTHrp as identified by radioligand binding techniques. These receptors are similar in characteristics to the receptors of renal tubular tissue. Both PTH and PTHrp appear to interact with the receptors of rabbit kidney microvessels and tubules.
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PMID:Binding of parathyroid hormone and parathyroid hormone-related protein to vascular smooth muscle of rabbit renal microvessels. 229 68

Paraendocrine syndromes are the remote effects of cancer that result from ectopic hormonal production. Recent investigations have concentrated in five areas that include the evaluation of diagnostic studies, the recognition of rare cases, the contribution of secondary hormones, the clinical distinctions of ectopic syndromes from endocrine disorders, and the efficacy of pharmaceutical agents in correcting hormonally induced biochemical imbalances. The three most common paraendocrine syndromes (humoral hypercalcemia of malignancy, the syndrome of inappropriate antidiuretic hormone production, and ectopic Cushing's syndrome) are the subject of this review.
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PMID:Paraendocrine syndromes. 836 80

Some hormones exert their action by inducing a rise in cytosolic calcium [Ca2+]i (calcium signal), and therefore, a blunting in hormone-induced calcium signal would engender resistance to the action of the hormone. Chronic renal failure (CRF) is associated with resistance to the action of a variety of hormones, a rise in [Ca2+]i and decrease in the amount of mRNA of one hormone receptor, the PTH-PTHrP receptor. We examined the calcium-signal induced by PTH, angiotensin II, vasopressin and glucagon in hepatocytes from CRF animals, evaluated the effect of the basal level [Ca2+]i on the calcium signal and explored the effect of [Ca2+]i on the mRNA of the receptors of these agonists. Hepatocytes from CRF rats have elevated basal levels of [Ca2+]i and display significantly reduced calcium signals induced by all these hormones, while the calcium signals were normal in PTX-CRF animals and those treated with verapamil both of which have normal levels of [Ca2+]i despite CRF. The calcium signals induced by dibutyryl cyclic AMP and G protein activator (GTP gamma S) were normal in hepatocytes from CRF animals despite the high levels of [Ca2+]i. Northern blotting experiments revealed that the levels of the mRNA of the receptors of PTH-PTHrP, angiotensin II and vasopressin were significantly reduced in hepatocytes from CRF animals but PTX-CRF rats and those treated with verapamil had either significantly greater or even normal amounts of the mRNA of these receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired agonist-induced calcium signaling in hepatocytes from chronic renal failure rats. 856 95

A system for the study of the regulation of the release of triacylglycerols by mammary gland slices was developed. By prelabelling the triacylglycerol pool with [3H]oleate measurements of release of both mass of triacylglycerol and of newly synthesized triacylglycerol have been made. Oxytocin and ovine prolactin stimulated release of triacylglycerol and protein, but the former was 40-fold more effective. Recombinant bovine prolactin was even less active than ovine prolactin, suggesting that contamination of the latter with oxytocin and/or vasopressin was partly responsible for its stimulatory effect on release. The findings support the view that the major effect of oxytocin is to stimulate contraction of myoepithelial cells and thus release secreted lipid stored in the lumen of the mammary gland alveoli. Ionomycin, a Ca2+ ionophore, also stimulated lipid release, but probably not by the usual apocrine route. Parathyroid hormone-related protein, a peptide produced by the mammary gland, did not stimulate release or antagonize the effects of oxytocin. Release of lipid was also measured in mammary gland slices from late-pregnant, early- and mid-lactating rats and lactating rats made prolactin-deficient. Hormonal stimulation in vitro showed the maturation of response seen in vivo on transition from late pregnancy to peak lactation. Prolactin deficiency resulted in decreased release of newly synthesized lipid in response to oxytocin.
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PMID:Regulation of milk lipid secretion: effects of oxytocin, prolactin and ionomycin on triacylglycerol release from rat mammary gland slices. 894 58

It has been suggested that PTH-related protein (PTHrP) is an endogenous modulator of cardiovascular systems. We have reported that PTHrP(1-34), but not PTH(1-34), causes the release of arginine-vasopressin (AVP) from the supraoptic nucleus (SON) of the hypothalamus in vitro through a novel receptor distinct from the PTH/PTHrP receptors (type I or type II) described previously. In this study, we have investigated the in vivo effects of PTHrP(1-34) on AVP secretion and its, messenger RNA (mRNA) expression in the SON in conscious rats. Intracerebroventricular (i.c.v.) administration of PTHrP(1-34) resulted in an increase in plasma AVP concentration in a dose-dependent manner (0-400 pmol/rat). The maximal effect was obtained at 15 min after i.c.v. administration of PTHrP(1-34). Neither PTHrP(7-34) nor PTH(1-34) had any effect on plasma AVP levels. PTHrP(1-34)-induced AVP secretion was antagonized by pretreatment with PTHrP(7-34) but not by that with PTH(1-34). In addition, in situ hybridization study revealed that AVP mRNA expression in the SON and paraventricular nucleus was significantly increased 30 min after i.c.v. administration of PTHrP(1-34) and reached a maximum at 180 min. Furthermore, in Northern blot analyses, AVP mRNA expression in the SON was increased to approximately a 2-fold of basal level by PTHrP(1-34). On the other hand, neither PTHrP(7-34) or PTH(1-34) had any effect on the mRNA expression. The PTHrP(1-34)-stimulated AVP mRNA expression was eliminated by pretreatment with PTHrP(7-34) but not with PTH(1-34). These results suggest that, in the central nervous system, PTHrP(1-34) is involved in AVP secretion through a novel receptor distinct from the PTH/PTHrP receptors reported previously, playing a role in the body water and electrolyte homeostasis.
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PMID:Centrally administered parathyroid hormone (PTH)-related protein(1-34) but not PTH(1-34) stimulates arginine-vasopressin secretion and its messenger ribonucleic acid expression in supraoptic nucleus of the conscious rats. 942 37

Parathyroid hormone-related protein (PTHrP) appears to play crucial roles in the cardiovascular system. Over the past few years it has become apparent that there is more than one receptor recognizing parathyroid hormone or PTHrP, or both, and that PTHrP is not only a potent vasodilator of vascular smooth muscle cell tone, but is also a regulator of vascular smooth muscle cell proliferation and a secretagogue of renin and vasopressin. Investigators in several laboratories have started to query whether PTHrP intervenes in vascular diseases such as hypertension, (re)stenosis-atherosclerosis and endotoxaemia.
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PMID:Parathyroid hormone-related peptide--a smooth muscle tone and proliferation regulatory protein. 944 59

We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. Nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca.
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PMID:Hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism. 1041 54

Secretin, glucagon, gastric inhibitory polypeptide (GIP), and parathyroid hormone (PTH) belong, together with vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase (AC)-activating polypeptide, to a family of peptides (the VIP-secretin-glucagon family), which also includes growth hormone-releasing hormone and exendins. All the members of this peptide family possess a remarkable amino-acid sequence homology, and bind to G-protein-coupled receptors, whose signaling mechanism primarily involves AC/protein kinase A and phospholipase C/protein kinase C cascades. VIP and pituitary AC-activating polypeptide play a role in the regulation of the hypothalamus-pituitary-adrenal (HPA) axis, and in this review we survey findings that also other members of the VIP-secretin-glucagon family may have the same function. Secretin and secretin receptors are expressed in the hypothalamus and pituitary gland, and secretin inhibits adrenocorticotropic hormone (ACTH) release. No evidence is available for the presence of secretin receptors in adrenal glands, but secretin selectively depresses the glucocorticoid response to ACTH of dispersed zona fasciculata-reticularis (ZF/R) cells. Glucagon and glucagon-like peptide-1 are contained in the hypothalamus, and all the components of the HPA axis are provided with glucagon and glucagons-like-1 receptors. These peptides exert a short-term inhibitory effect on stress-induced pituitary ACTH release and depress the ZF/R cell response to ACTH by inhibiting the AC/protein kinase A cascade; they also stimulate hypothalamic arginine-vasopressin release. GIP receptors are present in the ZF/R of the normal adrenals, and are particularly abundant in some types of adrenocortical adenomas and hyperplasias. GIP, through the activation of the AC/protein kinase A cascade, evokes a sizeable glucocorticoid secretagogue effect, leading to the identification of a food/GIP-dependent Cushing's syndrome. PTH and PTH-related protein are expressed in the hypothalamus and pituitary gland, and PTH and PTH-related protein receptors in all the components of the HPA axis. Both peptides enhance ACTH and arginine-vasopressin release, as well as stimulate aldosterone and glucocorticoid secretion of dispersed zona glomerulosa and ZF/R cells, respectively. The involvement of growth hormone-releasing hormone and exendins in the functional regulation of the HPA axis has not yet been extensively investigated.
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PMID:Secretin, glucagon, gastric inhibitory polypeptide, parathyroid hormone, and related peptides in the regulation of the hypothalamus- pituitary-adrenal axis. 1076 61

The acute tumor lysis syndrome (ATLS) is characterized by the rapid development of hyperuricemia, hyperkalemia, hyperphosphatemia, and acute renal failure (ARF). Hematologic malignancies are responsible for most cases of ATLS. Control of hyperuricemia and the achievement of a high urine flow are the mainstays of prevention. Urinary alkalinization should be performed only when hyperuricemia is present. Hypercalcemia occurs in 10% to 20% of patients with cancer at some time during the disease course. Parathyroid hormone-related protein (PTHrP) is the most common mediator of humoral hypercalcemia of malignancy (HHM), while local osteolysis is the principal mechanism in patients with bone metastasis. Hydration with saline and administration of pamidronate control hypercalcemia in most patients. Hyponatremia with an increase in total-body salt and water content, manifested as edema and/or ascites, is the most common electrolyte abnormality in cancer patients. Hyponatremia due to salt depletion may occur in patients who receive cisplatin. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) may occur in association with cancer of the lung, after high-dose cyclophosphamide, and during vigorous fluid administration in patients with chemotherapy-associated emesis. Lactic acidosis without tissue hypoperfusion may be seen in patients with extensive liver metastasis or with certain hematologic malignancies. In the latter cases, lactate levels parallel disease activity and chemotherapy often leads to resolution of the lactic acidosis. Idiopathic hyperammonemia has been described after intensive chemotherapy for hematological malignancies and following bone marrow transplantation.
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PMID:Metabolic emergencies in the cancer patient. 1086 20


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