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)

Many hormones initiate their biologic actions by augmenting the intracellular concentrations of 3',5'-adenosine monophosphate (cyclic AMP). The nucleotide has been found in body fluids; its determination in plasma and urine can be performed by a rapid, simple and specific method: the cyclic AMP assay kit of the Radiochemical Centre (Amersham, England). The assay is based on the competition between unlabelled cAMP and a fixed quantity of the tritium labelled compound for binding to a bovine muscle protein which has a high specificity and affinity for cAMP. Different factors must be considered in evaluating the 24 h urinary content of the nucleotide: the renal or extrarenal origin of cAMP and the functional status of the kidneys. In basal conditions the urinary cAMP excretion is significantly correlated with creatinine excretion (n = 67; r = 0.47; p less than 0.001) thus confirming that the most part of cAMP excreted is derived from the plasma by glomerular filtration. Parathyroid hormone (PTH) stimulates adenylate cyclase predominantly in the renal cortex, whereas vasopressin (ADH) stimulated the enzyme in the medulla; thus PTH and ADH could increase the amount of cAMP in the urine from the renal source. In a case of diabetes insipidus and infusion of ADH caused a prompt rise in cAMP urinary excretion. In 5 normals an infusion of bovine synthetic parathyroid hormone caused an increased excretion of cAMP that preceded the phosphaturic response. An infusion of salmon synthetic calcitonin caused a rise in phosphate excretion and no increase in cAMP urinary content. As it concerns the two calciotopic hormones, PTH and CT, it is reasonable to assume that renal receptors are distinct. The 24 h urinary excretion of cAMP in 55 control subjects (3613 +/- 1460 D.S. n moles) was contrasted with the lower excretion in 25 elderly subjects (70-93 years: 1804 +/- 699 n moles), with the high cAMP excretion in a patient with hyperparathyroidism (that fell to normal values following removal of the parathyroid adenoma) and with the low cAMP excretion in patients with primary or surgical hypoparathyroidism. The mean 24 h cAMP excretion in patients with renal insufficiency was significantly decreased when compared to control subjects. These findings and recent reports confirm that the 24 h urinary output of cAMP may be considered an useful index of pharathyroid function in man.
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PMID:[The diagnostic value of the determination of cyclic 3',5'-adenosine monophosphate (cAMP) in urine]. 19 Jun 33

Prolactin was shown to activate adenylate cyclase in broken cellular enzyme preparations from rat renal medulla. Likewise, vasopresin was effective on this enzyme system. Parathyroid hormone was similarly active in the renal cortex. The simultaneous administration of vasopressin and prolactin to medullary kidney slices did not result in an additive effect in stimulating medullary adenyl cyclase. Audioradiographic techniques revealed a selective and prolonged localization of intravenously injected 125I-prolactin to the thick limb of the loop of Henle, the distal tubule and the collecting duct. It is concluded that prolactin activates medullary adenylate cyclase, and may do so by occupying ADH receptors.
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PMID:Prolactin-induced stimulation of rat renal adenylate cyclase and autoradiographic localization to the distal nephron. 86 55

The mammalian renal thick ascending limb of Henle (TAL) reabsorbs approximately 55% of the filtered magnesium; accordingly, it is the major segment involved in control of renal Mg balance. This review discusses recent evidence for passive and active transport of Mg through the paracellular and transcellular pathways of the TAL, respectively. The properties of these pathways provide a basis for understanding the factors influencing magnesium reabsorption and hormonal controls regulating Mg balance. Normally, Mg absorption is load dependent, whether delivery is altered by increasing luminal Mg concentration or increasing the flow rate into the thick ascending limb. In contrast to the luminal concentration, elevation of peritubular (plasma) Mg and Ca inhibit divalent cation absorption by mechanisms that are not entirely clear. Magnesium reabsorption in the TAL is also closely associated with NaCl absorption so that factors that influence NaCl also affect magnesium. Magnesium deficiency results in a specific and apparently intrinsic cellular adaptation to increase Mg absorption in the TAL. Our greatest understanding of hormonal controls for Mg absorption have come from recent studies using a "hormone deprived" animal model. Parathyroid hormone, calcitonin, glucagon, and antidiuretic hormone act through a common second messenger, adenosine 3',5'-cyclic monophosphate, to limit Mg excretion by enhancing active Mg transport in the TAL. The integrated actions of these hormones and possibly others provide a sensitive means of control. Clearly, recent observations, using in vivo and in vitro microperfusion studies, have altered our thinking of TAL function and indicate that Mg transport is sensitively and specifically controlled within this segment.
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PMID:Control of magnesium transport in the thick ascending limb. 264 45

Parathyroid hormone (PTH) -degrading activity was studied using osteoblast-like UMR-106 cells. PTH-degrading activity was assessed by the amount of PTH fragments produced in the medium after exposure of intact human PTH-(1-84) to UMR-106 cells. PTH immunoreactivity recovered in trichloroacetic acid-soluble products of the medium and in fractions eluted from reverse-phase high-performance liquid chromatography (HPLC) was measured by radioimmunoassay using an antibody specific for the mid-region and C-terminus of PTH. In this study, intact UMR-106 cells but not extracellular enzymes cleaved human PTH(1-84) into fragments which were released into the medium (in a time- and temperature-dependent fashion). HPLC analysis of the PTH fragments depicted three immunoreactive peaks (peaks 1, 2 and 3) besides intact PTH, indicating a limited PTH-hydrolyzing activity of the cells. Furthermore, a 1000-fold molar excess of either hPTH-(3-34) or [Nle8,Nle18,Tyr34]hPTH-(3-34)amide inhibited PTH-degrading activity by 63% and 80% of control, respectively, whereas neither calcitonin, vasopressin nor growth hormone suppressed it. Additionally, HPLC analysis of the samples treated with [Nle8,Nle18,Tyr34]hPTH-(3-34)amide showed a reduction of the three peaks, suggesting an involvement of PTH receptor in the production of PTH fragments. This PTH-degrading activity was strongly inhibited by phenylmethylsulfonyl fluoride and chymostatin, but not by soybean trypsin inhibitor, elastatinal or inhibitors of cysteine, aspartic or metalloproteinases, indicating that it is due to a seryl chymotrypsin-like endopeptidase. Chymotrypsin-like activity seems to be solely responsible for PTH-degrading activity in intact UMR-106 cells, since all three PTH fragments were predominantly suppressed in the presence of chymostatin. Further analysis of chymotrypsin-digested products of hPTH-(1-84) eluted from HPLC exhibited five fragments detected by ultraviolet absorbance at 210 nm, three of which were measurable by PTH radioimmunoassay, each corresponding to the three PTH fragments produced by UMR-106 cells. To explore the cleavage sites of PTH further, amino acid analysis of chymotrypsin-cleaved products was performed. The results strongly support the view that the chymotrypsin-like enzyme in UMR-106 cells cleaved the hormone between residues 23-24 and 34-35, to produce, at least, hPTH-(24-84) and -(35-84). Our present study indicates that a chymotrypsin-like endopeptidase is solely responsible for limited hydrolysis of PTH by intact UMR-106 cells.
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PMID:Parathyroid hormone degradation by chymotrypsin-like endopeptidase in the clonal osteogenic UMR-106 cell. 291 1

Parathyroid hormone (PTH) has a variety of biologic effects which are both dependent and independent on activation of adenylate cyclase. We studied the effects of intact PTH and PTH fragments on water flow and Ca transport in isolated toad bladder sacs. As reported previously by us, PTH (1-84) significantly stimulated basal water flow in isolated toad bladder sacs. Synthetic PTH 1-34, 44-68, 53-84 and 65-84 (1 microgram/ml) had no effect on basal water flow after a 60-min incubation period. Intact PTH (1-84) and synthetic 1-34 PTH significantly inhibited both arginine-vasopressin and cyclic AMP-stimulated water flow. Synthetic PTH 44-68, 53-84 and 65-84 (1 microgram m/ml) had no effect on arginine-vasopressin or cyclic AMP-stimulated water flow after a 60-min incubation. Intact PTH (1-84) and synthetic 1-34 PTH significantly stimulated 45Ca uptake without affecting 45Ca efflux. Synthetic PTH 44-68, 53-84 and 65-84 had no effect on either 45Ca uptake or 45Ca efflux. Although these results suggest that the intact hormone is required for the maximal effect of PTH on water flow, substantial activity resides in the amino terminal fragment of the hormone. No activity per se resides in the carboxy terminal portion of the hormone as regards water flow. Alterations in Ca transport appear to mediate the effect of PTH on water flow. These effects are independent of activation of adenylate cyclase because these hormones also inhibit cyclic AMP-stimulated water flow.
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PMID:Effect of parathyroid hormone fragments on calcium transport in toad bladder. 303 17

Adenyl cyclase from plasma membrane fractions of rat renal cortex or medulla was assayed by measuring conversion of adenosine triphosphate labeled at the alpha-phosphate with (32)P to cyclic 3',5'-adenosine monophosphate labeled with 32P. Parathyroid hormone activated the enzyme primarily in cortex; vasopressin acted primarily in medulla. These experiments support the conclusion that cyclic adenosine monophosphate mediates the action of parathyroid hormone on the kidney and show that parathyroid hormone and vasopressin stimulate adenyl cyclase at anatomically separable areas within the kidney.
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PMID:Renal adenyl cyclase: anatomically separate sites for parathyroid hormone and vasopressin. 563 60

Parathyroid hormone- (PTH) stimulated adenylate cyclase activity in homogenates of rat renal cortex was inhibited by l-epinephrine. The specificity of the inhibition indicated that it was mediated by alpha 2-receptors. The inhibition of PTH-stimulated activity was greater than the inhibition of basal activity. The absolute decrease in adenylate cyclase activity produced by 10-4 M l-epinephrine was from 16.3 +/-0.6 (SE) to 11.2 +/- 0.6 pmol.min-1.mg-1 for activity stimulated by 10 microgram/ml PTH. Basal activity was decreased from 2.3 +/- 0.07 to 1.7 +/- 0.04. A similar inhibition of PTH-stimulated adenylate cyclase by l-epinephrine was demonstrated in preparations of renal cortical tubules. In contrast, the quantitative decrease in vasopressin-or calcitonin-stimulated activity by 10-4 M l-epinephrine was the same as the decrease in basal activity. These results demonstrate that PTH receptors that stimulated adenylate cyclase and alpha 2-adrenergic receptors that inhibit adenylate cyclase are present on the same cells in the renal tubules. Thus, a mechanism exists whereby alpha-adrenergic agonists can oppose the tubular actions of PTH via a direct inhibition of adenylate cyclase activity.
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PMID:Selective inhibition by epinephrine of parathyroid hormone-stimulated adenylate cyclase in rat renal cortex. 628 2

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

The effect of whole blood ionized calcium levels on vasopressin (AVP) secretion has been studied in 12 uremic hemodialysis patients (6 nephrectomized and 6 nonnephrectomized), 6 healthy subjects, and a sprue patient, first while she was hypocalcemic and again after her blood calcium had normalized. Changes in whole blood ionized calcium were induced by calcium infusion (3.15 mg Ca/kg BW h-1). In uremic patients, an increase in plasma AVP took place during infusion, and the changes in AVP were correlated to the changes in whole blood ionized calcium. In normals, no changes in AVP were found. In the sprue patient, an increase in plasma AVP correlated to whole blood ionized calcium was found in the hypocalcemic state, but this could not be demonstrated after treatment. Parathyroid hormone has been shown to facilitate calcium entry into cells, and it is proposed that the pathophysiological effect of calcium on AVP secretion in uremic patients is caused by the elevated parathyroid hormone level found in these patients.
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PMID:Calcium-stimulated vasopressin secretion in uremic patients: an effect mediated via parathyroid hormone? 741 83

Parathyroid hormone (PTH) has been implicated in hypertension, but PTH infusion results in vasodilation. PTH activates adenylate cyclase in vascular smooth muscle, but little is known about the factors that regulate PTH receptor/adenylate cyclase coupling in vascular cells. To characterize hormone-receptor signaling, we measured cyclic AMP levels in rat arterial smooth muscle cells in culture exposed to PTH (bovine 1-34). PTH yielded time- and concentration-dependent increases in cyclic AMP levels. Compared with isoproterenol, PTH was more potent, with a threshold at 2 x 10(-9) versus 5 x 10(-8) mol/L and half maximal responses at 10(-8) versus 2.4 x 10(-7) mol/L. PTH-induced increases in cyclic AMP were independent of extracellular calcium, cyclooxygenase metabolites, phospholipase C, and protein kinase C because PTH-induced increases in cyclic AMP were not prevented by variations in extracellular calcium, indomethacin, angiotensin II, vasopressin, and protein kinase C activators or inhibitors. PTH/adenylate cyclase coupling was G protein-dependent because increases in cyclic AMP were prevented by preincubation with cholera toxin but not with pertussis toxin. Prolonged exposure to PTH resulted in time- and concentration-dependent homologous desensitization of cyclic AMP responses. Desensitization occurred proximal to G protein/adenylate cyclase because after prolonged PTH, responses to forskolin and cholera toxin remained intact. Desensitization was independent of protein kinase A and receptor sequestration because cyclic AMP responses remained after prolonged exposure to forskolin and pretreatment with phenylarsine oxide, colchicine, and cytochalasin D. We conclude that in vascular smooth muscle cells, PTH is coupled to adenylate cyclase through a cholera toxin-sensitive G protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone/adenylate cyclase coupling in vascular smooth muscle cells. 751 68


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