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)

Previous studies demonstrated that in rat kidney, arginine-vasopressin (AVP), glucagon (GLU), calcitonin and parathyroid hormone exert similar effects on the thick ascending limb of Henle's loop (TALH). To ascertain the physiological significance of such multiple hormonal control of TALH function, it is necessary to establish whether one hormone can exert its effect on TALH, even when other hormones are present. We therefore compared renal responses to submaximal (1 ng/min) and maximal (10 ng/min) doses of glucagon in rats deprived of endogenous AVP, GLU, calcitonin and parathyroid hormone with the responses of similar rats given a maximal dose of AVP (40 pg/min). Administration of glucagon or AVP alone reduced Mg fractional excretion, but the reduction was more marked when both hormones were given together. Consequently, their effects were additive, at submaximal and maximal doses. In the presence of AVP + glucagon, urinary osmolality was also higher than in the presence of AVP alone (Umax: 1242 +/- 49 vs. 936 +/- 50 mosmol/kg; p less than 0.001). This latter effect may indicate that AVP and glucagon also exert additive effects on Na reabsorption in the TALH.
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PMID:Additive effects of glucagon and vasopressin on renal Mg reabsorption and urine concentrating ability in the rat. 382 66

We activated three known components of the adenylate cyclase system in renal membranes from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. The basal adenylate cyclase activity and responses to plasma membrane receptor activation by parathyroid hormone, isoproterenol and vasopressin were not different between the two strains. The response to prostaglandin E2 (PGE2), however, was less in the SHR than in the WKY at five, (P less than 0.05), 12 (P less than 0.01) and 16 (P less than 0.01) weeks of age. Activation of either the guanosine-5'-triphosphate (GTP) binding regulatory protein (N) with sodium fluoride (NaF) and guanyl-5'-yl-imidodiphosphate [Gpp(NH)p], or the catalytic unit with manganese chloride (MnCl2) or forskolin were not different between the two groups. When the medullary and cortical plasma membrane adenylate cyclase responses were studied separately, the observed decreased response to PGE2 (of SHR) was found to be entirely in the cortex. Also, the NaF response was reduced in the cortical region of the 12-week-old rats, a finding suggesting a possibility of a post receptor defect. These results show that there is a defective renal adenylate cyclase response specific to prostaglandin E2 in SHR. This defect could be related to the development of hypertension, by changing the natriuretic and/or renal vasodilating effects of these prostaglandins.
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PMID:Defective renal adenylate cyclase response to prostaglandin E2 in spontaneously hypertensive rats. 392 77

We evaluated the effects of human calcitonin (hCT) on electrolyte excretion in hormone-deprived rats, that is, in the absence of endogenous parathyroid hormone, antidiuretic hormone, thyrocalcitonin and glucagon, the effects of which might have interfered with those of exogenous calcitonin. Plasma hCT levels, measured by radioimmunoassay, varied from 0 to 32 ng/ml. In these rats, hCT decreased magnesium (Mg) and calcium (Ca) excretion in a dose-dependent fashion. Maximal decreases were observed for hCT plasma concentrations comprised between 3 and 5 ng/ml, and persisted at the highest doses. Sodium, potassium, water, and total solute excretions were constant in the calcitonin concentration range explored. The same was observed for phosphate, except that slight but significant phosphaturia was elicited by the highest doses. Calcium and phosphate infusions to attenuate the fall in plasma Ca and phosphate concentration subsequent to hCT infusion, did not alter the hormonal effect on Ca and Mg excretion. hCT can therefore directly modulate Mg and Ca reabsorption by the kidney at plasma concentrations within the physiological range. The maximal effects on Mg and Ca reabsorption were obtained at plasma concentrations which are generally reached after maximal stimulation of endogenous calcitonin secretion. It is suggested that in rats, endogenous secretion of calcitonin stimulates Ca and Mg renal reabsorption without modification of sodium and phosphate excretion.
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PMID:Modulation by calcitonin of magnesium and calcium urinary excretion in the rat. 399 91

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on the handling of water and electrolytes by the juxtamedullary nephrons were studied on rats with reduced circulating levels of antidiuretic hormone (ADH), parathyroid hormone, calcitonin, and glucagon, all of which stimulate the adenylate cyclase system of the thick ascending limb and the distal tubule. In such hormone-deprived rats and in hormone-deprived + dDAVP rats, the concentration of Na, Cl, and total solutes was lower in the ascending than in the descending limbs, whereas the inulin concentration was similar at both sites. dDAVP did not alter the fraction of NaCl remaining in the thin limbs, but tended to reduce that of Mg and Ca. On the other hand, dDAVP significantly increased the fraction of filtered K remaining from 65.8 +/- 5.2 to 107.3 +/- 15.8%. A direct correlation was observed between the fraction of filtered K remaining at the tip of the juxtamedullary loops and the fractional excretion rate of K in urine. Since dDAVP enhances distal K net secretion, as previously shown in our laboratory, these results indicate that the medullary recycling of K from nephron terminal segments to Henle's loop of juxtamedullary nephrons is stimulated by this peptide.
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PMID:Effects of dDAVP on rat juxtamedullary nephrons: stimulation of medullary K recycling. 402 56

Distal nephron epithelia of defined anatomical origin were microdissected from rabbit kidneys and individually explanted into an in vitro culture system. The 7 day monolayers grown from four different nephron epithelia were studied for the presence and amount of adenylate cyclase reaction product. In each case basal adenylate cyclase was compared with the enzyme reaction product after stimulation by arginine vasopressin, calcitonin, parathyroid hormone (PTH) and isoproterenol. In cortical collecting tubule cultures, the reaction was stimulated by vasopressin greater than isoproterenol greater than calcitonin. PTH had no effect. In cortical thick ascending loop of Henle cells, the stimulation was by calcitonin greater than vasopressin = PTH. Isoproterenol had no effect. In medullary ascending loop epithelia, stimulation was by vasopressin = calcitonin. Neither isoproterenol nor PTH had an effect. These observations indicate that adenylate cyclase is histochemically demonstrable in cultivated cells from rabbit distal nephron segments and that the enzyme activation by hormones is differential according to the epithelium of origin.
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PMID:Histochemical localization of hormone sensitive adenylate cyclase in defined nephron epithelia in culture. 403 Apr 8

Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl2 (serum calcium level, 12.8 +/- 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 +/- 2 mm Hg to 129 +/- 3 mm Hg, p less than 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 +/- 0.02 mm Hg/(ml/min)/kg body weight to 0.50 +/- 0.02 mm Hg/(ml/min)/kg body weight (p less than 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCl2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia.
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PMID:Mechanism of acute hypercalcemic hypertension in the conscious rat. 407 24

Thyrocalcitonin (TCT) increased the rate of accumulation of adenosine 3':5'-cyclic phosphate (cyclic AMP) when added to incubations containing washed particles from whole rat kidney, adenosine triphosphate (ATP), MgSO(4), and caffeine. The maximum stimulatory effect of TCT, 44 +/- 6.7 per cent, was always less than the 150 to 250 per cent increase produced by parathyroid hormone (PTH). The effect of both hormones together was no greater than that of PTH alone when each was present at a maximally effective concentration. Since neither TCT nor PTH altered the rate of degradation of cyclic AMP by the kidney preparation, it may be inferred that their effects on cyclic AMP accumulation are the result of increased formation of cyclic AMP. Adenyl cyclase activity in homogenates of renal cortex was stimulated to a greater extent by TCT and PTH than was that of medulla, whereas, as reported earlier, the effect of vasopressin was much larger with homogenates of medulla. The accumulation of cyclic AMP in incubations of rat kidney cortex slices was increased 20 to 60 per cent by TCT and 50 to 140 per cent by PTH. The accumulation of cyclic AMP in incubations of rat calvaria was increased about threefold with TCT and nine to tenfold with PTH, while reduced and alkylated TCT had less than 10 per cent of the activity of TCT. These observations are consistent with the view that the physiological effects of TCT and PTH in kidney and bone are secondary to the enhanced formation of cyclic AMP.
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PMID:Effect of thyrocalcitonin on adenosine 3':5'-cyclic phosphate formation by rat kidney and bone. 431 99

Properties of adenyl cyclase of normal adrenals and of a corticosterone-producing adrenal cancer of the rat have been compared. Enzyme activity was found in all particulate fractions of both tissues. The cyclase of the tumor as well as of the adrenals was stimulated by adrenocorticotropic hormone (ACTH) over similar concentration ranges. Unexpectedly, the tumor enzyme was also stimulated by epinephrine, norepinephrine, and thyroid-stimulating hormone (TSH). These hormones produced a dose-related effect over a concentration span that was comparable with that for ACTH. The tumor cyclase was not responsive to angiotensin Il, vasopressin, glucagon, insulin, growth hormone, parathyroid hormone, and thyrocalcitonin. ACTH was the only hormonal preparation that stimulated normal adrenal cyclase. These findings are compatible either with the possibility that the adenyl cyclase receptor of the tumor has undergone structural alteration with a consequent loss of specificity for ACTH or with the possibility that the tumor possesses several cyclase regulatory receptors.
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PMID:Abnormal hormone responses of an adrenocortical cancer adenyl cyclase. 432 11

Previous work has suggested that resistance to vasopressin in two strains of mice with nephrogenic deficiency of urinary concentration may entail a defect in the action of vasopressin at the cellular level. Several components involved in this action were therefore examined in vitro in renal medullary tissues from control mice (genotype VII +/+) and two genotypes with mild diabetes insipidus (DI +/+ nonsevere) and marked (DI +/+ severe) vasopressin-resistant concentrating defects. No significant differences were found in the affinity of adenylate cyclase for [8-arginine]-vasopressin (AVP), tested over a range of hormone concentration from 10(-10) to 10(-5) M. However, maximal stimulation of adenylate cyclase by saturating concentrations of AVP (intrinsic activity) was markedly decreased from control values in DI +/+ severe mice, and decreased to a lesser extent in DI +/+ nonsevere animals. A significant correlation was found between the activity of adenylate cyclase maximally stimulated by AVP in a given genotype, and the urine osmolality in the same animals. There were no significant differences in maximal stimulation of renal medullary adenylate cyclase in control experiments: not when stimulated nonspecifically by sodium fluoride, nor when stimulated by AVP in tissues from rats with induced water diuresis as compared to antidiuretic rats. Nor were there significant differences between VII +/+ and DI +/+ severe mice in the activity of renal cortical adenylate cyclase, either basal or when stimulated by parathyroid hormone. Furthermore, the abnormal genotypes did not differ significantly from control mice in the renal medullary activities of cyclic AMP phosphodiesterase or cyclic AMP-dependent protein kinase, nor in the content of microtubular subunits (assessed as colchicinebinding protein). The results are compatible with the view that impaired stimulation of renal medullary adenylate cyclase by vasopressin might be the sole or contributing cause of the vasopressin-resistant concentrating defect in the diseased mice; however, a causal relationship has not yet been proved.
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PMID:Cellular action of antidiuretic hormone in mice with inherited vasopressin-resistant urinary concentrating defects. 436 80

Peptide hormones labelled with radioactive iodine were partitioned into the aqueous two-phase polymer systems developed by Albertsson (1960) and the conditions required for separation of free from antibody-bound hormone have been worked out. Hormones studied included insulin, growth hormone, parathyroid hormone and [arginine]-vasopressin. Free and antibody-bound hormones show different distribution coefficients in a number of systems tested; two systems, the dextran-polyethylene glycol and dextran sulphate-polyethylene glycol system, give optimum separation. Free hormones distribute readily into the upper phase of these systems, whereas hormone-antibody complexes, as well as uncombined antibody, are found almost completely in the lower phase. Various factors including the polymer concentration, the ionic composition of the system, the nature of the hormone and the nature of added serum protein differentially affect the distribution coefficients for free and antibody-bound hormone. These factors can be adequately controlled so as to improve separation. The two-phase partition method has been successfully applied to measure binding of labelled hormone to antibody under standard radioimmunoassay conditions. It exhibits several advantages over the method of equilibration dialysis and can be applied to the study of non-immunological interactions.
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PMID:Distribution of free and antibody-bound peptide hormones in two-phase aqueous polymer systems. 467 74


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