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)

Hypouricemia seen with hyponatremia related to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) results from an increase in uric acid renal clearance. We studied the mechanism of the increase of uric acid excretion in 6 SIADH patients through pyrazinamide (PZA), which decreases tubular secretion of uric acid, and sulfinpyrazone (SPZ) which decreases post-secretory reabsorption of uric acid. 3 g of PZA decreased the absolute uric acid excretion from 428 +/- 244 to 105 +/- 47 micrograms/min (mean +/- SD, p less than 0.01), and 300 mg of SPZ increased the uric acid to creatinine clearance ratio from 0.31 +/- 0.05 to 0.52 +/- 0.05 mg/dl glomerular filtration rate (mean +/- SEM, p less than 0.001), which represent an increment about half of that observed in the control group. The increase of uric acid clearance in SIADH seems to result from a decrease in the post-secretory reabsorption of uric acid. After SPZ, we saw a decrease of natriuresis from 5.6 +/- 1.4 to 1.8 +/- 0.3 mmol/h (p less than 0.001), without any change of urinary flow or urinary potassium excretion.
Nephron 1985
PMID:Mechanisms of hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone. 397 80

1. A constant flow perfusion system using the isolated rat tail has been developed to facilitate the study of resistance vessel behaviour and the action of vasoactive drugs.2. Baseline resistance remains stable for several hours and dose response curves to bolus injections of pressor agents are reproducible when dialysed bovine serum albumen is used in the perfusion medium to maintain osmotic pressure.3. Noradrenaline, adrenaline, serotonin, vasopressin, angiotensin II, high potassium concentrations and sympathetic nerve stimulation constricted the vascular bed.4. Angiotensin I, bradykinin, histamine, acetylcholine and isoprenaline did not alter vascular resistance under baseline conditions.5. Maximal sensitivity to noradrenaline occurred at 32 degrees to 34 degrees C. Below 30 degrees C, resting tone increased and the pressor effect of noradrenaline was prolonged.6. Low concentrations of (+/-)-propranolol in the perfusate enhanced adrenaline and noradrenaline vasoconstriction, high concentration of (+/-)-propranolol had a direct pressor effect and did not affect catecholamine responses.7. The preparation is a simple and relatively inexpensive adjunct to established methods of studying resistance vessel behaviour under varying experimental conditions.
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PMID:Vascular resistance in the perfused isolated rat tail. 431 31

1. The effect of val(5)-angiotensin II amide, noradrenaline and vasopressin, on kidney volume and intrarenal distribution of carbon particles and thioflavine S was examined in the rat.2. Angiotensin produced a dose-dependent shrinkage of the kidney coinciding with the rise in systemic blood pressure. Noradrenaline and vasopressin, however, produced reduction in kidney volume only in much higher doses than were necessary to produce a pressor effect.3. An intravenous infusion of angiotensin sufficient to produce a diuretic response resulted in a striking increase in glomerular content of injected carbon particles, and a marked reduction in filling of the capillary plexuses of the subcortex and outer medulla. The reduction in outer medullary filling was also observed using the thioflavine S technique.4. Noradrenaline infused in amounts sufficient to produce diuresis, aortic constriction above the kidney and vasopressin injection produced no measurable change in carbon particle distribution.5. The reduction in capillary blood flow produced by angiotensin may result in impaired tubular reabsorptive capacity by reducing peritubular removal of reabsorbate, or by reducing oxygen availability. Thus the vasoconstrictor effects of angiotensin may explain its diuretic action.
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PMID:The effect of angiotensin, noradrenaline and vasopressin on blood flow distribution in the rat kidney. 433 28

1. The magnitude of the maximum constrictor response to nerve stimulation was measured in the saphenous, ear, inferior and superior mesenteric, renal and carotid arteries in the rabbit and corresponding arteries, except the ear and carotid, in the guinea-pig. The responses varied from an average rise of 350 mm Hg in the rabbit saphenous to almost no response in the rabbit carotid. The guinea-pig arteries gave consistently smaller responses than the rabbit. The response magnitude was unrelated to wall thickness or the presence of an active uptake mechanism for noradrenaline. The response did correlate with the density of adrenergic innervation, with the wall thickness to lumen ratio and with the function of the artery and the amount of connective tissue in its wall.2. The magnitude of the maximum constrictor response to noradrenaline and six other agonist drugs, acetylcholine, histamine, 5-HT, KCl, vasopressin and angiotensin II, was compared. In all arteries noradrenaline was the most powerful agonist. The maximum responses to nerve stimulation and to noradrenaline were compared. In the rabbit saphenous and ear arteries this ratio was almost 1, but in arteries such as the rabbit renal it fell below 0.5.3. Artery wall stiffness was measured from the pressure/volume relationship during distension of a closed length of artery. In a relaxed artery two components only were present, an early easily distended phase and a late relatively undistensible phase. Noradrenaline caused a third, early, very stiff phase to appear in the pressure/volume curves. This is probably due to contracted muscle. The increase in stiffness varied from 617% in the rabbit saphenous to 152% in the rabbit carotid. In conducting arteries such as the carotid the change in stiffness was a more sensitive index of noradrenaline action than vaso-constriction.4. During the measurement of wall stiffness stress relaxation was not noticeable in relaxed arteries but was prominent in arteries contracted by noradrenaline. Stress relaxation involved both the changes in wall stiffness and the ability to constrict and was reversible even in the continuing presence of agonist drugs.5. Nerve stimulation, even in arteries where its vasoconstrictor effects were equal to those of noradrenaline, gave only slight increases in artery wall stiffness, suggesting that even in these densely innervated arteries only a small fraction of the muscle is activated by nerve stimulation.
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PMID:Constrictor and compliance responses of some arteries to nerve or drug stimulation. 433 55

The frog urinary bladder undergoes, in some conditions, a marked increase of its water permeability when incubated in hypertonic media. This increase was observed with various nonpermeant solutes. It seems to result from the shrinkage of an osmo-sensitive compartment of the tissue, probably the epithelial cells. Many similarities were found between this effect and the physiological increase in water permeability (hydrosmotic response) elicited by antidiuretic hormone (ADH): both were dependent on the physiological state of the animals, and although the response was slower after hyperosmolar than after hormonal challenge, the patterns of response were similar, and in both cases markedly dependent on bathing solution temperature. Norepinephrine and prostaglandin E(1), which in this tissue reduce the hydrosmotic action of ADH, presumably by inhibiting the adenyl cylase also reduced the effect of hyperosmolarity. Conversely this effect was potentiated by incubation in the presence of oxytocin, exogenous cyclic AMP, and theophylline, conditions in which the intracellular concentration of cyclic AMP is increased. These data demonstrate that the response to hyperosmolarity is elicited, at least partly, by mechanisms also involved in the physiological hydrosmotic response to ADH.
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PMID:The effect of hypertonic media on water permeability of frog urinary bladder. Inhibition by catecholamines and prostaglandin E 1 . 434 37

Adrenergic and cholinergic agonists and antagonists were applied microelectrophoretically to over 700 neurons in the cat supraoptic nucleus, 20 percent of which were antidromically identified as neurosecretory cells. Norepinephrine uniformly depressed all sensitive cells. Acetylcholine caused both muscarinic depression and nicotinic excitation which were antagonized by atropine and dihydro-beta-erythroidine, respectively. These results support the hypothesis that norepinephrine and acetylcholine are directly involved in controlling the release of antidiuretic hormone.
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PMID:Supraoptic neurosecretory cells: adrenergic and cholinergic sensitivity. 439 31

The effects of the Ca2+-mobilizing hormones noradrenaline, vasopressin and angiotensin on the unidirectional influx of Ca2+ were investigated in isolated rat liver cells by measuring the initial rate of 45Ca2+ uptake. The three hormones increased Ca2+ influx, with EC50 values (concentrations giving half-maximal effect) of 0.15 microM, 0.44 nM and 0.8 nM for noradrenaline, vasopressin and angiotensin respectively. The actions of noradrenaline and angiotensin were evident within seconds after their addition to the cells, whereas the increase in Ca2+ influx initiated by vasopressin was slightly delayed (by 5-15s). The activation of Ca2+ influx was maintained as long as the receptor was occupied by the hormone. The measurement of the resting and hormone-stimulated Ca2+ influxes at different external Ca2+ concentrations revealed Michaelis-Menten-type kinetics compatible with a saturable channel model. Noradrenaline, vasopressin and angiotensin increased both Km and Vmax. of Ca2+ influx. It is proposed that the hormones increase the rate of translocation of Ca2+ through a common pool of Ca2+ channels without changing the number of available channels or their affinity for Ca2+.
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PMID:Noradrenaline, vasopressin and angiotensin increase Ca2+ influx by opening a common pool of Ca2+ channels in isolated rat liver cells. 608

The relationship between gastric blood flow and acid secretion has been studied by using a number of secretory stimulants and inhibitors and different techniques that measure gastric blood flow. Although there are conflicting data, there appears to be a consensus regarding the main aspects of this relationship. Agents that stimulate gastric acid secretion such as histamine, gastrin, cholinergic agents, and vagal stimulators also increase gastric blood flow. Other agents such as isoproterenol, epinephrine, and prostaglandins, which at low doses increase gastric blood flow, reduce gastric acid secretion at higher doses. Norepinephrine, vasopressin, and shock reduce gastric blood flow and thereby cause a decrease in secretion. Histamine H2-receptor antagonists reduce stimulated acid secretion and gastric blood flow. Histamine, gastrin, and acetylcholine have been shown to stimulate acid secretion in vitro. Therefore, these observations suggest that although blood flow is not a prerequisite for initiation of stimulated acid secretion, it can become rate-limiting at higher rates of secretion. Although the literature is replete with studies that attempt to characterize the relationship between gastric blood flow and acid secretion, conclusions have varied. Much of the difficulty has arisen because of the differences in technique used to measure gastric blood flow and the differences between anesthetized and unanesthetized animal preparations. Under some specific conditions, the different blood flow techniques give comparable results and this relationship can be defined.
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PMID:Blood flow and gastric secretion. 612 4

The effects of Pro-Leu-GlyNH2 (PLG), administered i.c.v. in doses of 3.5, 35, 350 and 3500 pmol, were studied on the alpha-MPT-induced disappearance of catecholamines in microdissected rat brain nuclei. PLG, dose-dependently, increased dopamine disappearance in the nucleus caudatus and globus pallidus, whereas a decrease in dopamine disappearance was observed in the nucleus dorsomedialis. Noradrenaline disappearance was decreased in the medial septal nucleus, anterior hypothalamic area and lateral amygdala. A tendency towards an increase in noradrenaline disappearance was observed in the nucl. supraopticus. These data show that PLG has a central site of action. The effects of PLG on dopamine disappearance are comparable to those previously found with vasopressin, while the effects of PLG on noradrenaline utilization show a striking similarity with those previously obtained with oxytocin.
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PMID:Pro-Leu-GlyNH2 affects dopamine and noradrenaline utilization in rat limbic-forebrain nuclei. 615 Jul 49

To further evaluate the interaction between vasopressin (AVP) and prostaglandin E2 (PGE2) in the kidney, the effects of AVP and PGE2 on cell cAMP content were examined in the isolated thick ascending limb of Henle (TAL) and the cortical collecting tubule (CCT) of rat kidney. Nephron segments were incubated in the presence of phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine (MIX), with 10 nM AVP and varying concentrations of PGE2 at 37 degrees C for 1-7 min, and the cAMP content was determined by radioimmunoassay. PGE2 suppressed the AVP-stimulated increase in cell cAMP in both medullary (MTAL) and cortical (CTAL) portions of the TAL in a dose-dependent manner. This inhibitory effect was evident at 0.28 nM PGE2 and maximum at 2.8-28 microM PGE2. By contrast, in the presence of MIX PGE2 did not inhibit AVP-stimulated cAMP increases in the CCT. However, in the absence of MIX, PGE2 suppressed cAMP accumulation in the CCT. These data suggest that PGE2 may suppress cell cAMP by inhibiting AVP-dependent cAMP formation in the TAL; PGE2 may suppress cAMP in the CCT by acting at a site(s) affected by MIX and not by inhibiting cAMP formation. The results show that although PGE2 may inhibit AVP-dependent cell cAMP accumulation in both TAL and CCT, the underlying cellular mechanisms may be different in these two distinct AVP-sensitive nephron segments.
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PMID:Effect of PGE2 on vasopressin-dependent cell cAMP in isolated single nephron segments. 619 77


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