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)

Na+-K+-ATPase was inhibited by 1 times 10-4M ethacrynic acid and mercuderamide, and by 1 times 10-3M hydrochlorothiazide and furosemide. A modification of Gilman's (1970) protein displacement assay has been used to measure c-AMP levels in toad bladder epithelial cells. Vasopressin (50 mU/ml) caused c-AMP levels to rise from 4.27 to 9.27 pmol/mg protein. Ethacrynic acid had no effect on cellular c-AMP levels after 10 min exposure to the drug, but at 90 min caused a reduction of both basal and vasopressin stimulated levels. Furosemide caused an apparent rise in c-AMP levels, dilution ratio measurements indicated interference by this drug in the assay procedure, mecuderamide also caused substantial interference with the c-AMP assay. Hydrochlorothiazide had no effect on basal or hormone stimulated levels of c-AMP. It was concluded that the inhibition of sodium transport produced by ethacrynic acid in toad bladder is probably due to inhibition of adenylate cyclase, an effect not shared by other dieuretics.
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PMID:The effect of diuretics on Na+-K+-ATPase and c-AMP levels in toad bladder epithelial cells. 16 90

A case of transient vasopressin-resistant diabetes insipidus is reported which developed during the seventh gestational month. Polyuria reached 4-6 L daily and urine osmolality remained dilute despite 21 hours of water deprivation followed by 5 U intramuscularly of aqueous pitressin, as well as four days of treatment with intranasal DDAVP (0.1-0.5 mL every 12 hours). Urinary excretion of prostaglandin E2, 1384 ng/24 hours, was fourfold that in nongravid subjects and a plasma arginine vasopressin level of 12 pg/mL was recorded. Indomethacin had no effect on urine osmolality but decreased urine volume markedly. Hydrochlorothiazide, also, decreased urine volumes, and this drug was used to manage the patient until delivery. The syndrome remitted in the puerperium, the patient concentrating her urine to 938 mOsm/kg when tested several months postpartum.
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PMID:Transient vasopressin-resistant diabetes insipidus of pregnancy. 376 91

1. The responses of the mean arterial pressure to (-)-noradrenaline, tyramine, angiotensin II-val(5)-amide, vasopressin and rat renin have been contrasted in renal hypertensive and in salt plus desoxycorticosterone hypertensive rats. The responses were measured in rats both unanaesthetized and rats anaesthetized with pentobarbitone.2. Responses of unanaesthetized, ganglion blocked renal hypertensive rats to noradrenaline, tyramine and vasopressin markedly exceeded, and to angiotensin II and renin were markedly smaller than, those of unanaesthetized ganglion blocked salt + DOC hypertensive animals. Responses to angiotensin and to renin were apparently enhanced in the latter animals.3. Hydrochlorothiazide and frusemide markedly reduced mean arterial pressure in salt + DOC hypertensive rats before and after ganglionic blockade.4. Neither diuretic caused significant reduction in the mean arterial pressures of unanaesthetized, renal hypertensive rats in the absence of ganglionic blockade: frusemide did so in anaesthetized and unanaesthetized rats after ganglionic blockade.5. Whereas the diuretics did not affect the responses of the renal hypertensive rats to pressor agents, frusemide and to a lesser extent hydrochlorothiazide tended to depress the responses to pressor agents in salt induced hypertension.6. Hydrochlorothiazide did not influence mean arterial pressure in unanaesthetized rats with neurogenic hypertension.
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PMID:Responses of mean arterial pressure to pressor agents and diuretics in renal hypertensive and salt hypertensive rats. 432 21

The effects of diazoxide and hydrochlorothiazide on vasopressin-induced increments in osmotic water flow and sodium transport across the frog bladder were studied. Diazoxide enhanced the vasopressin-induced osmotic water flow of the bladder, but did not affect the cyclic AMP- or theophylline-induced water flow. Hydrochlorothiazide did not affect the vasopressin-induced water flow. Our results suggest that diazoxide increased the water flow by inhibiting the activity of phosphodiesterase in bladder epithelial cells, whereas hydrochlorothiazide did not. On the other hand, both drugs suppressed the short-circuit current of the bladder membrane and inhibited the Na,K-dependent ATPase activity of the kidney cells. These results suggest that both drugs decreased sodium transport in the bladder by inhibiting Na,K-dependent ATPase activity.
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PMID:Effects of diazoxide and hydrochlorothiazide on water permeability and sodium transport in the frog bladder. 628 Feb 12

Our evaluation of hyponatremic patients is in a state of confusion because the assessment of the volume status of the patient and determinations of urine sodium concentrations (UNa) >30-40 mEq/L have dominated our approach despite documented evidence of many shortcomings. Central to this confusion is our inability to differentiate cerebral/renal salt wasting (C/RSW) from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), syndromes with diametrically opposing therapeutic goals. The recent proposal to treat most or all hyponatremic patients makes differentiation even more important and reports of C/RSW occurring without cerebral disease leads to a clinically important proposal to change cerebral to renal salt wasting (RSW). Differentiating SIADH from RSW is difficult because of identical clinical parameters that characterize both syndromes. Determination of fractional urate excretion (FEurate) is central to a new algorithm, which has proven to be superior to current methods. We utilized this algorithm and differences in physiologic response to isotonic saline infusions between SIADH and RSW to evaluate hyponatremic patients from the general medical wards of the hospital. In 62 hyponatremic patients, 17 (27%) had SIADH, 19 (31%) had reset osmostat (RO), 24 (38%) had RSW, 1 due to HCTZ and 1 Addison's disease. Interestingly, 21 of 24 with RSW had no evidence of cerebral disease and 10 of 24 with RSW had UNa < 20 mEqL. We conclude that 1. RSW is much more common than is perceived, 2.the term cerebral salt wasting should be changed to RSW 3. RO should be eliminated as a subclass of SIADH, 4. SIADH should be redefined 5. The volume approach is ineffective and 6. There are limitations to determining UNa, plasma renin, aldosterone or atrial/brain natriuretic peptides. We also present data on a natriuretic peptide found in sera of patients with RSW and Alzheimer's disease.
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PMID:Determining Fractional Urate Excretion Rates in Hyponatremic Conditions and Improved Methods to Distinguish Cerebral/Renal Salt Wasting From the Syndrome of Inappropriate Secretion of Antidiuretic Hormone. 3056 Jan 27