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)

To determine the mechanism by which vasopressin increases sodium transport in sodium-transporting, tight epithelia, we examined single amiloride-blockable Na channels in membrane patches from cultured distal nephron cells (A6) either before or after treatment with arginine vasopressin. Pretreatment of cells with vasopressin (40 mU/ml) for 40-50 min increases NPo (N, the number of Na channels; Po, the open probability of an individual Na channel). The increase in NPo is due to an increase in the number of conductive Na channels with little or no change in the open probability of individual Na channels. Pretreatment of cells for 1 h with 1 mM N6,2'-O-dibutyryladenosine 3', 5'-cyclic monophosphate (DBcAMP) also increased NPo. The increase in NPo caused by DBcAMP pretreatment is also due to the increase in the number of conductive Na channels with no change in the open probability of individual Na channels. Cells pretreated with cholera toxin (CTX; 250 ng/ml) for 4 h appeared similar to cells that had been treated with vasopressin or DBcAMP; that is, the number of Na channels per patch increased with little or no effect on the open probability of individual Na channels. For patches from many untreated cells, when the frequency of occurrence is plotted against the number of channels in an individual patch, the histogram consists of a single peak with a number of channels per patch of 2.0 +/- 1.5 (+/- SD, 126 patches). After pretreatment of cells with vasopressin, DBcAMP, or CTX, the same histogram contains two peaks after vasopressin of 1.8 +/- 1.2 and 9.2 +/- 1.5 (+/- SD, 38 and 53 patches, respectively). These observations suggest that pretreatment of cells with vasopressin, DBcAMP, or CTX may act by promoting insertion of clusters of new sodium channels.
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PMID:Effects of vasopressin and cAMP on single amiloride-blockable Na channels. 185 5

The effect of cyclophosphamide (CTX) on the renal handling of water and sodium and on plasma concentrations of vasopressin (AVP) and of the atrial natriuretic factor (ANF) was studied in the rabbit. When compared to controls, animals receiving CTX (100 mg/kg IV) showed an increase in the diuresis and natriuresis. In addition, ANF plasma concentrations increased by 84% between 4 and 8 hours after CTX, while AVP plasma concentrations remained unchanged. It is concluded that in the rabbit CTX has a diuretic and a natriuretic effect that may, at least in part, be related to the increase in ANF plasma concentrations.
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PMID:The effect of cyclophosphamide on arginine vasopressin and the atrial natriuretic factor. 295 Aug 59

To elucidate the mechanism of cyclophosphamide (CTX)-induced antidiuresis, plasma and urine volume as well as serum electrolytes, creatinine, osmolality, and appropriate hormones were monitored serially during 19 courses of chemotherapy. In spite of plasma hypotonicity and urinary hypertonicity, the plasma vasopressin concentrations were unaltered. Intravenous isotonic hydration did not prevent water retention, but did not lead to plasma hypotonicity, and compensated for modest urinary sodium losses. Furosemide diuresis did not prevent the development of hyponatremia in patients receiving hypotonic hydration. The results indicate that the origin of this self-limited syndrome is a direct effect of CTX on the renal tubule, permitting increased water reabsorption and sodium loss. The likelihood that water and salt imbalance will develop after CTX administration can be reduced by vigorous isotonic hydration, and pharmacological diuresis.
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PMID:Studies on the antidiuretic effect of cyclophosphamide: vasopressin release and sodium excretion. 746 88

Nitric oxide (NO) is known to be an important relaxant of contractile activity in various muscles including the human uterine arteries. It has been suggested that NO plays a role in modulation of vascular action of arginin vasopressin (AVP), a strong vasoconstrictor of the human uterine arteries. Therefore, the purposes of this study were to investigate an involvement of endogenous NO in regulation of responses of the human intrauterine arteries to AVP and examine the effect of exogenous NO on contractions of the human intrauterine arteries evoked by AVP. Pretreatment of the artery rings with L-NA, an inhibitor of NO synthase significantly increased the resting force and enhanced the artery responses to AVP. The opposite effect has been observed after administration of 10(-6) mol/L sodium nitroprusside (SNP). Pretreatment of the artery rings with 10(-7) M CTX, a blocker of Ca(2+)-sensitive potassium channels with large conductance, did not change significantly their responses to AVP. Glibenclamide (1.5.10(-6) mol/L), a blocker of ATP-dependent potassium channels and apamin (10(-8) M), a specific blocker of Ca(2+)-sensitive potassium channels with small conductance strongly enhanced the maximum responses of the artery rings to AVP. Pretreatment with CTX significantly decreased the relaxation induced by SNP while apamin attenuated the sensitivity to SNP resulted in rightward shift of the concentration-response curve to SNP. In conclusion, this study indicates that: NO plays a role in regulation of both the vascular tone of the human intramyometrial arteries and their response to AVP. Ca(2+)-sensitive K(+) channels with small and large conductance are involved in the SNP-induced relaxation of these arteries. The pathways of this relaxation cannot be sufficiently explained at this moment and need further investigation.
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PMID:Effect of nitric oxide on responses of the human uterine arteries to vasopressin. 1799 97