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248 results on '"Hayslett, J P"'

11. Dilutional hyponatremia in pre-eclampsia.

Author

Hayslett, John P., Katz, David L., Hayslett, J P, Katz, D L, and Knudson, J M

Subjects
PREECLAMPSIA, HYPONATREMIA, DISEASES in women, NEPHROTIC syndrome, VASOPRESSIN, EVALUATION of medical care, PREGNANCY, WATER, DISEASE complications, THERAPEUTICS
Abstract

Objective: The objective of this report is to describe a defect in water metabolism, characterized by hyponatremia, in patients with pre-eclampsia-induced nephrotic syndrom.Study Design: This was an observational study of 3 women.Results: Hyponatremia was observed in 3 women with pre-eclampsia characterized by various extrarenal manifestations, as well as by nephrotic syndrome with normal or nearly normal renal function. Restriction in water intake partially corrected hyponatremia before delivery in each case, and no complications were observed in the neonates. The mechanism of impaired excretion of water in these patients is proposed to involve persistent and inappropriate production of vasopressin through stimulation of the nonosmotic mechanism for vasopressin secretion in response to a reduction in effective plasma volume.Conclusions: These results indicate for the first time that women with pre-eclampsia are, at least when nephrotic, at risk for development of dilutional hyponatremia, which can cause neurologic complications that simulate those of eclampsia. [ABSTRACT FROM AUTHOR]

Published
1998
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12. Effect of glucocorticoids on rectal transport in normal subjects and patients with ulcerative colitis.

Author

Sandle, G I, Hayslett, J P, and Binder, H J

Abstract

The acute effects of single pharmacological doses of glucocorticoid hormones on net electrolyte and water transport and electrical potential difference (pd) in the rectum was studied in control subjects and in patients with either active or inactive ulcerative colitis, using a dialysis technique. Compared with 17 control subjects, nine patients with active ulcerative colitis exhibited marked decreases in net sodium absorption and rectal pd, while these transport parameters were normal in six patients with inactive ulcerative colitis. Intravenous administration of hydrocortisone hemisuccinate (100 mg) resulted five hours later in significant and quantitatively similar increases in net sodium and water absorption and pd in nine control subjects, seven patients with active ulcerative colitis, and six patients with inactive ulcerative colitis. Intravenous administration of methylprednisolone phosphate (40 mg) to eight control subjects produced increases in net sodium and water absorption and pd five hours later, which did not differ significantly from those produced by hydrocortisone; methylprednisolone induced similar changes in two patients with active ulcerative colitis. These results indicate that single pharmacological doses of glucocorticoids stimulate acute increases in rectal sodium and water absorption in control subjects and in patients with acute ulcerative colitis. The ability of systemically administered glucocorticoids to reduce diarrhoea in ulcerative colitis may therefore be related to direct effects on distal colonic sodium and water transport, as well as to their better known anti-inflammatory action. [ABSTRACT FROM PUBLISHER]

Published
1986

16. Wilson's disease with reversible renal tubular dysfunction. Correlation with proximal tubular ultrastructure.

Author

Elsas, Louis J., Hayslett, John P., Spargo, Benjamin H., Durant, Joseph L., Rosenberg, Leon E., Elsas, L J, Hayslett, J P, Spargo, B H, Durant, J L, and Rosenberg, L E

Subjects
HEPATOLENTICULAR degeneration, RENAL tubular transport, AUTOANTIBODY analysis, COPPER metabolism, ACUTE kidney failure, BIOPSY, COPPER, CREATININE, ELECTRON microscopy, GLOMERULAR filtration rate, GLOMERULONEPHRITIS, KIDNEY glomerulus, KIDNEY tubules, PENICILLAMINE, PROTEINURIA, SYSTEMIC lupus erythematosus, DISEASE complications
Abstract

Presents a study of Wilson's disease with reversible renal tubular dysfunction. Method of the study; results and discussion; Conclusion.

Published
1971
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18. Studies on the mechanism of non-oliguric experimental acute renal failure

Author

Appel, G. B., Siegel, N. J., Appel, A. S., and Hayslett, J. P.

Subjects
Male, Vasopressins, Water, Biological Transport, Rats, Inbred Strains, Acute Kidney Injury, urologic and male genital diseases, Kidney, Rats, Disease Models, Animal, Regional Blood Flow, Animals, Potassium Dichromate, Gentamicins, Research Article, Glomerular Filtration Rate
Abstract

Although acute renal failure, caused either by renal ischemia or nephrotoxic agents, is usually characterized by oliguria, a severe fall in glomerular filtration rate, and a fall in renal blood flow, some patients and experimental models display a non-oliguric pattern of renal injury. The present study was designed to evaluate the mechanism of preservation of high urinary flow rate under this condition. Following the administration of the aminoglycoside gentamicin to rats for five days, a decrease in concentrating ability was demonstrated, caused by impaired vasopressin-mediated water transport. Further treatment resulted in a fall in Cin to 15 percent of control, although RBF was reduced to only 67 percent of control, and urine flow rate rose above control levels. Induction of acute and renal failure with dichromate was associated with variable high or low urinary flow rates according to pre-injury intake of sodium. Urine volume correlated directly with cortical blood flow. These data suggest that the non-oliguric pattern of acute renal injury is caused by preservation of cortical perfusion in the setting of severe tubular injury.

Published
1981

21. Vasopressin-stimulated electrogenic sodium transport in A6 cells is linked to a Ca(2+)-mobilizing signal mechanism.

Author

Hayslett, J P, Macala, L J, Smallwood, J I, Kalghatgi, L, Gassala-Herraiz, J, and Isales, C

Abstract

Vasopressin is known to activate two types of cell surface receptors; V2, coupled to adenylate cyclase, and V1, linked to a Ca(2+)-dependent transduction system. We investigated whether arginine vasopressin (AVP) stimulation of electrogenic sodium transport in A6 cells, derived from Xenopus laevis, is mediated by activation of either one or both types of AVP-specific receptors. AVP caused a rapid increase in electrogenic sodium transport, reflected by the transepithelial potential difference (VT) and equivalent short circuit current (Ieq) measurements. AVP also rapidly increased intracellular Ca2+ (Ca2+i) and total inositol trisphosphate. The increase in Ieq was dependent on the rise in (Ca2+i), because 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) dose-dependently inhibited the Ieq response. There was no evidence, however, that activation of adenylate cyclase mediated AVP-stimulated Ieq; transport was not inhibited after AVP-induced activation of adenylate cyclase was abolished by 2',5'-dideoxyadenosine or when cAMP-dependent protein kinase (PKA) activity was abolished by the specific PKA inhibitor IP20. Further studies showed that although both forskolin and 8-(4-chlorophenylthio)-cAMP stimulated Ieq, this occurred by mechanisms independent of PKA activation. These results indicate that AVP-stimulated Na+ transport is mediated by a V1 receptor and a Ca(2+)-dependent mechanism.

Published
1995

22. Renal disease

Author

Kashgarian, M., Hayslett, J. P., and Spargo, B. H.

Subjects
Vasculitis, Hypertension, Renal, Nephritis, Amyloidosis, Kidney Tubular Necrosis, Acute, Kidney, Basement Membrane, Glomerulonephritis, Urinary Tract Infections, Humans, Immune Complex Diseases, Lupus Erythematosus, Systemic, Diabetic Nephropathies, Kidney Diseases, Research Article
Published
1977

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