Angiotensin-II and endothelin-1 levels in children with renoprival hypertension
University of Miami, Jackson Memorial Hospital, Department of Pediatrics, Division of Nephrology, PO Box 016960, Miami, FL 33101, USA.Pediatric Nephrology (Impact Factor: 2.86). 07/2001; 16(6):493-6. DOI: 10.1007/s004670100579
Children with end-stage renal disease (ESRD) often remain hypertensive despite bilateral nephrectomy and aggressive fluid removal on hemodialysis. We speculated that an extrarenal source of renin might contribute to the release of "tissular" angiotensin-II (AT-II) generating hypertension in anephric patients. At the same time, experimental evidence supports that peripheral AT-II vasoconstrictive effect is likely mediated by endothelin-1 (ET-1). Thus, it is conceivable that hypertension in ESRD patients may be due, in part, to a cascade involving vascular production and secretion of AT-II and ET-1. In order to establish the relationship between AT-II, ET-1, and blood pressure we performed a pilot study to measure predialysis systolic and diastolic blood pressures (SBP and DBP, respectively) and serum AT-II and ET-1 levels in 12 anephric children receiving hemodialysis. Predialysis AT-II and ET-1 levels were similar in all patients, and neither value correlated with their mean SBP or DBP. In patients with postdialysis hypertension, there was no correlation between predialysis AT-II and ET-1 plasma levels. We therefore find no evidence to suggest that vascular-mediated AT-II and/or ET-1 contributes significantly to hypertension in anephric patients.
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ABSTRACT: Unexplained hypertension was observed in three anephric children on hemodialysis. We investigated the possible involvement of a novel hypertensive extra-renal enzyme new pressor protein (NPP), related to coagulation beta-FXIIa. Currently, NPP activity can only be determined by a rat bioassay model. On study day 1, pre dialysis, patients 1, 2, and 3 were hypertensive and their plasmas raised rat systolic blood pressure (SBP) by 45, 34, and 9 mmHg, respectively. Post dialysis, patients 1 and 2 reached their estimated dry body weight and their systemic pressures dropped, while patient 3 remained hypertensive and hypervolemic. Their post-dialysis plasmas raised rat SBP by 22, 14, and 9 mmHg, respectively. On day 2, similar relationships between patient SBP, volume status, and plasma NPP-like activity in rats were observed. The characteristic rat BP responses, lack of inhibition by captopril (ruling out a renin-mediated effect), and inhibition by soybean trypsin inhibitor support co-identity with NPP. Plasma FXIIa (combined alpha-FXIIa and beta-FXIIa) was measured by immunoassay and found to be elevated in all patients. This investigation suggests that there is high endogenous NPP activity in the plasmas of these hypertensive hemodialysis patients, it changes with SBP and fluid volume, and is a possible contributor to their hypertension. Further studies are required to examine the wider applicability of these novel findings.Pediatric Nephrology 11/2003; 18(10):1025-31. DOI:10.1007/s00467-003-1246-6 · 2.86 Impact Factor
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ABSTRACT: Hypertension in subjects on long term dialysis is frequent. Its origins are found in extracellular volume overload, which is complicated by increased peripheral arterial resistance. The latter is affected by many systems, including that of renin-angiotensin, endothelin, nitric oxide, the sympathetic nervous system, and others. The interaction between these factors may explain why the control of hypertension in dialysis patients requires ongoing attention to the many aspects of good dialysis.NÃ©phrologie & ThÃ©rapeutique 10/2007; 3. DOI:10.1016/S1769-7255(07)80630-4 · 0.40 Impact Factor
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