AI Article Synopsis
- Endothelin (ET)-1 is produced in the kidneys and can be measured in urine as an indicator of renal function, prompting an investigation into urinary ET receptor types (ET(A) and ET(B)) in both normal and hypertensive patients.
- The study found intact ET(A) and ET(B) receptors in the urine of healthy and hypertensive individuals, with higher ET(A) levels in hypertensive patients compared to normotensive ones, while ET(B) levels were similar between the two groups.
- Both ET receptors were detected in kidney tubular cells and bladder tissue, with their levels in urine influenced by urine concentration, indicating that they are shed primarily based on urine flow dynamics, leaving open questions about
Article Abstract
Background/aims: Endothelin (ET)-1 is produced by most renal cell types. Renal tubular and vascular cells express both the ET receptors ET(A) and ET(B). Since significant amounts of ET-1 of renal origin were detected in human urine, urinary ET-1 has been used as an index for the capacity of renal ET-1 production. Here, we determine the existence of additional components of the intrarenal ET system, namely the ET(A) and ET(B) receptor subtypes, in the urine of normal and hypertensive subjects.
Methods: ET(A) and ET(B) receptors were detected in urine samples that were concentrated by TCA precipitation, Speedvac or ProteoSpin.
Results: Analysis of the human urine extracts revealed the existence of approximately 50 and 55 kDa of immunoreactive proteins, corresponding to ET(B) and ET(A), respectively, indicating that intact ET(A) and ET(B) are excreted in the urine of healthy subjects and hypertensive patients. Normotensive and hypertensive subjects had statistically comparable ET(B) excretion normalized to creatinine (0.58 +/- 0.16 vs. 0.83 +/- 0.17 microg/mg creatinine, respectively; p = 0.304). In contrast, ET(A) excretion was higher among hypertensive subjects (0.05 +/- 0.01 vs. 0.11 +/- 0.02 microg/mg creatinine; p = 0.0451). Immunostaining of ET(A) and ET(B) in the human urinary system revealed expression of both receptors, principally in tubular cells (mainly in medullary collecting ducts) and in the bladder urothelium, and ET(A) expression in the peritubular capillaries and arterioles. Urinary ET receptors closely and inversely correlated with indices of urine concentration, suggesting that their shedding is principally affected by urine flow.
Conclusion: ET receptors are present in human urine, conceivably originating within the urinary system. Their excretion is principally affected by urinary concentration. It remains to be determined whether urinary ET(A)/ET(B) is of physiological/pathophysiological relevance.
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