Feeding rats a low-protein (8%) diet (LPD) for 2 wk induces a facilitated urea transporter in rat initial inner medullary collecting ducts (IMCDs). To determine whether this is preceded by an increase in mRNA abundance, we designed degenerate polymerase chain reaction primers to the rabbit facilitated urea transporter (UT2; G. You, C. P. Smith, Y. Kanai, W.-S. Lee, M. Stelzner, and M. A. Hediger. Nature Lond. 365: 844-847, 1993) and amplified a 716-bp cDNA fragment to perform Northern analysis of the base or tip of rat inner medulla. In the base, the predominant transcript was a 2.9-kb band, which increased 55% after 1 wk on an LPD; there was no change in a 4-kb band. In the tip, the 4-kb band predominated, but neither band varied with an LPD. Next, we functionally characterized the induced urea transporter using microperfused initial IMCDs from rats fed an LPD for 2 wk. First, 100 pM arginine vasopressin (AVP) stimulated urea permeability (Purea); 10 nM AVP increased Purea further. Second, raising perfusate and bath osmolality to 690 mosmol/kgH2O (NaCl added) stimulated Purea; adding AVP (10 nM) increased Purea further. Third, thiourea reversibly inhibited AVP-stimulated Purea.(ABSTRACT TRUNCATED AT 250 WORDS)
J Clin Hypertens (Greenwich). 2010;12:96–103. ©2009 Wiley Periodicals, Inc. Hypertension is very common in dialysis patients. Disorders of mineral metabolism have been linked to vascular calcification and hypertension in dialysis. Fifty‐four hemodialysis patients were included in a cross‐sectional study in a dialysis unit during a 6‐month period. Linear regression analysis was done between averages of calcium and phosphorus (ca × ph) product and blood pressures (BPs). Ca × ph was significantly associated with systolic BP predialysis (P=.03, R=0.28), diastolic BP predialysis (P=.001, R=0.44), predialysis mean arterial pressure (MAP) (P=.002, R=0.4), and diastolic BP postdialysis (P=.03, R=0.26). No relationship was found with pulse pressures. Multilinear regression analysis was then done between ca × ph product and BPs adjusting for age, sex, hemoglobin, diabetes, albumin, parathyroid hormone, ultrafiltration volume, and average BP medications per patient. There was a strong positive association with predialysis systolic BP (P=.003, R2=0.49), predialysis MAP (P=.001, R2=0.51), and postdialysis MAP (P=.02, R2=0.65). No associations with pulse pressures were detected. The study findings suggest that ca × ph product is significantly associated with dialysis MAP and not pulse pressure. This is likely secondary to the stronger relationship with diastolic BP than with systolic BP. Prospective studies looking into the associated hemodynamic parameters related to arterial stiffness and endothelial dysfunction along with measures for calcifications would be very beneficial.
This study tested whether glucocorticoids regulate tubular urea transport. Urea permeability was measured in perfused inner medullary collecting duct (IMCD) subsegments from rats that underwent adrenalectomy, adrenalectomy plus replacement with a physiologic dose of glucocorticoid (dexamethasone), or sham operation. Compared with sham rats, basal urea permeability in terminal IMCD was significantly increased in adrenalectomized rats and reduced in dexamethasone-treated rats. Vasopressin significantly increased urea permeability in all three groups. In contrast, there was no difference in basal or vasopressin-stimulated urea permeability in initial IMCD between the three groups. Next, membrane and vesicle fraction proteins were isolated from inner medullary tip or base and Western analysis was performed by use of an antibody to the rat vasopressin-regulated urea transporter. Vasopressin-regulated urea transporter protein was significantly increased in both membrane and vesicle fractions from the inner medullary tip of adrenalectomized rats. There was no change in vasopressin-regulated urea transporter protein in the inner medullary base, and Northern analysis showed no change in urea transporter mRNA abundance in either inner medullary region. It was concluded that glucocorticoids can downregulate function and expression of the vasopressin-regulated urea transporter in rat terminal IMCD.
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