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. Expression, localization, and regulation of aquaporin-1 to -3 in rat urothelia. Am J Physiol Renal Physiol 282: F1034-F1042, 2002. First published January 29, 2002 10.1152/ajprenal.00136.2001.-Although mammalian urothelia are generally considered impermeable to constituents of urine, in vivo studies in several species indicate urothelial transport of water and solutes under certain conditions. This study investigates the expression, localization, and regulation of aquaporin (AQP)-1, -2, and -3 in ureteral and bladder tissues in 48-h dehydrated and water-loaded female Wistar rats. Immunoblots of homogenates of whole ureter and bladder identified characteristic ϳ28-and 35-to 44-kDa bands for AQP-1, -2, and -3. AQP-1 was localized to capillary and arteriole endothelial cells, whereas AQP-2 and -3 circumferentially lined the epithelial cell membranes except for the apical membrane of the epithelial cells adjacent to the lumens of both ureter and bladder. AQP-2 was also present in epithelial cell cytoplasm. Dehydration resulted in 160-200% increases of AQP-3 signal and 24-49% increases of AQP-2 signal but no change in AQP-1 signal on immunoblots of homogenates of ureters and bladders. AQPs in genitourinary tract urothelia likely play a role in the regulation of epithelial cell volume and osmolality and may play a role in bulk water movement across urothelia.Western blot analysis; immunocytochemistry; water transport IT IS GENERALLY ASSUMED THAT the mammalian lower urinary tract is an impermeable transit and storage system and that micturated urine is identical to that excreted by kidneys (7). In fact, recent in vitro studies have documented very low urothelial permeability to water, ions, and nonelectrolytes and demonstrated that a major permeability barrier resides in the apical luminal membrane of the epithelial cells ("umbrella cells") lining the bladder lumen (reviewed in Ref. 15;19).Although urothelial permeability to water and solutes may be low, it is finite, and the possibility that urine might be significantly modified in transit by the lower urinary tract is plausible given the large urothelial surface area and long elapsed time between egress of urine from collecting ducts and micturation. Indeed, significant net transport (both lumen to blood and blood to lumen) of solutes, including urea, creatinine, sodium, potassium, and chloride, usually down their respective blood/urine gradients, has been demonstrated in vivo in rabbits and rats and studies of perfused dog ureter (14, 29) and bladder (8,9,14,21,27). Furthermore, a number of studies have shown that rabbit and guinea pig urinary bladder epithelium contain an aldosterone-stimulated, amiloride-inhibited sodium transporter (2, 16), which has recently been identified by Northern blot analysis as the epithelial sodium channel (22). The epithelial sodium channel is known to be responsible for salt and fluid transport across epithelia of many tissues (6).Although isotopic movement of D 2 O or isotopically labeled water across mammalian urothelia has bee...

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Thirty-eight patients with chronic renal insufficiency who were in a dialysis program underwent studies of thyroid function and metabolic status. Mean values for serum total and free thyroxine (T4) concentrations and thyroxine-binding globulin capacity were within normal limits. Although mean serum total triiodothyronine (T3) concentration was normal, 43% of the group had low serum T3 and 54% had low serum free T3 concentrations. Serum thyrotrophin (TSH) concentrations were normal in all but four subjects who had very slight elevations. Metabolic status was assessed by various metabolic tests; mean values for each of these tests were normal, and the clinical index scores indicated that all patients were euthyroid. Results of metabolic testing were similar in patients with low and those with normal serum T3 concentrations. Low serum T3 measurements did not accurately reflect metabolic state in patients with chronic renal failure, whereas serum free T4 and TSH concentrations were reliable indicators of thyroid state.

Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta(1) (TGF-beta(1)) mRNA increase in rat skeletal muscle in response to a single acute exercise bout. Nitric oxide (NO) is released locally by muscle vascular endothelium and muscle fibers during exercise, contributes to the blood flow response to exercise, and regulates mitochondrial respiration. We hypothesized that a reduction in NO production, via NO synthase inhibition, would demonstrate a link between NO and the VEGF, bFGF, and TGF-beta(1) gene responses to exercise. To investigate this hypothesis, 9-wk-old female Wistar rats were divided into eight treatment groups (n = 6 each): 1) saline + rest, 2) saline + exercise, 3) 30 mg/kg N(omega)-nitro-L-arginine methyl ester (L-NAME, a known NOS inhibitor) + rest, 4) 30 mg/kg L-NAME + exercise, 5) 300 mg/kg L-NAME + rest, 6) 300 mg/kg L-NAME + exercise, 7) 300 mg/kg N(omega)-nitro-D-arginine methyl ester (D-NAME, inactive enantiomer of L-NAME) + rest, and 8) 300 mg/kg D-NAME + exercise. Exercise consisted of 1 h of running at 20 m/min on a 10 degrees incline. VEGF, TGF-beta(1), and bFGF mRNA from left gastrocnemius were analyzed by quantitative Northern blot. Submaximal exercise for 1 h increased VEGF mRNA 4.2-fold and TGF-beta(1) mRNA 1.5-fold in untreated rats but did not increase bFGF mRNA. The exercise-induced increase in VEGF mRNA was attenuated approximately 50% by 30 and 300 mg/kg L-NAME; the TGF-beta(1) mRNA increase was unaffected by 300 mg/kg L-NAME. In addition, 300 mg/kg D-NAME had no effect on the exercise-induced increase in VEGF mRNA. Administration of 300 mg/kg L-NAME had no effect on bFGF mRNA. These findings suggest that NO is important in the regulation of the VEGF gene response to exercise through increases in VEGF transcription or by increases in the VEGF mRNA half-life.