Urine concentration and avian aquaporin water channels

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Abstract
Although birds and mammals have evolved from primitive tetrapods and advanced divergently, both can conserve water by producing hyperosmotic urine. Unique aspects in the avian system include the presence of loopless and looped nephrons, lack of the thin ascending limb of Henle’s loop, a corticomedullary osmotic gradient primarily consisting of NaCl without contribution of urea, and significant postrenal modification of final urine. The countercurrent multiplier mechanism operates between the descending and ascending limbs of Henle via recycling of a single solute (NaCl) with no water accompaniment, forming an osmotic gradient along the medullary cone. Bird kidneys and developing rat kidneys share morphological and functional characteristics. Avian kidneys express aquaporin (AQP) 1, 2, and 4 homologues that share considerable homology with mammalian counterparts, but their distribution and function may not be the same. AQP2 expression in Japanese quail (q) evolves in the collecting duct of early metanephric kidneys and continues to increase in intensity and distribution during nephrogenesis and maturation. qAQP2 mRNA and protein are increased by arginine vasotocin (avian ADH), but vasotocin-induced enhancement of cAMP production and water permeability are less marked than in mammalian kidneys. Nephrogenesis is delayed by insufficient nutrition in avian embryos and newborns and results in fewer nephrons and an impaired water balance in adults. Diabetes insipidus quail with homozygous autosomal recessive mutation and an unaffected vasotocin system have low AQP2 expression, underdeveloped medullary cones. Comparative studies will provide important insight into integrative, cellular, and molecular mechanisms of epithelial water transport and its control by humoral, neural, and hemodynamic mechanisms.

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