Adaptation of proximal tubular structure and function: insights into compensatory renal hypertrophy.
Hypertrophy of the renal tubular cells, especially those of the proximal tubule (PT), accounts for the majority of the increase in kidney size that follows partial removal of renal mass. The propensity of PTs to enlarge appears to be closely linked to an elevation in glomerular filtration rate and may be related to altered tubular fluid flow rate. Hypertrophied PTs reabsorb fluid at an increased rate in vitro, which indicates an intrinsic adaptation of their transport capacity. The hypertrophied cells demonstrate a predominant increase in basolateral membrane area with little change in luminal surface area. This asymmetric structural hypertrophy does not, however, appear to be accompanied by functional asymmetry, for basolateral Na+-K+ pump activity increases roughly in proportion to the increase in cell protein. The activity of the Na+-H+ antiporter, on the other hand, is increased in the brush-border membrane of proximal tubules derived from animals with reduced renal mass. In view of the reported association of Na+-H+ antiport stimulation and mitogenesis in a variety of cell types, the increased activity of this transporter, possibly induced by an increase in tubular fluid flow rate, could be the local stimulus that initiates hypertrophy and determines the organ specificity of the response.
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D000222:Adaptation, Physiological; D000818:Animals; D001693:Biological Transport, Active; D005919:Glomerular Filtration Rate; D006984:Hypertrophy / Q000503:physiopathology; D007473:Ion Channels / Q000473:pathology / Q000502:physiology; D007687:Kidney Tubules, Proximal / Q000473:pathology* / Q000503:physiopathology; D011522:Protons; D051381:Rats; D012964:Sodium / Q000502:physiology
D007473:Ion Channels; D011522:Protons; D012964:Sodium