Renal water reabsorption: A physiologic retrospective in a molecular era

Abstract

The cloning and sequencing of the aquaporin water channels has been an enormous advance in the biomedical sciences, as recognized by the award of the Nobel Prize to Peter Agre last year. Among many other examples, expression of aquaporin proteins in Xenopus oocytes and other heterologous expression systems has confirmed two important models of renal function: the increase in the water permeability of the collecting duct by antidiuretic hormone (ADH), and the mechanism of near isosmotic volume reabsorption by the proximal tubule. These mechanisms were the subjects of intensive investigation by numerous investigators, including Thomas E. Andreoli, who is being honored by this symposium, and who developed many of the key concepts in these areas. His early work with artificial lipid bilayer membranes and the pore-forming antibiotic amphotericin provided the rigorous foundation in experimental and conceptual modeling techniques that he later applied to physiologic and pathophysiologic mechanisms in the kidney, which are summarized in this retrospective. Dr. Andreoli and his colleagues proposed a water channel mechanism for the action of ADH, which has been confirmed by the cloning and heterologous expression of aquaporin-2. They also proposed that volume reabsorption by the proximal tubule depended on a very high hydraulic conductivity and the development of luminal hypotonicity produced by active solute reabsorption. This model has also been confirmed in mice in which aquaporin-1 expression is knocked out, resulting in a low proximal tubule water permeability that exaggerates the development of luminal hypotonicity.

Diuretic activities of fayiren and coix seed in normal rats

“…ANP is an active polypeptide synthesized and secreted by the atrium, also known as atrial natriuretic factor or atrial natriuretic peptide, which has strong effects of sodium, diuretic, renin release and ALD secretion [30]. ADH is secreted by the hypothalamus and its main function is to promote water reabsorption [31]. This study found that coix seed and furosemide had signi cant effect on ADH; Coix seed and furosemide could promote the secretion of ANP and reduce plasma ALD content.…”

Hyponatremia in kidney transplant patients: its pathophysiologic mechanisms

“…Cortisol exerts a negative effect on antidiuretic hormone secretion, thus a cortisol deficit can promote inappropriate antidiuretic hormone release, in turn increasing the risk of developing hyponatremia [ 5 ]. The isolated cortisol deficit can be induced by any glucocorticoid axis damage [ 34 ].…”

“…Polyuria after kidney transplantation is not a rare condition, but massive polyuria is not common [ 34 ]. This entity can lead to significant sodium wasting and consequently to hyponatremia, and eventually to cerebral edema and seizure activity [ 26 ].…”