Hormonal Control of Urine Production

The volume of urine produced in a healthy individual is largely determined by circulating hormone levels, and in particular by levels of vasopressin. Vasopressin is a cyclic, nine-amino acid peptide. It is released from the posterior pituitary after having been transported there along the axons of neurons whose cell bodies are located in the paraventricular and supraoptic nuclei of the hypothalamus, the site of vasopressin synthesis. An increase in the rate of secretion of vasopressin results in a reduced urine production. Vasopressin acts on the renal distal tubules and collecting ducts to cause an increased permeability to water and hence an increased reabsorption of water from the filtrate. Therefore, a hyperosmotic urine can be formed and the solute load to be excreted can be accommodated in a small volume of water. A decrease in vasopressin secretion results in an increase in the volume of urine produced by causing a reduction in the permeability of the renal distal tubule and collecting ducts to water. Vasopressin secretion is largely influenced by changes in plasma osmolality. An increase in plasma osmolality results in a increased vasopressin secretion and vice versa. The vasopressin is released rapidly in response to the stimuli and begins to act within minutes. When the secretion is inhibited, the half-life of clearance from the circulation is approximately 10 minutes. Therefore, changes in body fluid tonicity are rapidly translated into changes in water excretion by this tightly regulated feedback system.

In addition to the influence of plasma osmolality on vasopressin secretion, other (nonosmotic) factors with an influence are baroregulation, nausea, and pharyngeal stimuli. A fall in blood pressure or blood volume will stimulate vasopressin release; vasopressin secretion is, however, less sensitive to these changes than to changes in osmolality. Nausea is an extremely potent stimulus to vasopressin secretion in man; vasopressin levels can increase 100- to 1000-fold in response to nausea induced by various chemical agents. After a period of water deprivation followed by access to drink, vasopressin levels fall before there is any change in plasma tonicity, suggesting activation of neuronal pathways from the oropharynx.

Aldosterone, a steroid hormone, is released into the circulation after synthesis by the zona glomeru-losa cells of the adrenal cortex. Its primary role, in terms of renal function, is to increase renal tubular reabsorption of sodium and in doing so will bring about an increased excretion of potassium and, in association with vasopressin, increase water reabsorption in the distal segments of the nephron. Aldosterone causes this response by increasing the activity of the peritubular sodium/potassium pump and by increasing the permeability of the luminal membrane to both sodium and potassium. The increased luminal permeability allows potassium to move down its concentration gradient from the inside of the membrane cells into the tubule lumen. The majority of the sodium present is reabsorbed into the cell down the concentration gradient. The sodium absorption and potassium excretion are closely correlated with a 3 sodium:2 potassium ratio. Chloride follows the sodium to maintain the electrical neutrality of the urine.

The release of aldosterone is determined by a number of factors including the renin-angiotensin system: A fall in blood or extracellular fluid volume increases renin production and, via angiotensin II, results in an increase in aldosterone secretion.

The presence in the renal filtrate of ions such as bicarbonate and sulphate, which are not reabsorbed, promotes secretion of potassium into the distal tubule of the nephron and will also result in an increased urinary loss of potassium.

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