Water renal regulation

Vander. A. J. Control of sodium and water excretion Regulation of plasma volume and osiiiolariiy. In Vander. A. J. (ed.). Renal Physiology. Sih ed. New York. McGraw-Hill. 1995. pp. 116-144. 37. 

Vasopressin (Rtressin Synthetic) and its derivatives, namely lypressin (Diapid) and desmopressin (DDAVP), regulate the reabsorption of water by the kidneys. Vasopressin is secreted by the pituitary when body fluids must be conserved. An example of this mechanism may be seen when an individual has severe vomiting and diarrhea with little or no fluid intake. When this and similar conditions are present, die posterior pituitary releases the hormone vasopressin, water in die kidneys is reabsorbed into die blood (ie, conserved), and die urine becomes concentrated. Vasopressin exhibits its greatest activity on die renal tubular epithelium, where it promotes water resoqition and smooth muscle contraction throughout die vascular bed. Vasopressin has some vasopressor activity. 

Vasopressin (antidiuretic hormone) is a peptide synthesized in the hypothalamus and secreted from the neurohypophysis of the pituitary gland. This substance plays an important role in the long-term regulation of blood pressure through its action on the kidney to increase reabsorption of water. The major stimulus for release of vasopressin is an increase in plasma osmolarity. The resulting reabsorption of water dilutes the plasma toward its normal value of 290 mOsM. This activity is discussed in more detail in Chapter 10 (the endocrine system) and Chapter 19 (the renal system). 

The maintenance of plasma volume and plasma osmolarity occurs through regulation of the renal excretion of sodium, chloride, and water. Each of these substances is freely filtered from the glomerulus and reabsorbed from the tubule none is secreted. Because salt and water intake in the diet may vary widely, the renal excretion of these substances is also highly variable. In other words, the kidneys must be able to produce a wide range of urine concentrations and urine volumes. The most dilute urine produced by humans is 65 to 70 mOsm/1 and the most concentrated the urine can be is 1200 mOsm/1 (recall that the plasma osmolarity is 290 mOsm/1). The volume of urine produced per day depends largely upon fluid intake. As fluid intake increases, urine output increases to excrete the excess water. Conversely, as fluid intake decreases or as an individual becomes dehydrated, urine output decreases in order to conserve water. 

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... 

The excretion of water soluble waste via the kidneys requires filtration followed by selective reabsorption from and secretion into the renal tubules. Regulation of normal blood pH within very strict limits due to proton secretion and bicarbonate reabsorption is a major role of the kidney. 

Assuming the capsular pressures opposing the movement of water out of the blood and into the top of the nephron are constant, the net filtration pressure is due largely to the blood pressure. Any fall in blood pressure can have a dramatic effect on the efficiency of filtration and therefore clearance of waste materials. So important is the pressure within the renal vasculature that the kidney is critical in regulating systemic blood pressure via the renin-angiotensin-aldosterone (RAA) axis, a physiological process which relies on transport mechanisms within the renal tubules. 

Aquaporins help water to pass through biological membranes. They form hydrophilic pores that allow H2O molecules, but not hydrated ions or larger molecules, to pass through. Aquaporins are particularly important in the kidney, where they promote the reuptake of water (see p. 328). Aquaporin-2 in the renal collecting ducts is regulated by antidiuretic hormone (ADH, vasopressin), which via cAMP leads to shifting of the channels from the ER into the plasma membrane. 

Vasopressin occurs in two variations arginine-vasopressin (AVP) and lysine-vasopressin (LVP), in which Arg is replaced by Lys. The conformation of these hormones is almost identical to that of oxytocin, except that the terminal tail is con-formationally free and not held by the ring. The physiological role of the vasopressins is the regulation of water reabsorption in the renal tubules (i.e., an antidiuretic action). In high doses, they promote the contraction of arterioles and capillaries and an increase in blood pressure hence the name of these hormones. Because of their very similar structures, OT and VP overlap in a number of effects. 

Many glomerular diseases, such as those associated with diabetes mellitus or systemic lupus erythematosus, exhibit renal retention of salt and water. The cause of this sodium retention is not precisely known, but it probably involves disordered regulation of the renal microcirculation and tubular function through release of vasoconstrictors, prostaglandins, cytokines, and other mediators. When edema or hypertension develops in these patients, diuretic therapy can be very effective. If heart failure is also present, see the warnings mentioned above. 

Vasopressin activates two subtypes of G protein-coupled receptors (see Chapter 17). Vi receptors are found on vascular smooth muscle cells and mediate vasoconstriction. V2 receptors are found on renal tubule cells and reduce diuresis through increased water permeability and water resorption in the collecting tubules. Extrarenal V2-like receptors regulate the release of coagulation factor VIII and von Willebrand factor. 

Regulates water balance Stimulates contraction of smooth muscles Increases renal tubular water reubsorption Releases anterior pituitary hormones... 

Mineralocorticoids are involved in controlling electtolyte and fluid levels.9,44 The primary mineralo-corticoid produced by the adrenal cortex is aldosterone. Aldosterone increases the reabsorption of sodium from the renal tubules. By increasing sodium reabsorption, aldosterone facilitates the reabsorption of water. Aldosterone also inhibits the renal reabsorption of potassium, thus increasing potassium excretion. Mineralocorticoid release is regulated by fluid and electrolyte levels in the body and by other hormones, such as the renin-angiotensin system. 

Hyponatremia is caused by an excess of total body water relative to total body sodium and can result from a number of underlying conditions, including the syndrome of inappropriate antidiuretic hormone secretion (SIADH), cirrhosis, and congestive heart failure (CHF). In each of these conditions, inappropriate production of arginine vasopressin (AVP) [also known as vasopressin or antidiuretic hormone (ADH)], a neurohormone that regulates renal electrolyte-free water reabsorption, contributes to enhanced renal water retention, leading to decreased serum sodium concentrations.7 Hyponatremia can be characterized as hypervolemic, euvolemic, or hypovolemic... 

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