Regulation of total body fluid volume is dependent on regulation of the extracellular fluid (ECF) volume. Control of ECF volume is mediated by osmoreceptors that affect ADH release.
ADH release responds to changes in ECF osmolality and the effective circulating volume (ECV) of blood. The ECV is the component of the ECF that actually perfuses tissues (this may not necessarily be identical to the intravascular volume, since there may be circumstances in which not all of the blood is involved in tissue perfusion). Reflexes controlling the release of ADH may be activated by changes in blood pressure, atrial filling, haemorrhage or stress. Thus, a response in ADH release takes place within minutes, and acts rapidly to correct a disturbance (Figure RE.11).
Osmoreceptors respond to changes in ECF osmolality. Since sodium salts are the main osmotically active solutes in the ECF, control of body fluid volume is dependent on the control of body sodium content. Man can conserve sodium very effectively, and urinary losses can be < 1 mmol/l. However, maximal sodium reabsorption can increase the excretion of K+ and H+, and so may disturb acid base balance. Changes in Na+ excretion are normally brought about by changes in tubular re-absorption. When disturbances of body fluid osmolality occur, disturbances in body sodium content (and consequently in body fluid volume) may take hours or even days to correct.
Primary control of sodium re-absorption is mediated by the release of systemic hormones renin, angiotensin and aldosterone. The effects of these hormones are modified by other mechanisms and also depend on changes in ECV. Overall regulation of sodium reabsorption is complex being influenced by the following factors:
Regulation of body sodium and extracellular volume
• Systemic hormones
• Starling forces in the peritubular capillaries
• Neurological reflexes
• Renal prostaglandins
• Atrial natriuretic peptide
Juxtaglomerular Apparatus and the Macula Densa
In a nephron the ascending limb of the loop of Henle re-enters the cortex to become the distal tubule, passing very close to its own Bowman's capsule. At this point it comes into contact with the afferent and efferent arterioles from its own glomerulus. This region of contact is the juxtaglomerular apparatus, and consists of renin containing granular cells in the walls of the afferent arterioles, and specialized cells, the macula densa, in the wall of the early distal tubule.
Renin is an enzyme synthesized and stored in the granular cells of the juxtaglomerular apparatus. It is released into the plasma when the body sodium content decreases. As noted above, body sodium content determines ECV and it is this relationship that determines renin release. There are three main ways in which decreases in ECV elicit increases in renin release.
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