Physiology Topics
Na+ diffuses through the apical membrane of principal cells of the distal convoluted tubule and collecting duct via Na+ leak channels. The cytosol concentration remains low as usual due to the Na+/K+ ATPases in the basolateral membrane. Principal cells also secrete a variable amount of K+ to adjust for dietary changes, by means of the ATPase and K+ leak channels in both the apical and basolateral membranes.
The hormone aldosterone increases Na+ and water reabsorption and K+ secretion by principal cells because it both increases the activity of existing ATPase pumps and channels and stimulates synthesis of new pumps and channels. If aldosterone levels are low, principal cells reabsorb few Na+ and secrete few K+. Too low aldosterone can cause an elevated blood level of K+, leading to cardiac arrhythmias.
Antidiuretic hormone (ADH) stimulates insertion of aquaporin-2 containing vesicles into the apical membrane of principal cells. This results in increase water permeability and reabsorption When osmoreceptors in the hypothalamus detect increases in plasma osmolarity (i.e. decreased water concentration), the hypothalamus signal through innervation to the pituitary for ADH release.
ADH controls whether urine is diluted or concentrated because of the countercurrent mechanism in the loop of Henle. Fluid leaving the proximal convoluted tubule is isotonic with plasma. Since the osmolarity of the interstitial fluid around the loop of Henle increases progressively, water is reabsorbed as filtrate flows along the descending limb. The osmotic gradient around the loop is established by Na+/+/2Cl- triplicate transporters in the ascending limb in combination with the inpermeability to water of that area of the tubule. As the filtrate reaches the later part of the distal tubule and collecting duct, additional water reabsorption is controlled by ADH. When ADH levels are low, the principal cells are impermeable to water and no further reabsorption occurs, resulting in diluted urine. As ADH levels increase, water permeability and reabsorption increase and urine becomes more concentrated.
In addition to the countercurrent mechanism, urea recycling further increases the osmolarity of the medulla. Duct cells deep in the medulla are permeable to urea, which then diffuses into the interstitial fluid and accumulates. Some diffuses into the tubular fluid, further increasing its urea concentration and generating more concentrated urine.
When blood volume decrease, the walls of afferent arterioles are less stretched, which triggers the juxtaglomerular cells to secrete renin. Sympathetic stimulation can also stimulate renin release. Renin clips off angiotensin I from angiotensinogen, a normal plasma protein synthesized in the liver. Angiotensin Converting Enzyme (ACE) in the lungs converts angiotensin I to angiotensin II, which affects renal physiology in four ways:
A large increase in blood volume sensed by receptors in cardiac tissue triggers the release of atrial natriuretic peptide (ANP), which inhibits Na+ and water reabsorption at the proximal convoluted tubule and collecting duct, and suppresses secretion of aldosterone and ADH. The result is increased Na+ and water excretion.
ANP and ADH are peptide hormones, therefore they act quickly. Aldosterone is a steroid hormone, acting more slowly through protein syntesis.
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