The secretion of K+ across the apical membrane of the collecting duct is passive.
About 75% of the excreted K+ is due to K+ filtered at the glomerulus
When aldosterone levels are high, the rate of K+ excretion will be high
Plasma aldosterone levels will rise in response to a rise in plasma K+ concentration
Will lead to a period of positive sodium balance where sodium accumulates in the body
Will normally cause a significant rise (e.g., >10 mOsm) in plasma osmolarity
Will result in the net loss of some water from the body.
All of the above
Proximal tubular sodium reabsorption is regulated by angiotensin II.
In principle cells in the distal tubule, sodium uptake involves secondary active transport
Na+ and Cl− transport by the thick ascending limb makes the medullary interstitium hyperosmotic.
Diuretic drugs increase the excretion of sodium by reducing apical sodium uptake
Will increase the water permeability of the apical membrane in the distal tubule and collecting ducts.
Will be triggered by a 5% reduction in blood volume
Will reduce the osmolarity of the excreted urine.
Will result in reduced cAMP levels in collecting duct principle cells.
Will cause the afferent arteriole to dilate
Will increase the apical-membrane potassium permeability in principle cells the collecting ducts
Will directly inhibit renin release.
Will occur in response to a decrease in the plasma angiotensin II concentration.
A change in renal sympathetic nervous system activity.
A rise in the plasma angiotensin II concentration.
A change in the flow rate of tubular fluid past the macula densa segment.
None of the above (since all can influence renin secretion).
ANP is secreted by the cardiac atria in response to increased stretch
ANP will increase GFR by dilating the afferent arteriole
ANP will not affect the secretion of renin
ANP reduces the Na+ permeability of the apical membrane of inner medullary collecting-duct cells.
Is a passive process that occurs in the vasa recta
Will not be affected by inhibition of ascending-limb sodium transport
Will result in the excretion of hypotonic urine when ADH levels are low
Does not involve the descending limb of Henle's loop
Will rise in response to a fall in the plasma bicarbonate concentration.
Will result in the release of bicarbonate into plasma.
Will be reduced by inhibition of cytosolic carbonic anhydrase.
All of the above.
Is converted into calcitriol in the kidney in response to an elevated plasma phosphate concentration
Activation to calcitriol in the kidney is suppressed by PTH.
In its activated form stimulates gastrointestinal calcium and phosphate absorption
Levels are suppressed when the plasma calcium concentration is low.
PTH increases renal calcium excretion and decreases renal phosphate excretion.
Release of calcium and phosphate from bone increases when osteoclasts are stimulated by PTH.
A calcium phosphate precipitate can be formed when the concentration of either ion rises substantially.
A fall in plasma phosphate levels can indirectly lead to a decrease in PTH secretion.
The low GFR reduces the filtered load of potassium.
Because K+ secretion is passive, the ability to secrete K+ depends on the total amount of tubular fluid that enters the distal tubules, and this is greatly reduced in these patients.
Renal K+ excretion is reduced by diuretics like furosemide that are often prescribed for these patients.
None of the above is a reasonable explanation
BP will rise because the pressure in the afferent arteriole will be reduced, thereby stimulating renin release and angiotensin II production.
BP will rise because aldosterone secretion will increase because of the high angiotensin II levels.
BP will rise because extracellular fluid volume will increase.
All of the above
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