Chapter 20 concept questions Flashcards
Does the apical membrane of a collecting duct cell have more water pores when vasopressin is present or when it is absent?
More water pores when vasopressin is present.
People who inherit vasopressin V2 receptor deficiency will have urine that is dilute or concentrated?
If vasopressin action is suppressed, the urine is dilute.
A scientist monitoring the activity of osmoreceptors notices that infusion of hyperosmotic saline (NaCl) causes increased firing of the osmoreceptors. Infusion of hyperosmotic urea (apenetrating solute)[p. 127] had no effect on the firing rate. Ifosmoreceptors fire only when cell volume decreases, explain why hyperosmotic urea did not affect them.
Hyperosmotic NaCl is hypertonic and shrinks the osmoreceptors, but hyperosmotic urea is hypotonic and causes them to swell. Because only cell shrinkage causes firing, osmoreceptors exposed to urea do not fire.
If vasopressin increases water reabsorption by the nephron, would vasopressin secretion be increased or decreased with dehydration?
Vasopressin levels would increase with dehydration.
Experiments suggest that there are peripheral osmoreceptors in the lumen of the upper digestive tract and in the hepatic portal vein[Fig. 14.1, p. 435]. What is the adaptive significance of osmoreceptors in these locations?
Osmoreceptors in the lumen of the digestive tract and hepatic portal vein would sense high-osmolarity food or drink that has been ingested and absorbed, before it is in the general circulation. This would allow an anticipatory, or feed-forward, secretion of vasopressin to conserve body water.
Explain why patients taking a loop diuretic that inhibits solute reabsorption excrete greater-than-normal volumes of urine.
Solutes that remain in the lumen when the NKCC symporter is inhibited force water to remain in the lumen with them, increasing the urine volume.
Loop diuretics that inhibit the NKCC symporter are sometimes called “potassium-wasting” diuretics. Explain why people who are on loop diuretics must increase their dietary K+ intake.
Diuretics that inhibit the NKCC symporter leave K+ in the tubule lumen, where it is likely to be excreted, thus increasing urinary K+ loss.
In Figure 20.9b, what forces cause
Na+ and K+ to cross the apical membrane?
Na+ and K+ are moving down their electrochemical gradients.
If a person experiences hyperkalemia, what happens to resting membrane potential and the excitability of neurons and the myocardium?
In hyperkalemia, resting membrane potential depolarizes. Excitable tissues fire one action potential but are unable to repolarize to fire a second one.
Laboratory values for ions may be reported as mg/L, mmol/L, or mEq/L. If normal plasma Na+ is 140 mmol/L, what is that concentration expressed as mEq/L?[Fig. 2.7, p. 42].
140 mmol/L = 140 mEq/L
A man comes to the doctor with high blood pressure. Tests show that he also has elevated plasma renin levels and atherosclerotic plaques that have nearly blocked blood flow through his renal arteries. How does decreased blood flow in his renal arteries cause elevated renin levels?
Atherosclerotic plaques block blood flow, which decreases pressure in the afferent arteriole and decreases GFR. Both events stimulate renin release.
Map the pathways through which elevated renin causes high blood pressure in the man mentioned in Concept Check 11.
Renin secretion begins a cascade that produces ANG II. ANG II causes vasoconstriction, acts on medullary centers to increase blood pressure, increases production of ADH and aldosterone, and increases thirst, resulting in drinking and an increased fluid volume in the body. All these responses contribute to increased blood pressure.
Why is it more efficient to put ACE in the pulmonary vasculaturethan in the systemic vasculature?
All blood passes through the pulmonary blood vessels with each circuit. Unless ACE was in every systemic blood vessel, some blood might not be exposed to ACE.
Incorporate the thirst reflex into Figure 20.8.
On the left side of Fig. 20.8, interneurons also lead from hypothalamic osmoreceptors to the hypothalamic thirst centers.
Map the pathway that begins with renal artery stenosis and ends with hypertension. (Hint: It involves the RAAS pathway.)
Narrowing of the renal artery decreases blood flow into the kidney and decreases afferent arteriole blood pressure and GFR. The kidney interprets this as low systemic blood pressure and initiates the RAS pathway to raise blood pressure. See Figure 20.10, starting at upper left.
