What is the major stimulus for the release of atrial natriuretic peptide (ANP) from cardiac atrial muscle fibers?
Explanation
This question identifies the primary physiological trigger for the release of ANP, a key natriuretic hormone involved in volume regulation.
Other questions
What is the normal concentration of potassium in the extracellular fluid, and what is the typical range of fluctuation around this value?
What percentage of the total body potassium is contained within the cells, as opposed to the extracellular fluid?
Which hormone is crucial for increasing the uptake of potassium into cells after a meal by stimulating the sodium-potassium ATPase pump?
What is the primary effect of metabolic acidosis on the distribution of potassium between intracellular and extracellular fluids?
What is the calculated normal rate of potassium filtration by the glomerular capillaries, given a GFR of 180 L/day and a plasma potassium concentration of 4.2 mEq/L?
In which specific parts of the renal nephron does most of the daily regulation of potassium excretion occur?
What is the primary function of the principal cells located in the late distal and cortical collecting tubules regarding potassium homeostasis?
Based on the data presented in Figure 30-4, which factor demonstrates a more significant impact on urinary potassium excretion when its concentration is increased from normal to five times normal?
What is one of the mechanisms by which increased extracellular fluid potassium concentration directly stimulates potassium secretion in the principal cells?
An increase in plasma potassium concentration of approximately 3 mEq/L can elevate the plasma aldosterone concentration from nearly zero to what level?
What is the primary mechanism by which acute acidosis decreases potassium secretion?
What percentage of the body's total calcium is found stored in the bones?
What is the normal concentration of ionized calcium in the extracellular fluid?
Which of the following is NOT one of the three main effects through which parathyroid hormone (PTH) regulates plasma calcium concentration?
Under normal conditions, what percentage of the calcium that is filtered at the glomerulus is reabsorbed by the renal tubules?
What is the principal pathway for the reabsorption of calcium in the proximal tubule?
Which of the following conditions would lead to a decrease in renal calcium excretion?
What is the approximate normal transport maximum for reabsorbing phosphate by the renal tubules?
What is the effect of increased plasma parathyroid hormone (PTH) on the renal handling of phosphate?
What is the primary site for the reabsorption of magnesium in the renal tubules, accounting for about 65 percent of the filtered load?
How does β-adrenergic stimulation affect the distribution of potassium in the body?
What percentage of filtered potassium is reabsorbed in the proximal tubule under normal conditions?
What is the primary function of type A intercalated cells in the late distal and collecting tubules in circumstances of severe potassium depletion?
What happens to potassium excretion when there is a high sodium intake, and why does it change little from normal?
What percentage of the total calcium in the plasma is bound to plasma proteins?
How does alkalosis affect the binding of calcium to plasma proteins and the susceptibility to hypocalcemic tetany?
What percentage of filtered calcium is reabsorbed in the proximal tubule?
What is the primary mechanism that controls phosphate excretion by the kidneys?
How does an increase in plasma phosphate concentration affect renal calcium excretion?
What is the normal total plasma magnesium concentration?
What is pressure natriuresis?
According to the renal-body fluid feedback mechanism for regulating arterial pressure, what is the direct consequence of an increased cardiac output?
What are the principal factors that can cause accumulation of fluid in the interstitial spaces (edema)?
How does the renin-angiotensin system respond to elevated sodium intake, and what is the effect on sodium excretion?
In patients with excessive aldosterone formation (Conn syndrome), why do the kidneys eventually 'escape' from sodium and water retention?
In congestive heart failure, blood volume can increase by what percentage?
What is the primary cause of renal sodium retention in nephrotic syndrome?
Which factor, when deficient, leads to clinically significant hyperkalemia due to accumulation in the extracellular space and renal retention?
What is the primary mechanism through which strenuous exercise can cause hyperkalemia?
What percentage of filtered potassium is reabsorbed in the loop of Henle?
What are the two types of special potassium channels in the luminal membrane of principal cells that allow for rapid potassium secretion?
What is the quantitative effect of a sevenfold increase in potassium intake on plasma potassium concentration when the aldosterone feedback system is blocked, according to the experiment shown in Figure 30-8?
Which dietary pattern is associated with a lower risk for hypertension and cardiovascular diseases?
What is the typical rate of dietary calcium intake, and how much is usually excreted in the feces?
In the thick ascending limb of the loop of Henle, what percentage of calcium reabsorption occurs through the paracellular route?
What is the primary role of type B intercalated cells in the late distal and collecting tubules when there is excess potassium in the body?
What is the primary physiological consequence of a severe decrease in GFR on potassium balance?
In a patient with primary aldosteronism (excess aldosterone), what is the typical effect on plasma sodium concentration?
What are the primary stimuli that increase salt appetite?