Aldosterone promotes Na+ retention and K+ loss because whenaldosterone levels increase, there is a low Na+ or high K+concentration in the blood. Review the Clinical Investigation:Primary Aldosteronism, Conn’s Syndrome and complete theinteractivities.
Read the overview and complete the interactivities thatfollow.
Karen is a 43-year-old lawyer with mild hypertension treatedwith an angiotensin receptor blocker. She visited her physiciancomplaining of muscle weakness, headaches, frequent urination, andunusually great thirst. Her blood pressure—particularly herdiastolic pressure—was significantly elevated. The physician notedthe absence of edema, and the presence of more PVCs (prematureventricular contractions) in her ECG than she had previously shown.Her urine sample displayed proteinuria and was slightly alkaline,and her blood test revealed that she had hypokalemia (low plasma K+concentration). More specialized blood tests measuring plasma reninactivity and aldosterone concentration were ordered. After theseresults were obtained, the physician ordered a test in which plasmaaldosterone concentration was measured before and after Karen dranka saline solution to determine the effects of sodium loading. Thephysician subsequently requested that Karen obtain an abdominal CTscan. Karen had significant diastolic hypertension without edema,hypokalemia, polyuria, and polydipsia (great thirst and drinking).Her urine sample was slightly alkaline, and her specialized bloodtests indicated an abnormally high ratio of plasma aldosterone torenin activity. When a sodium-loading test was performed, in whichKaren drank a saline solution, her plasma aldosterone concentrationremained elevated. The physician requested an abdominal CT scan,which showed a mass in her right adrenal gland.
QUESTIONS
1. How do the kidneys handle potassium, and how is thisregulated?
2. What is polyuria, and why might Karen have polyuria andpolydipsia?
3. Why would Karen’s urine be slightly alkaline?
4. What is the normal relationship between plasma renin andaldosterone?
5. How would plasma renin and aldosterone levels normallyrespond to sodium loading?
6. What is the likely explanation for Karen’s symptoms?
