1. Which of the following would increase glomerular filtration rate? (More than
ID: 162573 • Letter: 1
Question
1. Which of the following would increase glomerular filtration rate? (More than one answer may be correct)
Increased blood pressure
Increased solute concentration in the bowman capsule
Increased solute concentration in the blood
Decreased ADH
2. Explain the concept of a countercurrent multiplier system and how it works in the kidneys. What is the importance of this system to the function of the kidneys?
3. Many drugs prescribed to treat high blood pressure actually act on the kidneys. Why would this be a good target?
4. Explain one mechanism by which such drugs could work.
Explanation / Answer
Ques-1: Which of the following would increase glomerular filtration rate? (More than one answer may be correct)
Answer: Increased blood pressure
Reason:
The higher the mean arterial pressure (more blood pressure) due to more fluid or water content in the afferent arteriole may result in change in glomerular filtration rate with higher rate filtration rate but solute concentration in the blood also increases GFR rat. The high atrial natriuretic peptide also cause higher GFR rate
Que-3: Many drugs prescribed to treat high blood pressure actually act on the kidneys. Why would this be a good target?
Many drugs prescribed to treat high blood pressure actually act on the kidneys would be a good target, for example, patients with chronic kidney disease with hypertension are advised to take low salt diet. If they consume more salt content which accelerates the proteiurea and finally kidney and heart failure. Here angiotensin-converting enzyme (ACE) inhibitor and following a salt-restricted weight loss diet enable to reduce his hypertension. Renin is produced from kidneys. 135/96 is is a bit more blood pressure. ACE inhibitors (ex.lisinopril) improve dilation of blood vessels and reduce blood pressure and also stop reabsortion of more salts at the renal tubles so that renin acitivity is reduced.
: Mode of action: Angiotensin-converting enzyme (ACE) inhibitors inhibits angiotensin converting enzyme to convert angiotensin I to active antgotensin II. Threby there will be no more further resultant action to aldostrone production to absorb water or salts from the renal tubules and maintain homeostasis.
Stimulation of renin-angiotensin-aldosterone system: During hypertension, thiazide diuretics are preferred to prescribe along with Angiotensin converting enzyme inhibitors. Normally aldosterone activated Na+ - K+ exchanger reslut in loss of potassium thereby hypovolemia. Body normally respond to hypovolemia such as low sodium with ACE inhibitors as angiotensin II improves aldosterone production thereby more elimination of electrolytes including potassium. Thiaze diuretics specifically reduce hypovolemia by acting specifically on Na+-Ca2+-exchanger at the proximal convluted tubule to recover depleted sodium. Thaizide diuretics often improve reabsorption of potassium to reduce hypokalemia.
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