recap

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51.6 recap

Glomerular filtration is essential for kidney function and is sustained by autoregulatory mechanisms. These autoregulatory mechanisms include changes in dilation and constriction of the glomerular afferent arterioles and hormonal control over constriction of the efferent glomerular arteriole mediated by the renin–angiotensin–aldosterone system (RAAS). Angiotensin controls the release of aldosterone, which controls sodium reabsorption. Sensors that monitor blood pressure and blood osmolarity stimulate or inhibit the release of ADH, which controls the water permeability of the collecting duct.

learning outcomes

You should be able to:

  • Describe how renin, angiotensin, and aldosterone affect glomerular filtration rate and blood pressure.

  • Given an event that lowers blood pressure, predict the response of the renin−angiotensin−aldosterone system.

  • Describe ADH’s role in regulating kidney function in response to changes in blood osmolarity or blood pressure.

Question 1

What are the mechanisms whereby the afferent and efferent arterioles regulate the GFR, and how are those responses controlled?

The afferent and efferent arterioles regulate GFR by changing their resistance to flow. When blood pressure rises, the afferent arterioles respond by constricting and increasing their resistance. When blood pressure falls, the efferent arterioles respond by constricting and increasing their resistance. Constriction of the afferent arterioles decreases GFR, and constriction of the efferent arterioles increases GFR. Constriction of the afferent arterioles is due to the general property of smooth muscle – when stretched, it responds by contracting.

With a decrease in blood pressure and therefore a decrease in GFR, the feedback information is a fall in solute concentration in the distal tubule. In response, the macula densa cells signal the afferent arterioles to dilate and cause the efferent arterioles to constrict by releasing renin, which initiates the conversion of angiotensinogen to angiotensin, which in turn stimulates the efferent arterioles to constrict.

Question 2

Aldosterone stimulates activity of the Na+/K+ exchangers in the distal convoluted tubule and the initial segments of the collecting ducts. Aldosterone release is triggered by angiotensin. Given this information, what is the significance of the fact that the Na+/K+ exchanger in the tubule cells secretes two K+ ions for every three Na+ ions it reabsorbs?

The secretion of renin and the resulting production of active angiotensin are triggered by a fall in blood pressure and therefore a fall in GFR. One action of the reninangiotensinaldosterone system is to increase water reabsorption from the kidney to maintain blood volume. To reabsorb water, it is necessary to increase the reabsorption of Na+ to create the osmotic gradient that will pull water from the tubule fluid into the tubule cells. However, if the exchanger moved Na+ and K+ one for one, it would not create an osmotic gradient.

Question 3

If you drank a lot of salty chicken broth that had an osmotic concentration of 300 mosm/L, what two mechanisms would play roles in the response of your kidneys to excrete the excess fluid volume and excess Na+? Explain your answer.

The chicken broth has the same osmolarity as the body fluids, so its absorption from the gut would not increase the blood osmolarity, but it would increase blood volume and blood pressure. The increase in blood pressure would stimulate the carotid baroreceptors, resulting in an inhibition of ADH release. As a result of decreased ADH, the kidney would reabsorb less water and therefore produce more urine. In addition, the increased blood volume would stimulate the release of atrial natriuretic peptide, causing increased secretion of Na+ and therefore increased loss of water, thus reducing fluid volume, blood volume, and blood pressure.