Mikie H. answered • 05/02/19
Physiology tutor 2+ years
1)
A. Decreased, less. Decreased blood volume from dehydration decreases glomerular hydrostatic pressure from decreased renal blood flow and thus, GFR decreases. If GFR decreases, tubular load also decreases. This means there are less solutes, especially Na+, in the tubules, so when the load reaches the early distal convoluted tubule, macula densa detect hypotonic filtrate. Recall that in the renal system, adenosine does the opposite of what it did in the cardiovascular system due to different receptor chemistry. Adenosine causes vasoconstriction of afferent arterioles in the nephron instead of vasodilation. GFR can be restored in two ways. Increasing the radius of the afferent arteriole and decreasing the radius of the efferent arteriole. Angiotensin II controls the efferent arteriole diameter, so Adenosine controls the afferent arteriole diameter. If adenosine causes vasoconstriction and adenosine targets the afferent arteriole, then the macula densa release LESS adenosine to vasodilate the afferent arteriole.
2)
D. Decrease, increase. Now we have to figure out the urine concentration and output based on the activation of all of the “A” hormones. The “A” hormones that can help us figure this out are Aldosterone and ADH. Let’s examine ADH. ADH activates the insertion of aquaporins into the collecting duct in a process called facultative water reabsorption. Up to ~10% of water left in the tubule is reabsorbed. As water is reabsorbed into the blood, there is less water in the filtrate, so urine volume will decrease. In addition, this leaves more hypertonic filtrate so the urine will be more concentrated.
3)
B. High levels of K+. ADH will not help us determine this answer, so examine aldosterone. Aldosterone increases the activity of the principal cell basolateral NaK ATPase (1° active transport). This electrogenic protein pumps 2K+ into the basolateral membrane and 3Na+ out of the basolateral membrane into the interstitial fluid, which will then enter the peritubular capillaries by simple diffusion. As a result, more Na+ is reabsorbed into the blood. After K+ enters the basolateral cells, it leaks into the lumen. More K+ in the lumen means more K+ was secreted, and therefore, excreted. Recall E = F + S – R. The urine will have a higher concentration of K+. Aldosterone can also increase apical H+ ATPase activity, which pumps more H+ into the lumen, not less.
4)
D. High Angiotensin II, High Aldosterone, High ADH
This is RAAAS. In short, the low blood pressure causes the release of renin, ultimately leading to production of Angiotensin II, Aldosterone, and ADH. Thus, all hormone levels increase during compensation.
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Specifically,
In response to low renal blood flow, in this case from low blood pressure from dehydration, granular cells of the JGA release renin. Renin is an enzyme that cleaves and activates angiotensinogen I into angiotensin I. With low GFR, eventually the macula densa cells in the diluting segment of the nephron tubules detect hypo-osmotic filtrate and release less adenosine and more NO, which dilates the afferent arterioles. In addition, the macula densa cells indirectly activate granular cells too. Renin's production of Angiotensin I causes the next step in the cascade. Angiotensin I travels to the pulmonary capillaries; there, pulmonary endothelium produces the enzyme, ACE. ACE cleaves and activates angiotensin I into angiotensin II. Angiotensin II has various effects that all lead to increase blood pressure.
i) Angiotensin II constricts the efferent arterioles. The combination of dilated afferent arterioles and constricted efferent arterioles increases renal blood flow and GFR back to normal.
ii) Angiotensin II is a potent systemic vasoconstrictor. Vasoconstriction induces increased total peripheral resistance. To compensate and keep constant flow throughout the blood vessels, mean arteriole pressure also increases.
iii) Angiotensin II stimulates the production of Aldosterone from the Zona Glomerulosa of the Adrenal Cortices. Aldosterone is released into the blood and binds intracellular receptors of the principal cells of the late distal convoluted tubules and early regions of the collecting ducts. When aldosterone binds cytoplasmic receptors and the complex translocates to the nucleus to bind regulatory elements on DNA, this induces expression of proteins that increase the activity of the Na+/K+ pump of the principal cells. This increases reabsorption of Na+ into the peritubular capillaries and increases secretion of K+ into the tubules. The active transport of Na+ into blood vessels induces obligatory osmosis. Increased water flow into the blood vessels increases blood volume. With more water force per area inside the blood vessels, blood pressure increases
iv) Angiotensin II stimulates the secretion of ADH from the posterior pituitary gland. ADH travels to the blood and binds to V2 receptors on the cell membrane of cells lining the collecting duct and last region of the late distal convoluted tubule. This induces a cAMP-mediated signal transduction cascade, ultimately leading to the insertion of aquaporins and urea transporter proteins. Aquaporins and urea transporters allow for the reabsorption of water into the peritubular capillaries and urea into the renal medulla, respectively. This increases water volume in the blood. Finally, this increased volume also increases blood pressure.
