Salt And Water Balance Flashcards

1
Q

What changes stimulate ADH release? What senses these changes?

A

Increase in osmolarity and decrease in blood volume
Former : osmoreceptors (anterior hypothalamus)
Latter : baroreceptors (aortic arch and carotid sinus)

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2
Q

ADH action in basolateral membrane of principle cells of collecting duct

A

Binds V2 receptors
Gs protein coupled
PKA phosphorylates cytoskeletal elements causing vesicles containing AQP2 to fuse with apical membrane

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3
Q

Other than increasing AQP2 expression in principle cells, what else does ADH do? What receptors mediate these actions

A

Activates urea carriers (UT) in CD (increasing hypertonicity of interstitium of medulla) - V2 receptors

Stimulates NKCC in TALH
Vasoconstricts - especially descending vasa recta preventing wash out of hypertonicity
— both V1 receptors (Gq-coupled, IP3, Ca2+ activating kinase etc.)

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4
Q

Cardiovascular sensors of effective circulating volume?

A

Baroreceptors in carotid sinus and aortic arch
Stretch receptors in atria and pulmonary circulation
Pressure receptors in renal afferent arterioles

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5
Q

Renal sensors of effective circulating volume?

A

Macula densa (senses NaCl, depends on GFR, depends on ECV)

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6
Q
Affects on renin release:
1-increased Cl- in macula densa
2-increase A-II
3-Increase ADH
4-Increase SNS
5-Increase PGs
6-Increased pressure
A
1 - inhibit
2 - inhibit
3 - inhibit
4 - stimulate
5 - stimulate
6 - inhibit
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7
Q

A-II effects on adrenal cortex?

A

Aldosterone release

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8
Q

A-II cause vasconstriction on what in kidneys? Effects on peritubular capillaries?

A

Efferent arteriole, reducing hydrostatic pressure in peritubular capillaries increasing uptake of water from interstitium

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9
Q

Effects of A-II on proximal tubule?

A

A-II receptor Gs coupled, PKA activates Na/H increasing reabsorption

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10
Q

How does A-II help in increasing water content of body?

A

Stimulates ADH releases and increases thirst

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11
Q

Mechanism of action of ANP?

A

Antagonises RAAS by raising cGMP levels causing vasodilation raising GFR but inhibiting reabsorption to increase the fraction of the sodium load that is excreted

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