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Kaplan Qbank USMLE



Author12 Posts
  #1

What are the sites of action of ADH?

What are the two different types of receptors for ADH, where are they, and which G-Proteins are they associated with?

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  #2

while doing lithium I came across one receptor for ADH.

vasopressin V2 receptor blocked by lithium that is coupled to CAMP .That cause DI in lithium toxicity.

ADH acts on renal collecting ducts mainly.It adds water transporters to the membrane and controls ECF osmolarity mainly.


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  #3

ya V2 receptor in CT is G coupled and increases aquaporins. and V1a V1b are found in skin liver git etc. they cause cutaneous vasoconstriction and glycogenolysis. they are coupled to phospholipase C

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  #4

Yes.

V1 on Vascular Muslce -Gq coupled, activates PLC, increases IP3, Inc. Ca, Vasoconstriction.
V2 on Collecing Ducts -Gs coupled, acievates AC, increase cAPMP, puts water Channels CD.

What is the effect on cutaneous vasoconstriction? ADH is supposed to regulate volume and osmolarity, (increase vol and decrease osm.) so are there any effects on this by doing VC?




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Our greatest glory is not in never falling, but in rising every time we fall.

  #5

it causes vasoconstriction in supraphysiological concentrations

  #6

can you please explain further what are the effects of Vasoconstriction here?
Thanks.
I know release of ADH DOES cause VC, I'm just confused WHY ADH would produce vasoconstriction and what are the resulting effects...


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Our greatest glory is not in never falling, but in rising every time we fall.

  #7

Simply said, ADH has two target tissues (kidney, blood vessels) and two functions (antidiuresis, vasoconstriction) and two stimuli (hyperosmolarity, hypovolemia) and two names (antidiuretic hormone, vasopressine).

1. the kidney -
antidiuretic effect (increased water reabsorption)
via V2 receptors (cAMP mediated)
2. blood vessels -
vasoconstriction
via V1 receptors (PLC --- Ca2+----contraction of smooth muscle)

stimuli:
1. hyperosmolarity --- so increased ADH secretion ---- so increased water reabsorption ---- so decreased osmolarity (normalized) --- so decreased ADH secretion
2. hypovolemia --- so increased ADH secretion:
-2a. increased water reabsorption --- so increased blood volume --- so increased blood pressure
-2b. vasoconstriction --- so increased total peripheral resistence --- so increased blood pressure (BP=CO*TPR)



  #8

So, when there is hypovolemia, there is also decreased blood volume and decreased blood pressure. This is stimulus for ADH secretion which will increase blood pressure via increasing blood volume (by way of water reabsorption) and increasing vascular resistance (by way of vasoconstriction)

  #9

Mildus,
Its crystal clear now.. You cleared up all my doubts and questions...
Thanks so much.
grin

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Our greatest glory is not in never falling, but in rising every time we fall.

  #10

you're welcome smiling face

  #11

mildus, thank you very much also... but i've got a question... when the water is reasorbed, does the sodium follow as well..?? sorry if it's a stupid question..sad

  #12

ADH doesn't cause sodium absorption with water (because it acts on aquaporins), but aldosteron causes sodium reabsorption and water follows it







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