Review of ADH Regulation

by Amy Sussman, MD

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    00:01 Let's talk a little bit more about ADH and its regulation.

    00:04 So again, antidiuretic hormone or ADH is a decapeptide.

    00:07 It's synthesized in the supraoptic nucleus of the hypothalamus and it's secreted by the posterior pituitary.

    00:14 It's regulated by both osmotic and nonosmotic mechanisms.

    00:22 Now, there is two types of ADH receptors that ADH combined to.

    00:26 In terms of this top, what's most important is the V2 or Type 2 receptors that are located in the basal lateral surface of the collecting duct.

    00:34 That's what mediates water reabsorption.

    00:36 So again, we've got ADH, it binds to the basal lateral surface of that V2 receptor.

    00:41 It then causes stimulation of aquaporin channels into the apical membrane of the collecting duct to cell.

    00:48 ADH can also bind to V1A or Type1 A receptors that are located in the vasculature and help to control vascular tone.

    00:56 If you recall in the ICU in the critical care setting, we oftentimes use vasopressin as a vasopressor and our patients.

    01:05 so we just talked about before how there's two main mechanisms that stimulate ADH release from that posterior pituitary.

    01:12 One is an osmotic mechanism, meaning that our osmolarity gets high, and our body knows that we need to actually drink more water to bring that osmolarity down low.

    01:21 So that's our osmotic stimulus.

    01:24 The other is a nonosmotic stimulus.

    01:27 Stimulated by a decrease in volume.

    01:29 So let's go over what that means.

    01:31 In the Osmo regulation, things like serum osmolarity, when that gets high, that's sensed our sensors, our hypothalamic, osmoreceptors.

    01:41 When they sense an increase in osmolarity they will then produce and release ADH.

    01:48 ADH then acts at that kidney in order to insert those aquaporin channels so we reabsorb water.

    01:53 And at the same time we get thirsty, so we will drink water.

    01:59 In the situation of volume regulation, if we have too little volume, then remember our body wants to preserve that vascular tone in that vascular volume.

    02:08 So it wants us to reabsorb water.

    02:12 What's actually sensed is the effective tissue perfusion.

    02:16 So the actual sensors or our Macula densa our afferent arterial, our atria, and our carotid sinus.

    02:24 Our effectors are going to be the Renin Angiotensin Aldosterone System.

    02:28 So if I have too little perfusion, RAAS is going to be activated in order to reabsorb sodium.

    02:34 Atrial natriuretic peptide, and some of the ANP related peptides are going to be suppressed.

    02:39 We want to preserve our sodium.

    02:42 And then norepinephrine will be stimulated in order to increase vascular tone.

    02:45 And finally, ADH will be released.

    02:48 Why? Because ADH will help us reabsorb water and in concert with everything else, sodium, vasoconstriction we can preserve our vascular volume.

    03:00 So this is a graphical representation of what I'm talking about and the relationship between ADH release and these two different mechanisms.

    03:07 So on the left, what we can see is a graph on the y-axis of plasma ADH.

    03:13 The x-axis is plasma osmolality.

    03:16 So these were human subjects that basically were restricted from water.

    03:20 And as their osmolarity rises, you can see that there is a reliable relationship between ADH release.

    03:27 So at about 285 to 290 mOsm/kg, we can see that ADH is released.

    03:33 Remember, what happens when ADH is released is not only do we have those aquaporin channels that are inserted to reabsorb water.

    03:40 We also get very thirsty.

    03:42 So we're going to consume more water.

    03:45 Now, on the graphical representation on the right, this was actually an experiment done in rats, where they manipulated the total blood volume of rats.

    03:53 So on the y-axis, we have plasma ADH again, and on the x-axis, here we have blood volume depletion.

    04:01 And you can see that when rats were depleted by about 10% of their total body volume, that we have an increase in ADH, and this mechanism is so important that it will supersede osmolarity.

    04:14 Meaning that if our patients are hyperosmolar, but they have their total body volume is low, ADH will still be released even though they have a low osmolality.

    04:25 So it's a very important concept to understand.

    About the Lecture

    The lecture Review of ADH Regulation by Amy Sussman, MD is from the course Water Balance: Hypo- and Hypernatremia.

    Included Quiz Questions

    1. RAAS is activated in order to reabsorb sodium.
    2. Carotid body receptors sense intravascular volume depletion and inhibit the release of norepinephrine.
    3. ANP is secreted during volume depletion to decrease sodium excretion.
    4. ADH is released from the anterior pituitary gland in response to hypothalamic stimulation.
    1. The stimulatory effect of volume depletion supersedes the inhibitory control of hypoosmolarity.
    2. ADH binds to its V2 receptor to increase systemic vascular resistance.
    3. Hyperosmolarity is sensed by specialized receptors in the distal convoluted tubule.
    4. ADH is not released until plasma osmolality is >300 mOsm/kg.

    Author of lecture Review of ADH Regulation

     Amy Sussman, MD

    Amy Sussman, MD

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