Thirst and DI

[zhopv10]

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UW points out that serum Na is normal in nephrogenic DI due to intact thirst but is high in central DI. Is this just due to the close proximity of osmoreceptors in the hypothalamus controlling thirst and ADH production/release this leading to damage to both entities the majority of the time or is there something more to it?


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[slz1900]

I'm not 100% sure what you are asking, but remember that the main determinant of serum Na+ is volume. Intact thirst will preserve volume so Na+ will be normal. ADH is the main determinant of thirst, and it acts on the hypothalamus to stimulate it. In nephrogenic DI, ADH is produced and the hypothalamus is intact so thirst will be intact. In central DI, there is a lack of ADH so thirst will not be stimulated in the hypothalamus. Thirst is not directly controlled by osmoreceptors.

Edit: ADH is not the main factor in thirst since it is complicated and controlled by many different mediators.

 

[zhopv10]

I'm not 100% sure what you are asking, but remember that the main determinant of serum Na+ is volume. Intact thirst will preserve volume so Na+ will be normal. ADH is the main determinant of thirst, and it acts on the hypothalamus to stimulate it. In nephrogenic DI, ADH is produced and the hypothalamus is intact so thirst will be intact. In central DI, there is a lack of ADH so thirst will not be stimulated in the hypothalamus. Thirst is not directly controlled by osmoreceptors.

Thirst is not directly controlled by ADH nor is it the primary mediator. It is controlled by a handful of factors (osmolarity, volume status[probably mediated through ATII], AT2, other hormonal favors etc) that are sensed by the SFO and OVLT in the lamina terminalis. The actual perception of thirst is complex and mediated via a variety of brain areas through mechanisms not fully understood. Anyway, for increases in sodium osmoreceptors in the wall of the 3rd ventricle (SFO,OVLT) sense this and generate a response.

The question arose from a source stating that the populations of osmoreceptors that produce the ADH response and the thirst response were different, as evidenced by some data suggesting that the threshold for ADH is lower than thirst generation. However that is apparently fairly controversial and certainly not known for sure and even if it is true they would be very close together and not separated by any real anatomical space. So my original question was off (I was thinking the different receptors might be in different areas). However they all are mediated through the lamina terminalis it appears so if you knock out the hypothalamus you loose it all.
Ref: http://www.ncbi.nlm.nih.gov/m/pubmed/14739394/

Long story short: as you said if you loose the hypothalamus you loose both ADH and the thirst response, which is right and certainly good enough for boards, thanks so indeed thanks for pointing that out! forest through the trees phenomenon was occurring for me here I think haha.

As an interesting side note, there are cases of pts having DI post pituitary surgery from damage to the axons of the ADH secreting neurons in the hypothalamus. Can either be transient, or permanent. And an interesting feature is that these pts do have preserved thirst perception in most cases. http://www.medscape.com/viewarticle/558561_3


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[slz1900]

Thirst is not directly controlled by ADH nor is it the primary mediator. It is controlled by a handful of factors (osmolarity, volume status[probably mediated through ATII], AT2, other hormonal favors etc) that are sensed by the SFO and OVLT in the lamina terminalis. The actual perception of thirst is complex and mediated via a variety of brain areas through mechanisms not fully understood. Anyway, for increases in sodium osmoreceptors in the wall of the 3rd ventricle (SFO,OVLT) sense this and generate a response.

The question arose from a source stating that the populations of osmoreceptors that produce the ADH response and the thirst response were different, as evidenced by some data suggesting that the threshold for ADH is lower than thirst generation. However that is apparently fairly controversial and certainly not known for sure and even if it is true they would be very close together and not separated by any real anatomical space. So my original question was off (I was thinking the different receptors might be in different areas). However they all are mediated through the lamina terminalis it appears so if you knock out the hypothalamus you loose it all.
Ref: http://www.ncbi.nlm.nih.gov/m/pubmed/14739394/

Long story short: as you said if you loose the hypothalamus you loose both ADH and the thirst response, which is right and certainly good enough for boards, thanks so indeed thanks for pointing that out! forest through the trees phenomenon was occurring for me here I think haha.

As an interesting side note, there are cases of pts having DI post pituitary surgery from damage to the axons of the ADH secreting neurons in the hypothalamus. Can either be transient, or permanent. And an interesting feature is that these pts do have preserved thirst perception in most cases. http://www.medscape.com/viewarticle/558561_3


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Sorry if my answer oversimplified to the point of being incorrect. I do remember reading that ADH had a direct role in stimulating thirst though and like you said thirst regulation is extremely complicated and not well understood, so it seems unlikely that anything of that detail will be asked.

 

[zhopv10]

Sorry if my answer oversimplified to the point of being incorrect. I do remember reading that ADH had a direct role in stimulating thirst though and like you said thirst regulation is extremely complicated and not well understood, so it seems unlikely that anything of that detail will be asked.

No worries, and totally agreed. I only knew cause somewhat of the mech of thirst because of my major (neuro) and just thought I'd share the info. Totally not boards testable beyond what you said (I hope :0 )


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