Bartter's

[seminoma]

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From FC:

Due to the defective Na+/K+/2Cl- co-transporter, excess Na+, K+ and Cl- are delivered to the distal tubules, ultimately leading to the wasting of salt and water. The resulting volume contraction, along with increased levels of prostaglandins, leads to activation of the renin-angiotensin system, ultimately resulting in secondary hyperaldosteronism.

I understand that volume contraction leads to activation of the RAAS, but I thought prostaglandin synthesis was upregulated by RAAS activation (and not the other way around)?

 

[Suture15]

Well Aspirin does inhibit the RAAS system so it's not super odd that PGs may upregulate it.

 

[seminoma]

Well Aspirin does inhibit the RAAS system so it's not super odd that PGs may upregulate it.

Fair enough, but how does volume contraction upregulate PGs?

 

[Jabbed]

Fair enough, but how does volume contraction upregulate PGs?

My guess is that the source of the prostaglandins is from autoregulation of afferent arterial flow. Volume contraction > decreased blood flow > PGs dilate afferent artery > AT II constricts efferent artery > increased filtration fraction.

In this case the stimulus for PG increase is myogenic.

 

[seminoma]

My guess is that the source of the prostaglandins is from autoregulation of afferent arterial flow. Volume contraction > decreased blood flow > PGs dilate afferent artery > AT II constricts efferent artery > increased filtration fraction.

In this case the stimulus for PG increase is myogenic.

That makes sense. I always thought of the myogenic hypothesis as it pertains to volume expansion and RAAS as the equivalent for volume contraction. I guess it's a chicken/egg thing.. which doesn't really matter unless some test writer feels like being a jerk about it and writing one of those questions with mechanisms listed in a specific order as answer choices.