Nice explanation that makes sense, but your theory did not explain the intense afferent arteriolar vasoconstriction seen in HRS!Moreover, cirrhosis is a condition of high estrogen levels circulating into the bloodstream: defective liver function --> low levels of produced binding proteins --> estrogens are in their active forms, instead of being bound to proteins.
Estrogens cause vasodilation through mechanisms irrelevant to their classic interaction with the DNA, but instead through membrane endothelial receptors & NO.
This estrogen-induced vasodilation has been postulated to be responsible for palmar erythema, spider nevi, gynecomastia (spironolactone may also have a contribution, though) and even hepato-renal & hepato-pulmonary syndromes.
(The above is just a humble wannabe Ob-Gyn's contribution to a very fascinating, on pathophysiology grounds, topic )
Thank you Jajeek for the nice reference. But I still don't understand how peripheral arterial vasodilation leads to renal vasoconstriction!
- Peripheral arterial vasodilation with hyperdynamic circulation and subsequent renal vasoconstriction;