Having a little trouble understanding the mechanism of urine chloride in metabolic alkalosis...here's what I'm thinking.
Chloride-Responsive, i.e. vomitng.
Vomiting leads to volume depletion. Volume depletion leads to RAS. RAS increases chloride rentention in the PT via AngII and chloride retention in CDv via aldosterone. This leads to low urine Cl.
Chloride-Resistant, i.e. primary hyperaldosteronism
Aldosterone leads to volume expansion. Volume expansion leads to ANP. ANP leads to reduced sodium (and chloride) reabsorption in the late nephron. This results in an increase is chloride.
Are these mechanisms correct?
Chloride-Responsive, i.e. vomitng.
Vomiting leads to volume depletion. Volume depletion leads to RAS. RAS increases chloride rentention in the PT via AngII and chloride retention in CDv via aldosterone. This leads to low urine Cl.
Chloride-Resistant, i.e. primary hyperaldosteronism
Aldosterone leads to volume expansion. Volume expansion leads to ANP. ANP leads to reduced sodium (and chloride) reabsorption in the late nephron. This results in an increase is chloride.
Are these mechanisms correct?
