[1] Secondary hyperaldosteronism is a normal physiological response to decreased arterial blood volume, wherein hypovolemia activates the renin–angiotensin system to stimulate aldosterone synthesis and thus increase fluid retention.
[2] This increase in active sodium reabsorption generates an electrochemical gradient that leads to passive transfer of potassium from the tubular cells into the urine.
Signs of muscle weakness can include a plantigrade stance of the hindlimbs, cervical ventroflexion, inability to jump, lateral recumbency, or collapse.
Ocular signs of arterial hypertension include mydriasis, hyphema, or blindness due to retinal detachment and/or intraocular hemorrhages.
Imaging may also detect metastasis and usually includes radiographs of the chest in addition to abdominal ultrasound and/or computerized tomography (CT).
In cats with idiopathic bilateral nodular hyperplasia of the zona glomerulosa, the PAC may be slightly elevated or high normal.
[1] Bilateral primary hyperaldosteronism due to hyperplasia of the zona glomerulosa or metastasized adrenocortical adenocarcinoma should be treated medically.