Physiological actions of the mineralocorticoid aldosterone:

• While aldosterone stimulates $\text{H}^+$ secretion by alpha-intercalated cells, its primary classical homeostatic mandate is sodium/fluid retention and potassium regulation.
• Aldosterone promotes renal $\text{Na}^+$ reabsorption in the distal convoluted tubule and collecting duct, passively reabsorbing water and thereby defending the effective circulating arterial fluid volume.
• Aldosterone simultaneously stimulates potassium ($\text{K}^+$) excretion into the tubular lumen via principal cell ROMK channels, maintaining systemic potassium homeostasis.
• Systemic osmolality is primarily controlled by Antidiuretic Hormone (ADH/vasopressin) and the thirst center, not aldosterone.

Physiology of enteroglucagon (GLP-1 and GLP-2 proglucagon products):

• Pancreatic glucagon and insulin primarily regulate systemic blood glucose levels.
• Enteroglucagon (specifically glucagon-like peptide 2, GLP-2, cleaved from proglucagon in intestinal endocrine L-cells) functions as a potent trophic hormone that stimulates mucosal epithelial proliferation, inhibits enterocyte apoptosis, and regulates growth and repair of the intestinal crypt-villus architecture.
• Enteroglucagons generally inhibit, rather than stimulate, gastric emptying and motility.
• Gastric acid secretion is stimulated by gastrin and histamine, and inhibited by enteroglucagons.

Chemical classification of endogenous opioid peptides:

• Steroids are cyclopentanoperhydrophenanthrene derivatives (e.g., cortisol, estrogen).
• Lipids are water-insoluble biomolecules (fatty acids, triacylglycerols).
• $\beta$-Endorphin is an endogenous opioid neuropeptide consisting of a 31-amino acid polypeptide chain ($Tyr-Gly-Gly-Phe-Met-\dots$) produced by tissue-specific proteolytic cleavage of the large precursor prohormone pro-opiomelanocortin (POMC) in the pituitary and hypothalamus.
• Carbohydrates are polyhydroxy aldehydes or ketones.

Etiology of Cushing's syndrome (hyperadrenocorticism):

• Progesterone is a luteal progestational steroid not characteristically elevated in Cushing's.
• Primary excess of aldosterone causes Conn's syndrome (hyperaldosteronism).
• Testosterone hypersecretion causes virilization, not classic Cushing's syndrome.
• Cushing's syndrome (hyperadrenocorticism, common in canine clinical practice) is caused by chronic, sustained overproduction of the glucocorticoid hormone cortisol by the adrenal cortex (zona fasciculata), either due to an ACTH-secreting pituitary adenoma or an autonomous functional adrenal tumor.