Note that aldosterone, the end product of the mineralocorticoid pathway, does not cause negative feedback inhibition on ACTH or CRH production.

spell out Adrenal Insufficiency in the table legend.

high

nodule

add space

increasing the expression of sodium channels, potassium channels, and the Na+/K+ ATPase in the distal tubule of the kidney.

binding

(DOC to corticosterone to 18-hydroxycorticosterone to aldosterone)

and starts with secretion of the protease renin from the juxtaglomerular cells of the kidney. Renin catalyzes the conversion of angiotensinogen, made in the liver, to angiotensin I that is converted to angiotensin II by the protease angiotensin-converting enzyme (ACE). (Students are often confused by and miss the fact that renin and ACE are proteases, so better to explain it here, as it is also illustrated in figure 4.)

as well as other peptides.

precursor

precursor

increase in sympathetic activity, and a decrease in NaCl passing through the renal nephron, as detected by the salt-sensing macula densa cells. (if "interesting" mechanistic text on a slide is not explained a little bit, it is very annoying for the students. But they can do without all the things that angiotensin II does for now.)

start new line- will increase list to 14 SLOs

I will NOT test out

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