The renin-angiotensin-aldosterone system. Past, present and future.
"The present results indicate that there is a close relationship between the incretory function of the kidney, which is shown by the discharge of renin and similar materials, and the function of the adrenal cortex, especially the zona glomerulosa, which is the place of production of the sodium-retaining hormone aldosterone . Salt load inhibits the production of renin and aldosterone, while salt deprivation stimulates the production of both. The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." ... "Under these conditions the development of experimental renal hypertension could be explained as follows: the narrowing of the renal artery stimulates the secretion of renin which itself increases the formation or discharge of mineralocorticoid hormones (aldosterone or similarly acting corticoids). The resulting retention of sodium does not lead to the normal reduction of renin secretion in the ischemic kidney, so that corticoid production in the adrenal cortex is further stimulated despite no need for it."
D000450:Aldosterone / Q000502:physiology*; D000804:Angiotensin II / Q000502:physiology*; D000808:Angiotensinogen / Q000096:biosynthesis / Q000302:isolation & purification; D000818:Animals; D004792:Enzyme Precursors / Q000502:physiology; D006801:Humans; D008901:Mineralocorticoids / Q000378:metabolism; D011945:Receptors, Angiotensin / Q000502:physiology; D012083:Renin / Q000032:analysis / Q000502:physiology*; D014018:Tissue Distribution
D004792:Enzyme Precursors; D008901:Mineralocorticoids; D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D000804:Angiotensin II; D000450:Aldosterone; D012083:Renin