title: Atrial natriuretic hormone, the renin-aldosterone axis, and blood pressure-electrolyte homeostasis.
abstract: The renin-angiotensin-aldosterone axis exerts major control over sodium and potassium balance and arterial blood pressure. These three functions are continuously regulated by changes in angiotensin II and aldosterone levels in response to wide variations in dietary intake of sodium and potassium. In addition, changes in intrarenal physical factors cause changes in the supply of distal tubular sodium that, in turn, work to determine sodium and potassium excretion and to modulate the release of renal renin. However, certain aspects of sodium homeostasis cannot be fully explained either by the activity of the renin system or by intrarenal physical factors, and this has led investigators to search for other natriuretic hormonal mechanisms. Recently, it has become clear that atrial tissue contains a group of peptides, at least one of which is probably secreted as a regulatory hormone. In animals, these atrial peptides produce immediate, marked natriuresis associated with a rise in glomerular filtration rate (but no alteration of total renal flow) and a simultaneous decrease in arterial blood pressure. Atrial peptides also inhibit renal renin secretion and adrenal cortical secretion of aldosterone, and they oppose the vasoconstrictive action of angiotensin II. One of these atrial peptides may therefore be the long-sought natriuretic hormone, though in a different form and shape than was envisioned. The fact that atrial peptide works to oppose the renin system at four points suggests that this new hormone could have a major complementary role in long-term regulation of blood pressure and electrolyte homeostasis. In this construction the renin system primarily defends sodium balance and blood pressure, with the atrial hormone having an increasing counter-influence in situations involving high blood pressure or sodium surfeit. We can soon expect to learn more about this atrial hormone, including which peptide is the active circulating hormone, what induces or inhibits its release, and what part it plays in cardiovascular diseases.
authors.forename: J H
authors.initials: JH
authors.lastname: Laragh
mesh_terms: D000450:Aldosterone / Q000378:metabolism; D000595:Amino Acid Sequence; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000032:analysis / Q000502:physiology* / Q000627:therapeutic use; D001775:Blood Circulation; D001794:Blood Pressure / Q000187:drug effects; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D011188:Potassium / Q000378:metabolism; D012079:Renal Circulation; D012083:Renin / Q000502:physiology; D012084:Renin-Angiotensin System; D012964:Sodium / Q000378:metabolism; D014882:Water-Electrolyte Balance
chemical_list: D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D012083:Renin; D011188:Potassium