Atrial natriuretic peptide causes pre-glomerular vasodilatation and post-glomerular vasoconstriction in rat kidney

• Published in: Nature (London) Vol. 324; no. 6096; p. 473
• Main Authors: Marin-Grez, M, Fleming, J T, Steinhausen, M
• Format: Journal Article
• Language: English
• Published: England 04.12.1986
• Subjects: Animals; Atrial Natriuretic Factor - pharmacology; Atrial Natriuretic Factor - physiology; Kidney - drug effects; Kidney - physiology; Kidney Glomerulus - blood supply; Kidney Glomerulus - drug effects; Kidney Glomerulus - physiology; Rats; Renal Circulation - drug effects; Vasoconstriction - drug effects; Vasodilation - drug effects
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/324473a0

Atrial natriuretic peptide (ANP) can be extracted from rat hearts, and is found to increase fluid excretion by the kidneys when injected into test animals. The mechanism of ANP action is still unclear. ANP may reduce sodium reabsorption in the renal tubules, but it is also known that it increases the rate of glomerular filtration in the kidney, and relaxes preparations of smooth muscle, including one made from arteries that supply the kidney. To clarify its mode of action, we have studied directly the effects of semi-purified and synthetic ANP on blood vessels in the kidney of anaesthetized rats. We found that ANP causes a vasodilatation of the blood vessels which supply the glomeruli and a vasoconstriction of the arterioles which drain them. This substantiates the finding that increased filtration pressure participates in the natriuretic response.