Differential effects of angiotensin II and noradrenaline on tubular rejection of sodium produced by ANP in rats

• Published in: Clinical and experimental hypertension. Part A, Theory and practice Vol. 13; no. 4; p. 489
• Main Authors: Reddy, S, Salipan-Moore, N, Györy, A Z
• Format: Journal Article
• Language: English
• Published: United States 1991
• Subjects: Angiotensin II - pharmacology; Angiotensin-Converting Enzyme Inhibitors - pharmacology; Animals; Atrial Natriuretic Factor - pharmacology; Blood Pressure - drug effects; Glomerular Filtration Rate - drug effects; Hematocrit; Kidney Tubules - metabolism; Male; Natriuresis - drug effects; Norepinephrine - pharmacology; Rats; Rats, Inbred Strains; Saralasin - pharmacology; Sodium - blood; Sodium - metabolism
• ISSN: 0730-0077
• DOI: 10.3109/10641969109045065

The effect of Atrial Natriuretic Peptide (ANP) on renal tubular sodium handling (FENa) in the presence of converting enzyme inhibition (CEI), the AII antagonist Saralasin (SAR), noradrenaline (NA) and angiotensin II (AII) infusions was investigated. FENa and increases in FENa produced by ANP were significantly lower with CEI (p less than 0.03 and 0.0001) or SAR (p less than 0.02 and 0.02) against control (Vehicle + ANP). Mean arterial pressures (MAP) were also reduced. Returning MAP to 107 +/- 2 mmHg with NA (+CEI+ANP), did not change FENa (1.22% +/- 0.16 to 1.25% +/- 0.18, p greater than 0.66) whereas without CEI but with ANP (MAP 113 +/- 2 mmHg) FENa was significantly increased by NA (2.34% +/- 0.36, p less than 0.02). With AII+CEI+ANP, MAP was restored to 110 +/- 5 mmHg, and FENa was highly significantly increased (0.99% +/- 0.20 to 3.04% +/- 0.39, p less than 0.0003) in excess of that expected due to pressure effects alone. It is concluded the additional effect of AII on FENa (3.04 versus 1.25% with NA) at equivalent perfusion pressures are due to a separate additive phenomenon of AII and ANP both causing tubular rejection of Na.