Differential Effects of Angiotensin II and Noradrenaline on Tubular Rejection of Sodium Produced by Anp in Rats

Abstract

The effect of Atrial Natriuretic Peptide (ANP) on renal tubular sodium handling (FE_Na) in the presence of converting enzyme inhibition (CEI), the AII antagonist Saralasin (SAR), noradrenaline (NA) and angiotensin II (AII) infusions was investigated. FE_Na and increases in FE_Na produced by ANP were significantly lower with CEI (p < 0.03 and 0.0001) or SAR (p < 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 FE_Na (1.22%±0.16 to 1.25%±0.18, p > 0.66) whereas without CEI but with ANP (MAP 113±2 mmHg) FE_Na was significantly increased by NA (2.34%±0.36, p < 0.02). With AII+CEI+ANP, MAP was restored to 110±5 mmHg, and FE_Na was highly significantly increased (0.99%±0.20 to 3.04%±0.39, p < 0.0003) in excess of that expected due to pressure effects alone. It is concluded the additional effect of All on FE_Na (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.

Key Words:

• Atrial Natriuretic Peptide
• Converting Enzyme Inhibition
• Na Transport
• Renal Perfusion Pressure