Depressor Effects and Release of Atrial Natriuretic Peptide during Norepinephrine or Angiotensin II Infusion in Man*

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Abstract
α-Human atrial natriuretic peptide (αhANP) is the major circulating form of ANP in man. The potential of synthetic ahANP to antagonize the pressor action of norepinephrine (NE) or angiotensin II (All) and a possible influence of NE or All pressor infusions on circulating immunoreactive ANP (irANP) were investigated in 14 normal young subjects. After titration of doses to increase mean blood pressure by about 20 mm Hg, NE or All was infused at a constant rate for 110 min. Mean blood pressure (BP) was similar during NE and All infusions [109 ± 4 (±SEM) and 108 ± 3 mm Hg, respectively]. However, synthetic ahANP injected in stepwise increasing doses of 10, 40, and 75 µg caused significantly greater (P < 0.001) BP reductions during NE infusion. ahANP lowered BP progressively from 147/91 ± 5/3 to136/70 ± 5/3 mm Hg during NE infusion (P < 0.001) and only minimally from 133/96 ± 3/3 to 132/89 ± 4/4 during All infusion. Heart rate was elevated more (P < 0.01) after ahANP injection during NE infusion. Endogenous plasma irANP increased significantly after 20 min of NE or All pressor infusion (P < 0.01 and P< 0.05, respectively); this rise was more pronounced (P < 0.05) during NE (from 25 ± 2 to 80 ± 20 pg/ml) than during All (from 21 ± 3 to 31 ± 3 pg/ml) infusion. These findings suggest that ahANP interacted preferentially with noradrenergic as compared to angiotensinergic BP control. Conversely, for a given rise in BP, NE elicited a greater rise in circulating irANP.