Effect of Atrial Natriuretic Peptide on the Vasopressin Response to Osmotic and Hemorrhagic Stimuli in Dogs

Abstract

Abstract Effect of atrial natriuretic peptide (ANP) on the vasopressin response to osmotic stimulation (Experiment I) as well as to hemorrhage (Experiment II) was investigated in anesthetized dogs. Moreover, cardiovascular function and renal water and electrolyte excretion were studied. In Experiment I, 2.5 M NaCI, containing 0.02 mug.kg (1) of ANP, was infused intravenously at a rate of 0.2 ml.kg(-1), min (1) after one bolus injection of 0.75 mug.kg (1) ANP (HSA group). In the control group, 2.5 M NaCI alone (HS group) was infused. The infusion was continued for 75 min. In Experiment II, 0.15 M NaCI, containing the identical dose of ANP to Experiment I (HA group), or 0.15 M NaCI alone (H group) was infused intravenously during bleeding at a rate of 1 ml.kg(-1).min (-1) for 40 min. In Experiment I, infused ANP suppressed the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and attenuated ANP release and a rise in arterial and central venous pressures in response to plasma volume expansion, without the enhanced natriuresis. In Experiment II, infused ANP neither impaired the vasopressin response to bleeding nor potentiated a fall in mean arterial pressure and central venous pressure. In conclusion, ANP at physiological and/or supraphysiological range may suppress the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and to hemorrhage. In addition, ANP given intravenously may attenuate ANP release and a rise in blood pressure without any natriuresis.