Angiotensin II (A-II) has been shown to stimulate plasma arginine vasopressin (AVP) secretion in experimental animals, although offsetting effects from a rise in arterial pressure may obscure the effect. A rise in plasma norepinephrine (NE) may have several effects on plasma AVP because of changes in arterial pressure and central adrenergic stimulation. As little data exist concerning these neuro-humoral interrelationships in humans, the current investigation was performed to examine the role of acute changes in plasma NE and A-II in the control of arginine vasopressin (AVP). The question is of potential importance because of diffuse disturbances in neurohumoral control in diseases such as hypertension and congestive heart failure. We measured heart rate, arterial pressure, and plasma AVP during 2.5 and 5.0 μg/min infusions of NE, and during .05 and .10 μg/kg/min infusions of A-II. NE increased mean blood pressure from 81 ± 11 mm Hg to 87 ± 16 mm Hg at 2.5 μg/min and to 93 ± 16 mm Hg at 5.0 μg/min (p < .001). Heart rate was unchanged during the 2.5 μg/min infusion but declined from 58 ± 9 beats/min to 54 ± 9 beats/min during the 5.0 μg/min infusion (p = NS). Plasma AVP, 3.0 ± 0.9 pg/mL, did not change. During A-II infusions, mean arterial pressure increased from 81 ± 13 mm Hg to 92 ± 17 mm Hg and 112 ± 21 mm Hg at the two rates (p < .001); heart rate declined from 61 ± 6.8 beats/min to 59 ± 9.1 beats/min and 56 ± 11.3 beats/min (p = NS). Plasma AVP, 3.2 ± 0.6 pg/mL, again did not change, although a nonsignificant trend toward a rise occurred between the first and second dose intervals. Thus, neither the rise in arterial pressure caused by an increase in plasma NE, nor a rise in plasma NE itself, decreases plasma AVP in normal humans. A rise in A-II to high levels may stimulate AVP, but only minimally, although offsetting baroreceptor effects are not excluded. These data do not suggest a major role for either increased NE or A-II in the regulation of basal AVP levels in normal humans. Whether increased NE or A-II affects AVP in disease states with abnormal baseline levels remains to be determined.
Bibliographical noteFunding Information:
This work was conducted during Dr. Steven Goldsmith's tenure as recipient of Clinical Investigator Award #5R08 HL00895-04 from the National Heart, Lung and Blood Institute, which also provided the funding for this study.