LEFT-HEART AND ARTERIAL BARORECEPTORS INTERACT IN CONTROL OF PLASMA VASOPRESSIN, RENIN, AND CORTISOL IN AWAKE DOGS

Arterial hypotension induced by constriction of the ascending aorta (A A) causes increases in left atrial pressure (LAP) and plasma atrial na triuretic peptide (ANP), but no change in plasma arginine vasopressin (AVP), plasma renin activity (PRA), or cortisol. In the present study, we tested the hypothesis that the rise in left heart pressure during constriction of the AA suppressed the stimulation of AVP, renin, and c ortisol secretion in response to arterial hypotension. Dogs were prepa red with inflatable cuffs around the AA, the pulmonary artery (PA), an d the thoracic inferior vena cava (IVC) and with catheters in the left and right atria and abdominal aorta. In one series of experiments, th e AA was constricted to lower mean arterial pressure (MAP) 10 or 20% b elow control for 15 min. Then, either the PA or the IVC was constricte d to bring LAP back to control levels but without altering the degree of arterial hypotension. Constriction of the AA alone led to significa nt increases in LAP and plasma ANP but no change in plasma AVP, cortis ol, or PRA. Reducing LAP to control levels by constriction of either t he PA or IVC led to significant and similar increases in plasma AVP, c ortisol, and PRA. Plasma ANP fell significantly 10 min after LAP was n ormalized by constriction of the NC but not when LAP was normalized by constriction of the PA, because PA constriction caused a significant rise in right atrial pressure that stimulated ANP secretion. The incre ases in plasma AVP and PRA after normalizing LAP by constriction of th e PA were compared with the increases obtained during identical falls in MAP induced by constriction of the IVC alone, a maneuver that lower s LAP below control. The increases in plasma AVP in the two conditions were identical, indicating that the stimulation of left heart barorec eptors alone can account for the suppression of AVP secretion in respo nse to unloading arterial baroreceptors. In contrast, there was a grea ter rise in PRA during hypotension caused by constriction of the NC al one compared with the condition in which LAP was normalized but plasma ANP remained elevated. This suggests that increased left heart pressu re inhibits renin secretion in response to arterial hypotension by ref lex mechanisms and by increased plasma ANP concentration.