Andersen J L, Andersen L J, Thrasher T N, Keil L C, Ramsay D J
Department of Physiology, School of Medicine, University of California, San Francisco 94143.
Am J Physiol. 1994 Mar;266(3 Pt 2):R879-88. doi: 10.1152/ajpregu.1994.266.3.R879.
Arterial hypotension induced by constriction of the ascending aorta (AA) causes increases in left atrial pressure (LAP) and plasma atrial natriuretic 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 cortisol secretion in response to arterial hypotension. Dogs were prepared with inflatable cuffs around the AA, the pulmonary artery (PA), and the thoracic inferior vena cava (IVC) and with catheters in the left and right atria and abdominal aorta. In one series of experiments, the AA was constricted to lower mean arterial pressure (MAP) 10 or 20% below control for 15 min. Then, either the PA or the IVC was constricted to bring LAP back to control levels but without altering the degree of arterial hypotension. Constriction of the AA alone led to significant increases in LAP and plasma ANP but no change in plasma AVP, cortisol, or PRA. Reducing LAP to control levels by constriction of either the PA or IVC led to significant and similar increases in plasma AVP, cortisol, and PRA. Plasma ANP fell significantly 10 min after LAP was normalized by constriction of the IVC 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 increases in plasma AVP and PRA after normalizing LAP by constriction of the PA were compared with the increases obtained during identical falls in MAP induced by constriction of the IVC alone, a maneuver that lowers LAP below control. The increases in plasma AVP in the two conditions were identical, indicating that the stimulation of left heart baroreceptors alone can account for the suppression of AVP secretion in response to unloading arterial baroreceptors. In contrast, there was a greater rise in PRA during hypotension caused by constriction of the IVC alone compared with the condition in which LAP was normalized but plasma ANP remained elevated. This suggests that increased left heart pressure inhibits renin secretion in response to arterial hypotension by reflex mechanisms and by increased plasma ANP concentration.
升主动脉（AA）缩窄所致动脉性低血压会使左心房压力（LAP）和血浆心房利钠肽（ANP）升高，但血浆精氨酸血管加压素（AVP）、血浆肾素活性（PRA）或皮质醇无变化。在本研究中，我们检验了以下假设：AA缩窄期间左心压力升高抑制了因动脉性低血压而对AVP、肾素和皮质醇分泌的刺激。给犬在AA、肺动脉（PA）和胸段下腔静脉（IVC）周围安置可充气袖带，并在左、右心房和腹主动脉置入导管。在一系列实验中，将AA缩窄以使平均动脉压（MAP）比对照降低10%或20%，持续15分钟。然后，缩窄PA或IVC以使LAP恢复到对照水平，但不改变动脉性低血压的程度。单独缩窄AA导致LAP和血浆ANP显著升高，但血浆AVP、皮质醇或PRA无变化。通过缩窄PA或IVC将LAP降至对照水平导致血浆AVP、皮质醇和PRA显著且类似地升高。通过缩窄IVC使LAP恢复正常10分钟后血浆ANP显著下降，但通过缩窄PA使LAP恢复正常时血浆ANP未下降，因为缩窄PA导致右心房压力显著升高，刺激了ANP分泌。将通过缩窄PA使LAP恢复正常后血浆AVP和PRA的升高与单独缩窄IVC导致MAP同等下降期间（该操作使LAP低于对照）所获得的升高进行比较。两种情况下血浆AVP的升高相同，表明仅左心压力感受器的刺激就能解释因动脉压力感受器卸载而对AVP分泌的抑制。相反，与LAP恢复正常但血浆ANP仍升高的情况相比，单独缩窄IVC所致低血压期间PRA升高幅度更大。这表明升高的左心压力通过反射机制和血浆ANP浓度升高抑制因动脉性低血压而引起的肾素分泌。
