Contribution of cardiac and arterial baroreceptors to enhanced vasopressin release during hemorrhage with autonomic blockade.
During episodes of blood loss, several apparently redundant mechanisms are activated to maintain arterial blood pressure. This study was designed to examine one such compensatory mechanism involving enhanced vasopressin release during hemorrhage when the autonomic nervous system (ANS) is pharmacologically blocked. First, to confirm that this compensatory mechanism exists in canines, conscious dogs were hemorrhaged under normal conditions and during ANS blockade. In dogs with intact cardiac nerves (intact, n = 7), hemorrhage at 0.8 ml/kg/min increased plasma vasopressin (PAVP) from 3.0 +/- 0.7 to 6.6 +/- 2.4 and 78 +/- 50 pg/ml at blood losses of 10 and 20 ml/kg, respectively. At the same amount of blood loss during hemorrhage with ANS blockage, PAVP was enhanced significantly from 33 +/- 17 to 230 +/- 90 and 610 +/- 270 pg/ml. ANS blockade did not, however, alter the hemorrhage-induced increases in plasma renin activity. Next, to examine the afferent mechanisms responsible for the enhanced PAVP response, cardiac-denervated dogs (CD, n = 9) were hemorrhaged with and without ANS blockade. Without blockade, PAVP increased from 3.7 +/- 0.9 to 5.2 +/- 0.8 and 26 +/- 11 pg/ml at blood losses of 10 and 20 ml/kg. PAVP was significantly higher in response to hemorrhage with ANS blockade, increasing from 17 +/- 6 to 76 +/- 18 and 330 +/- 80 pg/ml. The rise in PAVP in the CD dogs suggested that peripheral baroreceptors were involved in eliciting vasopressin release under these conditions. Therefore, the influence of arterial baroreceptors was examined by infusing norepinephrine during hemorrhage in order to maintain blood pressure constant. Under these conditions, PAVP increased significantly in the intact dogs at 10 ml/kg blood loss, but did not change in the CD dogs. These results demonstrate that the enhanced release of AVP during hemorrhage with ANS blockade can be mediated either by cardiac or arterial baroreceptors; however, the maximum response is elicited only when both sets of receptors are functioning normally.
Zhu
J L
JL
Division of Experimental Medicine, St. Luke's Hospital and Foundation, Kansas City, Missouri 64111.
Leadley
R J
RJ
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood / Q000378:metabolism*; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D001794:Blood Pressure; D002302:Cardiac Output; D003714:Denervation; D004285:Dogs; D005260:Female; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D006470:Hemorrhage / Q000097:blood / Q000503:physiopathology*; D018738:Hexamethonium / Q000494:pharmacology; D019832:N-Methylscopolamine; D009638:Norepinephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D012016:Reference Values; D012083:Renin / Q000097:blood; D012602:Scopolamine Derivatives / Q000494:pharmacology
D012602:Scopolamine Derivatives; D001127:Arginine Vasopressin; D018738:Hexamethonium; D012083:Renin; D019832:N-Methylscopolamine; D009638:Norepinephrine