Atrial distension, arterial pulsation, and vasopressin release during negative pressure breathing in humans

Citation
B. Pump et al., Atrial distension, arterial pulsation, and vasopressin release during negative pressure breathing in humans, AM J P-HEAR, 281(4), 2001, pp. H1583-H1588
Citations number
29
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
281
Issue
4
Year of publication
2001
Pages
H1583 - H1588
Database
ISI
SICI code
0363-6135(200110)281:4<H1583:ADAPAV>2.0.ZU;2-J
Abstract
During an antiorthostatic posture change, left atrial (LA) diameter and art erial pulse pressure (PP) increase, and plasma arginine vasopressin (AVP) i s suppressed. By comparing the effects of a 15-min posture change from seat ed to supine with those of 15-min seated negative pressure breathing in eig ht healthy males, we tested the hypothesis that with similar increases in L A diameter, suppression of AVP release is dependent on the degree of increa se in PP. LA diameter increased similarly during the posture change and neg ative pressure breathing (-9 to -24 mmHg) from between 30 and 31 +/- 1 to 3 4 +/- 1 min (P < 0.05). The increase in PP from 38 +/- 2 to 44 +/- 2 mmHg ( P < 0.05) was sustained during the posture change but only increased during the initial 5 min of negative pressure breathing from 36 +/- 3 to 42 +/- 3 mmHg (P < 0.05). Aortic transmural pressure decreased during the posture c hange and increased during negative pressure breathing. Plasma AVP was supp ressed to a lower value during the posture change (from 1.5 +/- 0.3 to 1.2 - 0.2 pg/ml, P < 0.05) than during negative pressure breathing (from 1.5 +/ - 0.3 to 1.4 +/- 0.3 pg/ml). Plasma norepinephrine was decreased similarly during the posture change and negative pressure breathing compared with sea ted control. In conclusion, the results are in compliance with the hypothes is that during maneuvers with similar cardiac distension, suppression of AV P release is dependent on the increase in PP and, furthermore, probably una ffected by static aortic baroreceptor stimulation.