RIGHT ATRIAL PRESSURE AND ANP RELEASE DURING PROLONGED EXERCISE IN A HOT ENVIRONMENT

Citation
H. Nose et al., RIGHT ATRIAL PRESSURE AND ANP RELEASE DURING PROLONGED EXERCISE IN A HOT ENVIRONMENT, Journal of applied physiology, 76(5), 1994, pp. 1882-1887
Citations number
29
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
5
Year of publication
1994
Pages
1882 - 1887
Database
ISI
SICI code
8750-7587(1994)76:5<1882:RAPAAR>2.0.ZU;2-D
Abstract
To investigate the relationship between right atrial pressure (RAP) an d atrial natriuretic peptide (ANP) release during prolonged exercise i n a hot environment (30 degrees C, 20% relative humidity), we studied with a Swan-Ganz catheter five male volunteers exercising on a cycle e rgometer at 60% of peak aerobic power for 50 min. The ANP level increa sed from 14 +/- 3 (SE) to 69 +/- 10 pg/ml (P < 0.001) during the first 10 min of exercise as RAP rose from 4.3 +/- 0.8 to 6.9 +/- 1.1 mmHg ( P < 0.001). The 10-min ANP level was significantly correlated with RAP (r = 0.88, P < 0.05) but not with heart rate, pulmonary arterial bloo d temperature, plasma norepinephrine, or plasma epinephrine. The 10-mi n RAP value was inversely correlated with blood volume (r = -0.98, P < 0.01) and also with stroke volume (r = -0.96, P < 0.01). In the next 20 min of exercise, ANP continued to increase to 101 +/- 12 pg/ml (P < 0.02 vs. 10 min) and remained at this level until 50 min of exercise, whereas RAP decreased and reached a level not significantly different from baseline at 50 min (5.7 +/- 1.0 mmHg; P < 0.01 vs. 10 min). This dissociation of ANP and RAP may have been related to the significant increases from the 10-min values of heart rate, blood temperature, nor epinephrine (all P < 0.01), and epinephrine (P < 0.02) during the same period. These results suggest that ANP release is primarily controlle d by atrial distension at the onset of exercise but that other stimula tors may be involved thereafter. The lower ANP release in subjects wit h a higher blood volume at 10 min may have been caused by an attenuate d increase in RAP due to a larger stroke volume.