Right atrial pressure and ANP release during prolonged exercise in a hot environment

• Published in: Journal of applied physiology (1985) Vol. 76; no. 5; p. 1882
• Main Authors: Nose, H, Takamata, A, Mack, G W, Kawabata, T, Oda, Y, Hashimoto, S, Hirose, M, Chihara, E, Morimoto, T
• Format: Journal Article
• Language: English
• Published: United States 01.05.1994
• Subjects: Adult; Atrial Function; Atrial Natriuretic Factor - blood; Blood Pressure - physiology; Blood Volume - physiology; Body Temperature - physiology; Catecholamines - blood; Exercise - physiology; Hematocrit; Hemoglobins - metabolism; Hot Temperature - adverse effects; Humans; Male; Stroke Volume - physiology
• ISSN: 8750-7587
• DOI: 10.1152/jappl.1994.76.5.1882

To investigate the relationship between right atrial pressure (RAP) and atrial natriuretic peptide (ANP) release during prolonged exercise in a hot environment (30 degrees C, 20% relative humidity), we studied with a Swan-Ganz catheter five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min. The ANP level increased 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 blood temperature, plasma norepinephrine, or plasma epinephrine. The 10-min 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, norepinephrine (all P < 0.01), and epinephrine (P < 0.02) during the same period. These results suggest that ANP release is primarily controlled by atrial distension at the onset of exercise but that other stimulators may be involved thereafter.