Menstrual status and plasma vasopressin, renin activity, and aldosterone exercise responses

The effects of menstrual cycle phase (early follicular vs. midluteal) and menstrual status (eumenorrhea vs. amenorrhea) on plasma arginine vasopressin (AVP), renin activity (PRA), and aldosterone (ALDO) were studied before and after 40 min of submaximal running (80% maximal O2 uptake). Eumenorrheic runners were studied in the early follicular and midluteal phases determined by urinary luteinizing hormone and progesterone and plasma estradiol and progesterone assays; amenorrheic runners were studied once. Menstrual phase was associated with no significant differences in preexercise plasma AVP or PRA, but ALDO levels were significantly higher during the midluteal phase than the early follicular phase. Plasma AVP and PRA were significantly elevated at 4 min after the 40-min run in the eumenorrheic runners during both menstrual phases and returned to preexercise levels by 40 min after exercise. Plasma ALDO responses at 4 and 40 min after exercise were higher in the midluteal phase than the early follicular phase. Menstrual status was associated with no significant differences in preexercise AVP or PRA; however, ALDO levels were significantly higher in the amenorrheic runners. After exercise, responses in the amenorrheic runners were comparable with the eumenorrheic runners during the early follicular phase. Thus, submaximal exercise elicits significant increases in plasma AVP and PRA independent of menstrual phase and status. However, plasma ALDO is significantly elevated during the midluteal phase, exercise results in a greater response during this menstrual phase, and amenorrheic runners have elevated resting levels of ALDO.     

Plasma vasopressin, renin activity, and aldosterone responses to maximal exercise in active college females

The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p less than 0.05) from a pre-exercise concentration of 3.8 +/- 0.5 to 15.8 +/- 4.8 pg X ml-1 following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5 +/- 0.5 pg X ml-1 and increased to 16.7 +/- 5.9 pg X ml-1 after the exercise test. PRA increased (p less than 0.05) from a pre-exercise value of 1.6 +/- 0.6 to 6.8 +/- 1.7 ngAI X ml-1 X hr-1 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4 +/- 0.6 ngAI X ml- X hr-1), as was the elevation found after maximal exercise (8.3 +/- 1.9 ngAI X ml- X hr-1). Pre-season plasma ALDO increased (p less than 0.05) from 102.9 +/- 30.8 pg X ml-1 in the pre-exercise period to 453.8 +/- 54.8 pg X ml-1 after the exercise test. In the post-season the values were 108.9 +/- 19.4 and 365.9 +/- 64.4 pg X ml-1, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Responses of plasma human atrial natriuretic factor to high intensity submaximal exercise in the heat

No data exists regarding responses of human atrial natriuretic factor (ANF) to exercise in the heat. The purpose of this study was to examine the responses of plasma ANF to high intensity submaximal (71% +/- 0.9 VO2max) exercise in the heat over an eight day acclimation period. Fourteen healthy males volunteered to participate in the study. Subjects performed intermittent exercises on a treadmill (0% grade) during 50 min of each 100 min trial in an environmental chamber maintained at 41.2 +/- 0.5 degrees C, 39.0 +/- 1.7% relative humidity. Blood was obtained from an antecubital vein after standing 20 min in the heat prior to exercise, and immediately after exercise. Measures were compared on days 1, 4 and 8. ANF did not change pre- to post-exercise nor did it change over the eight day heat acclimation period despite other heat acclimation adaptations. Conversely, plasma aldosterone (ALDO), renin activity (PRA) and cortisol (COR) all increased (p less than 0.05) pre- to post-exercise on each day but again no changes were observed over the eight day period. These data support that ANF may not increase when ALDO and PRA increases are observed.     

Plasma renin activity, aldosterone and catecholamine levels when swimming and running

The purpose of this study was to determine the response of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and catecholamines to two graded exercises differing by posture. Seven male subjects (19-25 years) performed successively a running rest on a treadmill and a swimming test in a 50-m swimming pool. Each exercise was increased in severity in 5-min steps with intervals of 1 min. Oxygen consumption, heart rate and blood lactate, measured every 5 min, showed a similar progression in energy expenditure until exhaustion, but there was a shorter time to exhaustion in the last step of the running test. PRA, PAC and catecholamines were increased after both types of exercise. The PRA increase was higher after the running test (20.9 ng AngI X ml-1 X h-1) than after swimming (8.66 ng AngI X ml-1 X h-1). The PAC increase was slightly greater after running (123 pg X ml-1) than swimming (102 pg X ml-1), buth the difference was not significant. Plasma catecholamine was higher after the swimming test. These results suggest that the volume shift induced by the supine position and water pressure during swimming decreased the PRA response. The association after swimming compared to running of a decreased PRA and an enhanced catecholamine response rule out a strict dependence of renin release under the effect of plasma catecholamines and is evidence of the major role of neural pathways for renin secretion during physical exercise.     

Plasma prostaglandins, renin, and catecholamines at rest and during exercise in hypertensive humans

Plasma prostaglandins (PGE and PGF alpha), catecholamine concentration, and plasma renin activity (PRA) were measured during an uninterrupted graded exercise test on the bicycle ergometer in 11 hypertensive patients. Blood was withdrawn from the brachial and pulmonary arteries after 30 min of recumbent rest, after 15 min of rest sitting, and at the final work load of the exercise test, which averaged 143 +/- 16.5 W. Exercise did not provoke a significant change in these plasma PGE or PGF alpha concentrations, whereas a rise (P less than 0.001) in arterial PRA and (nor)epinephrine concentration was observed. It is thus unlikely that PGE or PGF alpha is an important determinant of PRA release during exercise, although circulating levels of PGE and PGF alpha do not necessarily reflect release rate or activity in the kidney.     

Effects of dietary copper on human autonomic cardiovascular function

Heart rate and blood pressure responses during supine rest, orthostasis, and sustained handgrip exercise at 30% maximal voluntary contraction were determined in eight healthy women aged 18-36 years who consumed diets varying in copper and ascorbic acid content. Copper retention and plasma copper concentration were not affected by diet. Enzymatic, but not immunoreactive, ceruloplasmin was lower (p less than 0.05) after the low copper and high ascorbic acid diet periods. Diet had no effect on resting supine heart rates, orthostatic responses in heart rate and blood pressure, or standing resting blood pressure. Systolic and diastolic blood pressures were increased significantly (p less than 0.05) during the handgrip test at the end of the low copper and ascorbic acid supplementation periods. Also, the ratio of enzymatic to immunoreactive ceruloplasmin decreased significantly during these dietary treatments. The mean arterial blood pressure at the end of the handgrip test was negatively (p less than 0.0004) correlated with the ceruloplasmin ratios. These findings indicate a functional alteration in human blood pressure regulation during mild copper depletion.     

Role of skin blood flow and sweating rate in exercise thermoregulation after bed rest.

Two potential mechanisms, reduced skin blood flow (SBF) and sweating rate (SR), may be responsible for elevated intestinal temperature (T(in)) during exercise after bed rest and spaceflight. Seven men underwent 13 days of 6 degrees head-down bed rest. Pre- and post-bed rest, subjects completed supine submaximal cycle ergometry (20 min at 40% and 20 min at 65% of pre-bed rest supine peak exercise capacity) in a thermoneutral room. After bed rest, T(in) was elevated at rest (+0.31 +/- 0.12 degrees C) and at the end of exercise (+0.33 +/- 0.07 degrees C). Percent increase in SBF during exercise was less after bed rest (211 +/- 53 vs. 96 +/- 31%; P < or = 0.05), SBF/T(in) threshold was greater (37.09 +/- 0.16 vs. 37.33 +/- 0.13 degrees C; P < or = 0.05), and slope of SBF/T(in) tended to be reduced (536 +/- 184 vs. 201 +/- 46%/ degrees C; P = 0.08). SR/T(in) threshold was delayed (37.06 +/- 0.11 vs. 37.34 +/- 0.06 degrees C; P < or = 0.05), but the slope of SR/T(in) (3.45 +/- 1.22 vs. 2.58 +/- 0.71 mg x min-1 x cm-2 x degrees C-1) and total sweat loss (0.42 +/- 0.06 vs. 0.44 +/- 0.08 kg) were not changed. The higher resting and exercise T(in) and delayed onset of SBF and SR suggest a centrally mediated elevation in the thermoregulatory set point during bed rest exposure.     

Prolonged exercise following diuretic-induced hypohydration effects on fluid and electrolyte hormones.

To investigate the hypothesis that a reduction in plasma volume (PV) induced by diuretic administration would result in an increase in the fluid and electrolyte hormonal response to exercise, ten untrained males (VO(2) peak = 3.96 +/- 0.14 l/min) performed 60 min of cycle ergometry at 61 % VO(2) peak twice. The test was carried out once under control conditions (CON) (placebo) and once after 4 days of diuretic administration (DIU) (Novotriamazide; 100 mg triamterene and 50 mg hydrochlorothiazide). Calculated resting PV decreased by 14.6 +/- 3.3 % (p < 0.05) with DIU. No difference in plasma osmolality was observed between conditions. For the hormones measured, differences (p < 0.05) between conditions at rest were noted for plasma renin activity (PRA) (0.62 +/- 0.09 vs. 5.61 +/- 0.94 ng/ml/h), angiotensin I (ANG 1) (0.26 +/- 0.03 vs. 0.56 +/- 0.08 ng/ml), aldosterone (ALD) (143 +/- 14 vs. 1603 +/- 302 pg/ml), arginine vasopressin (AVP) (4.13 +/- 1.1 vs. 9.58 +/- 1.6 pg/ml) and atrial natriuretic peptide (alpha-ANP) (11.5 +/- 2.8 vs. 6.33 +/- 1.0 pg/ml). The exercise resulted in increases (p < 0.05) in PRA, ANG I, ALD, AVP, alpha-ANP. DIU led to higher levels of PRA, ANG I, and ALD (p < 0.05) and lower levels of alpha-ANP (p < 0.05) compared to CON. Arginine vasopressin was not affected by the loss of PV. For the catecholamines--norepinephrine (NE) and epinephrine (EPI)--only NE was higher during exercise with DIU compared to CON (p < 0.05). For PRA and ALD, the higher levels observed during exercise with DIU could be explained both by higher resting levels and a greater increase during exercise itself. For ANG I and NE, the effect of DIU only manifested itself during exercise. In contrast, the lower alpha-ANP observed during exercise with DIU was due to the lower resting levels. These results support the hypotheses that hypohydration leads to alterations in the secretion of all of the fluid and electrolyte hormones with the exception of AVP. The specific mechanisms of these alterations remain unclear, but appear to be related directly to the decrease in PV.     

Effect of prostaglandin inhibition by indomethacin on plasma active and inactive renin concentration in men.

The effect of inhibition of prostaglandin synthesis by indomethacin on active renin and on acid-activable inactive renin was studied in nine healthy, sodium-replete men, both at rest and exercise. These volunteers were investigated after pretreatment with placebo or indomethacin, 150 mg daily for 3 days. Indomethacin induced a decrease in active (p = 0.004), total (p less than 0.001), and inactive (p = 0.02) renin at rest recumbent on average by 42, 19, and 8%, respectively, and at rest sitting on average by 45, 15, and 3%, respectively. Inhibition of prostaglandins with indomethacin reduced (p less than 0.001) active and total renin at each level of work load but not (p = 0.32) inactive renin. However, the exercise-induced stimulation (p less than 0.05) of active and total renin still occur during indomethacin. Indomethacin reduced (p less than 0.001) at rest sitting and at maximal exercise the plasma concentrations of immunoreactive prostaglandins E2 by 50 and 54%, respectively, prostaglandin F2 alpha by 36 and 39%, respectively, and 13,14-dihydro-15-keto-prostaglandin F alpha by 38 and 60%, respectively. The urinary excretion of immunoreactive prostaglandin E2 and F2 alpha was also reduced.     

Central venous pressure in humans during short periods of weightlessness

Central venous pressure (CVP) was measured in 14 males during 23.3 +/- 0.6 s (mean +/- SE) of weightlessness (0.00 +/- 0.05 G) achieved in a Gulfstream-3 jet aircraft performing parabolic flight maneuvers and during either 60 or 120 s of +2 Gz (2.0 +/- 0.1 Gz). CVP was obtained using central venous catheters and strain-gauge pressure transducers. Heart rate (HR) was measured simultaneously in seven of the subjects. Measurements were compared with values obtained inflight at 1 G with the subjects in the supine (+1 Gx) and upright sitting (+1 Gz) positions, respectively. CVP was 2.6 +/- 1.5 mmHg during upright sitting and 5.0 +/- 0.7 mmHg in the supine position. During weightlessness, CVP increased significantly to 6.8 +/- 0.8 mmHg (P less than 0.005 compared with both upright sitting and supine inflight). During +2 Gz, CVP was 2.8 +/- 1.4 mmHg and only significantly lower than CVP during weightlessness (P less than 0.05). HR increased from 65 +/- 7 beats/min at supine and 70 +/- 5 beats/min during upright sitting to 79 +/- 7 beats/min (P less than 0.01 compared with supine) during weightlessness and to 80 +/- 6 beats/min (P less than 0.01 compared with upright sitting and P less than 0.001 compared with supine) during +2 Gz. We conclude that the immediate onset of weightlessness induces a significant increase in CVP, not only compared with the upright sitting position but also compared with the supine position at 1 G.     

Reproducibility of plasma catecholamine concentrations at rest and during exercise in man

The purpose of this study was to test the reproducibility of plasma norepinephrine (NE) and epinephrine (E) concentrations, at rest and during exercise, in man. Twelve young men were evaluated on two occasions (one week apart) at rest in supine and sitting positions and during dynamic exercise on bicycle ergometer: 5 min at a low intensity workload (heart rate = 131-133 bt min-1) and 5 and 20 min at a higher intensity (174-175 bt min-1). Mean plasma NE and E concentrations were not significantly different (p less than 0.05) on the two occasions in any of the experimental situations. However large within-subject variations were present, and the "standard errors of a single measurement" corrected for the variability of the catecholamine assay, ranged from 14 to 50% for NE and 14 to 37% for E. These results indicate that the mean plasma NE and E concentrations observed in a group of subjects are reproducible from one week to the other, but that individual plasma NE and E concentrations are not. This lack of reliability of a single determination of plasma catecholamine concentrations might be due to cyclic variations of plasma NE and E concentrations over time.     

Baroreflex during exercise in different postures before and after 20-days bed rest

Vagal-cardiac baroreflex functions in young healthy humans (n=6) were investigated in four different conditions; supine rest, seated rest, supine and seated exercise (50 watts) before and after 20-day horizontal bed rest. By selectively stimulating carotid baroreceptors using a neck pressure and suction technique, the primary finding was that the baroreflex sensitivity tuation at which we observed a tendency for an attenuation (0.05相似文献   

Left ventricular hemodynamics during exercise recovery

The directional response of human left ventricular stroke volume during exercise recovery is unclear. Stroke volume has been reported to increase and decrease over exercise values during early recovery. The confounding variable may be posture. With the use of pulsed Doppler ultrasound, we tested the hypothesis that there is a significant difference between seated and supine stroke index (SI) during passive recovery from seated ergometer exercise. Thirteen subjects aged 26 +/- 2 yr performed two seated cycle ergometer exercise tests to 70% of predicted maximum heart rate (HR). Recovery was supine on one test and seated on the other. Cardiac index (CI), HR, and SI were calculated during rest, exercise, and 10 min of recovery. At rest, SI and CI were significantly (P less than 0.01) less and HR significantly (P less than 0.01) greater when the subjects were seated than when they were supine. At the last exercise work load, no significant differences were found in any measured variable between tests. During recovery, supine SI was maximal 180 s postexercise (99 +/- 14 ml/m2) and exceeded (P less than 0.01) resting supine (81 +/- 14 ml/m2) and peak exercise (77 +/- 14 ml/m2) SI by 22 and 29%, respectively. Seated SI was constant at peak exercise levels for 2 min. Seated and supine recovery CI never exceeded exercise values. Systolic and diastolic blood pressure recovery curves were similar in the two postures. We conclude that posture significantly affects SI during recovery from submaximal seated exercise. These results have implications for choice of recovery posture after stress testing in cardiac patients where it is desirable to minimize ventricular loading.     

Lower body negative pressure exercise plus brief postexercise lower body negative pressure improve post-bed rest orthostatic tolerance.

Orthostatic intolerance follows actual weightlessness and weightlessness simulated by bed rest. Orthostasis immediately after acute exercise imposes greater cardiovascular stress than orthostasis without prior exercise. We hypothesized that 5 min/day of simulated orthostasis [supine lower body negative pressure (LBNP)] immediately following LBNP exercise maintains orthostatic tolerance during bed rest. Identical twins (14 women, 16 men) underwent 30 days of 6 degrees head-down tilt bed rest. One of each pair was randomly selected as a control, and their sibling performed 40 min/day of treadmill exercise while supine in 53 mmHg (SD 4) [7.05 kPa (SD 0.50)] LBNP. LBNP continued for 5 min after exercise stopped. Head-up tilt at 60 degrees plus graded LBNP assessed orthostatic tolerance before and after bed rest. Hemodynamic measurements accompanied these tests. Bed rest decreased orthostatic tolerance time to a greater extent in control [34% (SD 10)] than in countermeasure subjects [13% (SD 20); P < 0.004]. Controls exhibited cardiac stroke volume reduction and relative cardioacceleration typically seen after bed rest, yet no such changes occurred in the countermeasure group. These findings demonstrate that 40 min/day of supine LBNP treadmill exercise followed immediately by 5 min of resting LBNP attenuates, but does not fully prevent, the orthostatic intolerance associated with 30 days of bed rest. We speculate that longer postexercise LBNP may improve results. Together with our earlier related studies, these ground-based results support spaceflight evaluation of postexercise orthostatic stress as a time-efficient countermeasure against postflight orthostatic intolerance.     

Circadian variations in plasma renin activity, catecholamines and aldosterone during exercise in women

Four women were studied at 0400 h and 1600 h to determine if their hormonal and hemodynamic responses to exercise varied with the circadian cycle. Esophageal temperature was measured during rest and exercise (60% peak VO2; 30 min) in a warm room (Ta = 35 degrees C; PH2O = 1.7 kPa). Venous blood samples were drawn during rest and exercise and hemoglobin concentration (Hb), hematocrit (Hct), plasma osmolality (Posm), plasma protein concentration (Pp), colloid osmotic pressure (COP), plasma renin activity (PRA), cortisol, aldosterone, norepinephrine (NE) and epinephrine (E) were determined. Changes in plasma volume (PV) were estimated from changes in Hb and Hct. The relative hemoconcentration (-11.2%) was similar at 0400 h and 1600 h, but the absolute PV was smaller at 1600 h than at 0400 h (p = 0.03). The responses of Posm, Pp and COP to exercise were unaffected by time of day. Although PRA was not different at the two times of day, PRA was 244% greater during exercise at 1600 h, but only 103% greater during exercise at 0400 h. The normal circadian rhythms in plasma aldosterone (p = 0.043) and plasma cortisol (p = 0.004) were observed. Plasma aldosterone was 57% greater during exercise, while plasma cortisol did not change. The change in E and NE was greater at 0400 h, but this was due to the lower resting values of the catecholamines at 0400 h. These data indicate that time of day generally did not affect the hormonal or hemodynamic responses to exercise, with the exception that PRA was markedly higher during exercise at 1600 h compared to 0400 h.     

Effect of central hypervolemia on cardiac performance during exercise

To investigate the effect of different levels of central blood volume on cardiac performance during exercise, M-mode echocardiography was utilized to determine left ventricular size and performance during cycling exercise in the upright posture (UP), supine posture (SP), and head-out water immersion (WI). At submaximal work loads requiring a mean O2 consumption (Vo2) of 1.2 1/min and 1.5 1/min, mean left ventricular end-diastolic and end-systolic dimensions were significantly greater (P less than 0.05) with WI than UP. In the SP during exercise, left ventricular dimensions were intermediate between UP and WI. Heart rate did not differ significantly among the three conditions at rest and at submaximal exercise up to a mean Vo2 of 1.8 1/min. However, at a mean Vo2 of 2.4 1/min, heart rate in the UP was significantly greater than WI (P less than 0.01) and the SP (P less than 0.05). Maximal Vo2 did not differ statistically in the three conditions. These data indicate that a change in central blood volume results in alterations in left ventricular end-diastolic and end-systolic dimensions during moderate levels of exercise and a change in heart rate at heavy levels of exercise.     

Ventilatory and blood gas dynamics at onset and offset of exercise in the pony

The purpose of these experiments was to examine the temporal pattern of arterial carbon dioxide tension (PaCO2) to assess the relationship between alveolar ventilation (VA) and CO2 return to the lung at the onset and offset of submaximal treadmill exercise. Five healthy ponies exercised for 8 min at two work rates: 50 m/min 6% grade and 70 m/min 12% grade. PaCO2 decreased (P less than 0.05) below resting values within 1 min after commencement of exercise at both work rates and reached a nadir at 90 s. PaCO2 decreased maximally by 2.5 and 3.5 Torr at the low and moderate rate, respectively. After the nadir, PaCO2 increased across time during both work rates and reached values that were not significantly different (P greater than 0.05) from rest at minute 4 of exercise. Partial pressure of O2 in arterial blood and arterial pH reflected hyperventilation during the first 3 min of exercise. At the termination of exercise PaCO2 increased (1.5 Torr) above rest (P less than 0.05), reaching a zenith at 2-3 min of recovery. These data suggest that VA and CO2 flow to the lung are not tightly matched at the onset and offset of exercise in the pony and thus challenges the traditional concept of blood gas homeostasis during muscular exercise.     

Hemodynamic response to converting enzyme inhibition at rest and exercise in humans

The response of the systemic circulation to acute inhibition of the converting enzyme with 25 mg of oral Captopril (Squibb) was studied in six normal sodium-replete male volunteers at rest and during exercise, together with its effects on exercise capacity for graded uninterrupted exercise. In recumbent subjects at rest Captopril did not affect arterial pressure or heart rate, and plasma renin activity rose 2.5-fold (P less than 0.05). In subjects in the sitting position, at rest and during exercise until exhaustion, Captopril reduced mean brachial intra-arterial pressure by an average of 7 Torr in comparison to placebo (P less than 0.001). Captopril's hypotensive effect was caused by a reduction of systemic vascular resistance (P less than 0.01), without changes of cardiac output (measured by CO2 rebreathing), heart rate, or stroke volume. Plasma renin activity was significantly higher during Captopril (P less than 0.001). Peak oxygen uptake and exercise duration were the same after administration of Captopril or placebo. The data demonstrate that the renin-angiotensin system is not involved in the homeostasis of blood pressure in supine sodium-replete humans, but has a modest role in blood pressure regulation when posture is changed from supine to upright. The orthostatic effect of Captopril is maintained during upright exercise. Furthermore the reduction of systemic vascular resistance by Captopril does not affect peak oxygen uptake.     

Relationship between plasma renin activity and physical fitness in normal subjects

The relationship between plasma renin activity (PRA) at rest and physical fitness was studied in 40 normal young subjects on a liberal sodium intake. Plasma renin activity was measured in arterial blood withdrawn at the end of a 30-min period of rest in recumbency, while physical fitness was expressed by the highest oxygen uptake achieved during an uninterrupted graded exercise test performed in the sitting position on an electromagnetically braked ergometer bicycle (peak VO2). Log PRA correlated significantly and inversely with peak VO2 adjusted for body weight (r = -0.34; P less than 0.05) in single regression analysis. Using multiple regression and adjusted peak VO2, age, urinary sodium excretion and mean intra-arterial pressure as independent variables, no combination of two or more independent variables yielded significant partial correlation coefficients with log PRA. This correlation suggests that PRA at rest is inversely related to the subject's physical fitness.     

Immersion diuresis without expected suppression of vasopressin

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20-35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersion experiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at the end of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed when there is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.