Effect of head-down tilt on basal plasma norepinephrine and renin activity in humans

The effects of loading cardiopulmonary baroreceptors on basal norepinephrine and renin activity were studied in six normal subjects. Loading of cardiopulmonary baroreceptors was accomplished by a 60-min 30 degrees head-down tilt with small supplemental saline infusions. Central venous pressure was measured continuously by intrathoracic catheter; arterial pressure was measured indirectly by cuff. During the tilt, central venous pressure increased from 5.1 +/- 1.3 to 8.9 +/- 1.7 mmHg (P less than 0.001), whereas arterial pressure was unchanged. Plasma norepinephrine (185 +/- 85 pg/ml) and plasma renin activity (3.9 +/- 5.7 ng . ml-1 . h-1) did not change. Moderate sustained loading of cardiopulmonary baroreceptors is therefore without effect on unstressed plasma norepinephrine and renin activity in normal humans, suggesting that the tonic inhibitory effects of these receptors on these neurohumoral control systems are not readily increased in the basal state.     

Comparison of acute cardiovascular responses to water immersion and head-down tilt in humans.

The hypothesis was tested that acute water immersion to the neck (WI) compared with 6 degrees head-down tilt (HDT) induces a more pronounced distension of the heart and lower plasma levels of vasoconstrictor hormones. Ten healthy males underwent 30 min of HDT, WI, and a seated control (randomized). During WI, left atrial diameter and stroke volume increased to the same extent as during HDT. Cardiac output increased by 1 l/min more during WI than during HDT. (P < 0.05). Plasma atrial natriuretic peptide increased during WI (P < 0.05) but not during HDT, whereas plasma norepinephrine, vasopressin, and renin activity were suppressed similarly. Mean arterial pressure decreased by 9 mmHg (P < 0.05) during HDT and was unchanged during WI, and heart rate decreased more during HDT (P < 0.05). Arterial pulse pressure increased considerably more during HDT than during WI. In conclusion, the hypothesis was not confirmed because the cardiac atria were similarly distended by acute HDT and WI and the release of vasoconstrictor hormones were suppressed to the same extent.     

Antigravity suit inflation: kidney function and cardiovascular and hormonal responses in men

To investigate the effects of lower body positive pressure (LBPP) on kidney function while controlling certain cardiovascular and endocrine responses, seven men [35 +/- 2 (SE) yr] underwent 30 min of sitting and then 4.5 h of 70 degrees head-up tilt. An antigravity suit was applied (60 Torr legs, 30 Torr abdomen) during the last 3 h of tilt. A similar noninflation experiment was conducted where the suited subjects were tilted for 3.5 h. To provide adequate urine flow, the subjects were hydrated during the course of both experiments. Immediately after inflation, mean arterial pressure increased by 8 +/- 3 Torr and pulse rate decreased by 16 +/- 3 beats/min. Plasma renin activity and aldosterone were maximally suppressed (P less than 0.05) after 2.5 h of inflation. Plasma vasopressin decreased by 40-50% (P less than 0.05) and plasma sodium and potassium remained unchanged during both experiments. Glomerular filtration rate was not increased significantly by inflation, whereas inflation induced marked increases (P less than 0.05) in effective renal plasma flow (ERPF), urine flow, osmolar and free water clearances, and total and fractional sodium excretion. No such changes occurred during control. Thus, LBPP induces 1) a significant increase in ERPF and 2) significant changes in kidney excretory patterns similar to those observed during water immersion or the early phase of bed rest, situations that also result in central vascular volume expansion.     

Cardiorespiratory responses of animals to passive orthostasis after intermittent hypoxia during head-down tilt

Cardiorespiratory responses induced by upright tilt before and after intermittent hypoxia during head-down tilt, were investigated in rabbits. Arterial blood pressure, heart rate, central venous pressure, transmural filling pressure of the heart (calculated as the product of esophageal and central venous pressure), breathing frequency, esophageal pressure were measured in supine (baseline), head-down and upright posture. Our results indicate a reduction in orthostatic responses in cardiovascular system after intermittent hypoxia.     

Altered baroreflex function after tail suspension in the conscious rat

Experiments were performed on conscious chronically instrumented rats to determine the contribution of peripheral V2-vasopressinergic receptors in any alteration of baroreceptor reflex (BRR) sensitivity on release from 1 wk of 30 degrees head-down tilt resulting from tail suspension. Initial experiments determined changes in plasma volume (PV) occurring over this period by use of the Evans Blue dye dilution technique. PV was determined immediately before tail suspension and on day 7 of the stimulus. PV, erythrocyte volume, and total blood volume were all significantly diminished on day 7, whereas hematocrit was unchanged. Other rats were instrumented with pulsed Doppler flow probes on the ascending aorta for determination of cardiac output and with arterial and venous catheters 7-10 days before study. Immediately before tail suspension, control cardiac output, mean arterial blood pressure, and heart rate values were determined. In addition, BRR sensitivity was estimated both before and after intravenous administration of a V2-receptor antagonist by assessing the slope of the pulse interval-mean arterial blood pressure relationship in response to a series of pressor doses of phenylephrine. BRR sensitivity was determined on the last day of head-down tilt, 1 min after release from tail suspension, and 10 min after administration of a specific V2-vasopressinergic antagonist. BRR sensitivity tended to fall on day 7 of tail suspension compared with control and was significantly increased after release. However, BRR sensitivity was not altered by intravenous V2 antagonist administration either before tail suspension or after release.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10 degrees head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased approximately 2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: -3.1 +/- 0.6 and -3.3 +/- 1.0 versus -5.0 +/- 0.6 units.beat(-1).mmHg(-1) (P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.     

Arterial pulse pressure and vasopressin release during graded water immersion in humans

Previous results indicate that arterial pulse pressure modulates release of arginine vasopressin (AVP) in humans. The hypothesis was therefore tested that an increase in arterial pulse pressure is the stimulus for suppression of AVP release during central blood volume expansion by water immersion. A two-step immersion model (n = 8) to the xiphoid process and neck, respectively, was used to attain two different levels of augmented cardiac distension. Left atrial diameter (echocardiography) increased from 28 +/- 1 to 34 +/- 1 mm (P < 0.05) during immersion to the xiphoid process and more so (P < 0.05), to 36 +/- 1 mm, during immersion to the neck. During immersion to the xiphoid process, arterial pulse pressure (invasively measured in a brachial artery) increased (P < 0.05) from 44 +/- 1 to 51 +/- 2 mmHg and to the same extent from 42 +/- 1 to 52 +/- 2 mmHg during immersion to the neck. Mean arterial pressure was unchanged during immersion to the xiphoid process and increased during immersion to the neck by 7 +/- 1 mmHg (P < 0.05). Arterial plasma AVP decreased from 2.5 +/- 0.7 to 1.8 +/- 0.5 pg/ml (P < 0. 05) during immersion to the xiphoid process and significantly more so (P < 0.05), to 1.4 +/- 0.5 pg/ml, during immersion to the neck. In conclusion, other factors besides the increase in arterial pulse pressure must have participated in the graded suppression of AVP release, comparing immersion to the xiphoid process with immersion to the neck. We suggest that when arterial pulse pressure is increased, graded distension of cardiopulmonary receptors modulate AVP release.     

Central venous pressure and plasma arginine vasopressin in man during water immersion combined with changes in blood volume

To investigate the influence of central venous pressure (CVP) changes on plasma arginine vasopressin (pAVP), 8 normal male subjects were studied twice before, during and after immersion to the neck in water at 35.1 degrees +/- 0.1 degrees C (mean +/- SE) for 6 h. After 2 h of immersion, blood volume was either expanded (WIEXP) by intravenous infusion of 2.0 1 of isotonic saline during 2 h or reduced by loss of 0.5 1 of blood during 30 min (WIHEM). The two studies were randomised between subjects. WIEXP increased CVP, systolic arterial pressure (SAP), diuresis, natriuresis, kaliuresis and osmolar clearance compared to WIHEM while haematocrit, haemoglobin concentration and urine osmolality decreased. Heart rate, mean arterial (MAP) and diastolic arterial pressure, plasma osmolality, plasma sodium, plasma potassium and free water clearance did not differ significantly in the two studies. pAVP was significantly higher after 6 h in WIHEM than after 6 h in WIEXP (2.0 +/- 0.2 vs. 1.6 +/- 0.2 pg X ml-1, mean +/- SE; P less than 0.05). pAVP values were corrected for changes in plasma volume due to infusion in order properly to reflect AVP secretion. In conclusion, there was a weak, but significant, negative correlation between CVP and pAVP during the two studies, while during recovery from WIHEM and WIEXP decrements in SAP and MAP correlated significantly and strongly with increases in pAVP. It is therefore concluded that it is the arterial baroreceptors rather than the cardiopulmonary mechanoreceptors which are of importance in AVP regulation in man.     

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

During an antiorthostatic posture change, left atrial (LA) diameter and arterial pulse pressure (PP) increase, and plasma arginine vasopressin (AVP) is suppressed. By comparing the effects of a 15-min posture change from seated to supine with those of 15-min seated negative pressure breathing in eight healthy males, we tested the hypothesis that with similar increases in LA diameter, suppression of AVP release is dependent on the degree of increase in PP. LA diameter increased similarly during the posture change and negative pressure breathing (-9 to -24 mmHg) from between 30 and 31 +/- 1 to 34 +/- 1 mm (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 change and increased during negative pressure breathing. Plasma AVP was suppressed 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 seated control. In conclusion, the results are in compliance with the hypothesis that during maneuvers with similar cardiac distension, suppression of AVP release is dependent on the increase in PP and, furthermore, probably unaffected by static aortic baroreceptor stimulation.     

Arginine vasopressin, circulation, and kidney during graded water immersion in humans

Ten normal males rested sitting upright at an air temperature of 28 degrees C for 5.5 h (control, C) and underwent 4 h of graded water immersion (WI) to the umbilicus (UI), to the chest (CI), and to the neck (NI), respectively (water temperature = 34.5 degrees C), on different experimental days. Plasma arginine vasopressin (PAVP) was suppressed during WI compared with C and maximally so during NI. However, there was no change in PAVP comparing CI with UI even though central venous pressure (CVP) increased. CVP increased during CI and NI compared with C but was unchanged during UI, whereas cardiac output (rebreathing method), stroke volume, and plasma volume increased to approximately the same level during all three steps of WI compared with C. Heart rate and total peripheral vascular resistance decreased during UI, CI, and NI. Systolic arterial pressure (SAP) and pulse pressure (PP) were increased gradually from prestudy related to the degree of WI. Also diuresis, natriuresis, kaliuresis, osmotic excretion, and clearance were increased gradually compared with C, whereas free water clearance (CH2O) gradually decreased. There were weak negative but statistically significant correlations between PAVP and CVP and between changes in PAVP from prestudy and corresponding changes in SAP and PP. Furthermore, a statistically significant and negative correlation between CH2O and natriuresis could be established. We conclude that graded immersion gradually increases central blood volume and decreases PAVP. However, not only cardiopulmonary mechanoreceptors but also arterial baroreceptors may play a role in AVP suppression during WI in humans. In hydropenic subjects the suppression of PAVP during WI is apparently not effective in counteracting the decrease in CH2O induced by increased solute excretion.     

Effects of dehydration on the vasopressin response to immersion

Nine healthy volunteers underwent three experimental procedures in random order. The protocols were 4 h of thermal dehydration followed by 2 h of head-out water immersion, 4 h of thermal dehydration followed by 2 h of chair rest, and 6 h of rest in the supine position. Four hours of heat exposure (50 degrees C) resulted in a body weight loss of approximately 3.5%. Plasma osmolality rose by approximately 5 mosmol/kg, mean arterial pressure (MAP) decreased from 85 to 78 mmHg, and body temperature increased from 36.8 to 38.6 degrees C. As a consequence of the combined action of hypertonicity, hypovolemia, hypotension, and hyperthermia, plasma arginine vasopressin (AVP) increased from 2.1 to 8.1 pg/ml after 4 h thermal dehydration. Changes in body weight, plasma osmolality, body temperature, and MAP were similar after either a subsequent 2 h of water immersion or 2 h of chair rest. However, during chair rest plasma AVP remained elevated (8.4 pg/ml), whereas during immersion plasma AVP decreased from 8.1 to 4.7 pg/ml. This was probably due to the central hypervolemia induced by immersion. Our results support the hypothesis that central hypervolemia rather than hypotonicity is the primary stimulus for AVP suppression during water immersion in dehydrated subjects. During the early immersion period hypoosmolality might contribute to the AVP suppression.     

Central transmural venous pressure and plasma arginine vasopressin during negative pressure breathing in man

After overnight food and fluid restriction, 8 normal healthy males were examined in the upright sitting position before (prestudy), during and after (recovery) negative pressure breathing (NPB) with a pressure (P = difference between airway pressure and barometric pressure) of -9.6 +/- 0.5 to -10.4 +/- 0.4 mm Hg for 30 min. Plasma arginine vasopressin (pAVP) did not change significantly comparing prestudy with 10 and 30 min of NPB or comparing recovery with NPB at 10, 20 or 30 min. However, at 20 min of NBP, pAVP was slightly lower than at prestudy (p less than 0.05). Central venous pressure (CVP) decreased significantly during NPB, and central transmural venous pressure (CVP-P) increased significantly from -0.9 +/- 0.8 mm Hg to 3.8 +/- 0.7, 4.3 +/- 0.7 and 4.5 +/- 0.6 mm Hg (p less than 0.001) after 10, 20 and 30 min, respectively. Systolic, diastolic and mean arterial pressure and heart rate did not change significantly during NPB. Diuresis, natriuresis, kaliuresis, osmotic excretion and clearance were slightly increased during the recovery hour after NPB compared to prestudy, while urine osmolality decreased during NPB (n = 6). However, none of these changes were significant. There was no significant correlation between CVP-P and pAVP. In conclusion, -10 mm Hg NPB for 30 min in upright sitting subjects did not change pAVP consistently, while CVP-P was significantly increased and HR and arterial pressures were unchanged. This lends support to the concept that arterial baroreceptors and not cardiopulmonary mechanoreceptors are of importance in regulating AVP secretion in man.     

Hemodynamic adjustments to head-up posture in the partly arboreal snake, Elaphe obsoleta

Radioactively-labeled microspheres were used to quantify adjustments of regional blood flows in 15 snakes (Elaphe obsoleta) subjected to 45 degrees head-up tilt. Heart rate and peripheral vascular resistance increased during tilt to compensate for the passive drop of pressure at the head. Two snakes failed to regulate blood pressure, but in 13 others arterial pressure increased at midbody (where passive changes in pressure are unexpected due to tilt alone) and arterial pressure at the head averaged 67% of the pretilt value. Tissue blood flow was reduced significantly in visceral organs, posterior skin and posterior skeletal muscle, but was maintained at pretilt levels in brain, heart, lung and anterior tissues. Ventricular systemic output averaged 24 ml/min X kg in horizontal posture and 9.4 ml/min X kg during tilt. Comparable values for pulmonary output were 4 and 6.5 ml/min X kg. Patterns of intraventricular shunting of blood acted to maintain pulmonary flow during tilt. A large right-to-left shunt (mean 76%) was present in horizontal snakes, but the shunted fraction declined during tilt (mean 54%). Left-to-right shunt increased during tilt from 7% to 14%.     

Hemodynamic and hormonal effects of prolonged anti-G suit inflation in humans.

This study examined the hemodynamic consequences of prolonged lower body positive-pressure application and their relationship to changes in the plasma concentration of the major vasoactive hormones. Six men [36 +/- 2 (SE) yr] underwent 30 min of sitting and then 3 h of 70 degrees head-up tilt. An antigravity suit was applied (60 Torr legs, 30 Torr abdomen) during the last 2 h of tilt. In a similar noninflation experiment, the endocrine responses were measured in the suited subjects tilted for 3 h. Two-dimensional echocardiography was used to calculate ventricular volume and cardiac output. Measurements were made 30 min before and 30 and 90 min after inflation. Immediately after inflation, mean arterial pressure increased by 7 +/- 2 Torr and heart rate decreased by 16 +/- 4 beats/min. Left ventricular end-diastolic volume and systolic volume increased significantly (P less than 0.05) at 30 and 90 min of inflation. Cardiac output increased after 30 min of inflation and returned to the preinflation level at 90 min. Plasma norepinephrine and plasma renin activity were maximally suppressed after 15 and 90 min of inflation, respectively (P less than 0.05). No such hormonal changes occurred during control. Plasma sodium, potassium, and osmolality remained unchanged during both experiments. Thus, prolonged application of lower body positive pressure induces 1) a transient increase in cardiac output and 2) a marked and sustained decrease in plasma norepinephrine and plasma renin activity, which reflect an inflation-induced decrease in sympathetic activity.     

Atrial natriuretic peptide and vasopressin in human plasma

Using a specific radioimmunoassay for atrial natriuretic peptide (ANP), plasma immunoreactive ANP was measured in 17 normal subjects and 83 patients with various diseases. Plasma ANP concentration in normal subjects was 14.1 +/- 1.7 pg/ml (mean +/- S.E.). Relatively high plasma ANP concentrations were detected in patients with diabetes mellitus, hyperthyroidism, atrial fibrillation and liver cirrhosis. Plasma ANP concentrations in the patients correlated positively with mean arterial blood pressure and plasma AVP concentrations. Plasma ANP concentrations in the patients also had positive correlations with left atrial dimension and left ventricular diastolic dimension determined by echocardiography. Another positive correlation was observed in the patients between plasma AVP concentrations and mean arterial blood pressure. These results suggest that ANP is a volume regulatory hormone but also that ANP may be involved in the blood pressure regulating system.     

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg(-1)·min(-1)) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg(-1)·min(-1)) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure and central venous pressure (CVP). Because the elevation in blood pressure could have potentially inhibited AVP secretion via baroreceptor reflexes, the effect of ANG II on blood pressure was attenuated by the simultaneous infusion of nitroprusside. ANG II alone produced a remarkable increase in plasma AVP levels when infused with nitroprusside, whereas the simultaneous ANP intravenous infusion (10 ng·kg(-1)·min(-1)) abolished the increase in plasma AVP levels induced by ANG II when blood pressure elevation was attenuated by nitroprusside. Thus, ANG II increased AVP secretion and ANP inhibited not only basal AVP secretion but also ANG II-stimulated AVP secretion in humans. These findings support the hypothesis that circulating ANP modulates AVP secretion, in part, by antagonizing the action of circulating ANG II.     

Reduced orthostatic tolerance following 4 h head-down tilt

The cardiovascular responses to a 10-min 1.22 rad (70 degrees) head-up tilt orthostatic tolerance test (OST) was observed in eight healthy men following each of a 5-min supine baseline (control), 4 h of 0.1 rad (6 degrees) head-down tilt (HDT), or 4 h 0.52 rad (30 degrees) head-up tilt (HUT). An important clinical observation was presyncopal symptoms in six of eight subjects following 4 h HDT, but in no subjects following 4 h HUT. Immediately prior to the OST, there were no differences in heart rate, stroke volume, cardiac output, mean arterial pressure and total peripheral resistance for HDT and HUT. However, stroke volume and cardiac output were greater for the control group. Mean arterial pressure for the control group was less than HDT but not HUT. Over the full 10-min period of OST, the mean arterial pressure was not different between groups. Heart rate increased to the same level for all three treatments. Stroke volume decreased across the full time period for control and HDT, but only at 3 and 9 min for HUT. There was a higher total peripheral resistance in the HDT group than control or HUT. The pre-ejection period to left ventricular ejection time ratio was less in HDT than for control or HUT groups. These data indicate a rapid adaptation of the cardiovascular system to 4 h HDT that appears to be inappropriate on reapplication of a head to foot gravity vector. We speculate that the cause of the impaired orthostatic tolerance is decreased tone in venous capacitance vessels so that venous return is inadequate.     

Postural cardiovascular reflexes: comparison of responses of forearm and calf resistance vessels

Simultaneous measurements were made of changes in vascular resistance in the forearm and calf in response to moving from supine to sitting or to head-down tilt. The subjects were healthy male volunteers, 21-63 yr. Blood flows were measured by venous occlusion plethysmography using mercury-in-Silastic strain-gauges. The gauges were maintained at the same level relative to the heart during the postural changes. Arterial blood pressure was measured by auscultation; heart rate was counted from the plethysmograms. Changing from supine to sitting caused a decrease in forearm blood flow from 4.13 +/- 0.14 to 2.16 +/- 0.19 ml.100 ml-1.min-1. Corresponding calf flows were 4.21 +/- 0.32 and 4.40 +/- 0.59 ml.100 ml-1.min-1. There was no change in mean arterial blood pressure, and heart rate increased by 8.0 +/- 1.5 beats/min. Arrest of the circulation of both legs with occlusion cuffs on the thighs before sitting, to prevent pooling of blood in them, reduced the degree of forearm vasoconstriction. Neck suction (40 Torr) during sitting, to oppose the decrease in transmural pressure at the carotid sinuses, inhibited the vasoconstriction. During a 30 degrees head-down tilt, there was a dilatation of forearm but not of calf resistance vessels. A Valsalva maneuver caused a similar constriction of both vascular beds. Thus, when changes in vascular resistance in forearm and calf are compared, the major reflex adjustments to changes in posture take place in the forearm.     

Cardiovascular responses to military antishock trouser inflation during standing arm exercise

Military antishock trousers (MAST) inflated to 50 mmHg were used with 12 healthy males (mean age 28 +/- 1 yr) to determine the effects of lower-body positive pressure on cardiac output (Q), stroke volume (SV), heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP), total peripheral resistance (TPR), and O2 uptake (VO2) during graded arm-cranking exercise. Subjects were studied while standing at rest and at 25, 50, and 75% of maximal arm-cranking VO2. At each level, rest or work was continued for 6 min with MAST inflated and for 6 min with MAST deflated. Order of inflation and deflation was alternated at each experimental rest or exercise level. Measurements were obtained during the last 2 min at each level. Repeated-measures analysis of variance revealed significant increases (P less than 0.001) in Q, SV, and MABP and a consistent decrease in HR with MAST inflation. There was no apparent change in Q/VO2 between inflated and control conditions. There was no effect of MAST inflation on VO2 or TPR. MAST inflation counteracts the gravitational effect of venous return in upright exercise, restoring central blood volume and thereby increasing Q and MABP from control. HR is decreased consequent to increased MABP through arterial baroreflexes. The associated decrease in TPR is not observed, being offset by the mechanical compression of leg vasculature with MAST inflation.     

Acute head-down tilt decreases the postexercise resting threshold for forearm cutaneous vasodilation.

The purpose of this study was to evaluate the role of baroreceptor control on the postexercise threshold for forearm cutaneous vasodilation. On four separate days, six subjects (1 woman) were randomly exposed to 65 degrees head-up tilt and to 15 degrees head-down tilt during a No-Exercise and Exercise treatment protocol. Under each condition, a whole body water-perfused suit was used to regulate mean skin temperature (T(sk)) in the following sequence: 1) cooling until the threshold for vasoconstriction was evident; 2) heating ( approximately 7.0 degrees C/h) until vasodilation occurred; and 3) cooling until esophageal temperature (T(es)) and (T(sk)) returned to baseline values. The Exercise treatment consisted of 15 min of cycling exercise at 70% maximal O(2) uptake, followed by 15 min of recovery in the head-up tilt position. The No-Exercise treatment consisted of 30 min resting in the head-up tilt position. After the treatment protocols, subjects were returned to their pretreatment condition, then cooled and warmed again consecutively. The calculated T(es) threshold for cutaneous vasodilation increased 0.24 degrees C postexercise during head-up tilt (P < 0.05), whereas no difference was measured during head-down tilt. In contrast, sequential measurements without exercise demonstrate a time-dependent decrease for head-up tilt (0.17 degrees C) and no difference for head-down tilt. Pretreatment thresholds were significantly lower during head-down tilt compared with head-up tilt. We have shown that manipulating postexercise venous pooling by means of head-down tilt, in an effort to reverse its impact on baroreceptor unloading, resulted in a relative lowering of the resting postexercise elevation in the T(es) for forearm cutaneous vasodilation.