Skip to main content
NCBI home page
The Journal of Physiology logoLink to The Journal of Physiology
. 1999 Sep 1;519(Pt 2):623–628. doi: 10.1111/j.1469-7793.1999.0623m.x

Contribution of the leg vasculature to hypotensive effects of an antiorthostatic posture change in humans

Bettina Pump 1, Morten Schou 1, Anders Gabrielsen 1, Peter Norsk 1
PMCID: PMC2269521  PMID: 10457077

Abstract

  1. Previous results from our laboratory have shown that vasodilatation in the legs prevents mean arterial pressure (MAP) from increasing during water immersion. Therefore, we tested the hypothesis that vasodilatation in the legs is necessary for the hypotensive effects to occur during a moderate antiorthostatic posture change.

  2. Ten healthy males underwent a 5 min posture change from upright seated to horizontal supine (SUP) and back to seated again with (OCCL-SUP) and without simultaneous total arterial (154 ± 1 mmHg) thigh occlusion, and a control seated period, also with and without arterial occlusion. Cardiac output (CO) was measured by a non-invasive foreign (N2O) gas rebreathing technique.

  3. MAP (brachial auscultation) decreased during SUP from 94 ± 3 to 84 ± 2 mmHg (P < 0.0001) and total peripheral vascular resistance (TPR = MAP/CO, n = 8) decreased by 15 ± 4 % (P < 0.001). During OCCL-SUP, MAP decreased from 98 ± 2 to 90 ± 2 mmHg (P < 0.005) and TPR decreased by 14 ± 3 % (P < 0.01).

  4. In conclusion, vasodilatation in the legs is not necessary for the decrease in MAP to occur during a moderate antiorthostatic manoeuvre. Therefore, vasodilatation in more central vascular beds (e.g. abdomen) can alone account for the hypotensive effects.

During a moderate antiorthostatic posture change in humans from seated to supine, mean arterial pressure (MAP) decreases (Pump et al. 1997). The mechanism for this involves cardiopulmonary low- and arterial high-pressure receptor stimulation, which induces peripheral vasodilatation and a decrease in heart rate (HR) (Rowell, 1993). That the muscle vascular bed is sensitive to changes in baroreceptor stimulation has been known for decades (Öberg, 1964). It is not known, however, which vascular beds are the most important for the vasodilatation that induces the decrease in MAP in humans.

During water immersion to the neck (another model that induces central volume expansion), MAP remains unchanged (Johansen et al. 1997). If, however, the blood supply to the legs is simultaneously occluded by thigh cuff inflation of 250 mmHg, MAP increases by 10-12 mmHg, compared with the effects of occlusion without immersion (Johansen et al. 1997). This observation suggests that vasodilatation in the vascular beds of the legs is pivotal for maintaining MAP unchanged during water immersion in humans.

Several investigators have previously used limb blood flow as a reflection of change in peripheral vascular resistance during posture changes in humans (Skagen, 1983; Sander-Jensen et al. 1986; Kassis, 1989; Breit et al. 1993; Stout et al. 1995). The relative contribution of the vascular beds in the legs to the changes in total peripheral vascular resistance (TPR) and arterial pressures during ortho- and antiorthostatic manoeuvres in humans, however, is not known.

Because an intact vascular bed in the legs is important to keep MAP unchanged during water immersion, in this study we tested the hypothesis that the vascular beds of the legs are likewise a pivotal contributor to the decrease in MAP during a moderate antiorthostatic manoeuvre in humans. In order not to change the position of the legs, whereby local veno-arterial reflexes are stimulated, we used a model that we have described previously (Pump et al. 1997), where the legs are kept horizontal, while the upper body is tilted from upright vertical to horizontal.

METHODS

Ten male subjects (aged 25 ± 1 (s.e.m.) years (range, 22-30 years); height, 181 ± 1 cm (range, 174-188 cm); and weight, 79 ± 3 kg (range, 63-91 kg)) completed the experiment. Four additional subjects originally entered the study but did not complete the protocol because of the occurrence of vasovagal presyncopal symptoms (three subjects during a session with occlusion and one subject before the start of the experiment). Data from these four subjects are not presented. All were non-smokers, had a negative history of cardiovascular and kidney diseases and were healthy as indicated by the results of a questionnaire similar to that used for class 1 examination of professional pilots, a normal physical examination, arterial blood pressure (< 140/90 mmHg), electrocardiogram (unipolar), and urine tests (strips) for glucose, leucocytes, erythrocytes and protein. None of the subjects took any medication for at least 1 month prior to the study. Informed consent was obtained after the subjects had read a description of the experimental protocol, which was approved by the Ethics Committee of Copenhagen (KF 01-347/93) and was in compliance with the Declaration of Helsinki.

The subject fasted for 12 h before the experiment and reported at the laboratory at 08:00 h. He was weighed and thereafter placed in the seated position and instrumented with electrodes for HR determination and with cuffs around the right upper arm and left index finger for determination of arterial pressures. In addition, cuffs (20 cm × 88 cm) were placed around both thighs, as close to the genitofemoral region as possible, to induce arterial occlusion of the femoral arteries. The subject rested in the seated position for 30 min before the start of the experiment.

The experiment thereafter consisted of four sessions each lasting 15 min, two with and two without occlusion: (1) a control (SEAT) session for 15 min, in which the subject was seated with his trunk vertical with back and neck support and with the legs placed horizontally; (2) 5 min of being seated as described in (1), 5 min in the supine position, by tilting the trunk from vertical within 5 s (SUP), and then again 5 min of being seated; (3) 15 min of being seated as in (1) combined with arterial occlusion of the legs by thigh cuffs (OCCL-SEAT); and (4) posture changes similar to (2) but with simultaneous arterial occlusion of the legs during the 15 min (OCCL-SUP). The passive posture changes were performed by manually tilting the back support from vertical to horizontal. The sessions were separated by 30 min of the subject being seated, and performed in a balanced, randomized sequence order between subjects.

The subjects wore the thigh cuffs throughout the experiment, but they were only inflated during OCCL-SEAT and OCCL-SUP. The cuffs were inflated within 30 s, immediately before the start of the OCCL sessions, and the cuff pressure was adjusted so that it was 10 mmHg higher than systolic arterial pressure at heart level plus the pressure corresponding to the hydrostatic pressure difference between mid-heart and mid-thigh level (mean cuff pressure = 154 ± 1 mmHg). The subjects reported minor discomfort during OCCL, in the form of a tingling sensation in the legs, but no pain. The discomfort was similar during OCCL-SEAT and OCCL-SUP.

Systolic (SAP) and diastolic (DAP) arterial pressures were measured in the brachial artery (auscultation) and MAP was calculated from DAP + 1/3 arterial pulse pressure.

Left atrial diameter was measured by echocardiography (Aloka SSD 500, Simonsen & Weel) as described previously (Pump et al. 1997) during end-expiration, as an average of measurements from three M-mode pictures obtained from: (1) the parasternal long axis view (LAD) and (2) a 2-dimensional (2-D) apical four-chamber view (LADa). The 2-D measurements were obtained immediately before opening of the mitral valves, as determined from the video recordings. All the measurements were performed blind.

HR and mean arterial pressure in an index finger (MAPp, photoplethysmography; 2300 Finapres, Ohmeda) were measured continuously as described previously (Pump et al. 1997).

At the end of each 5 min period and after completion of the previously described measurements, cardiac output (CO) was measured in eight of the subjects by a rebreathing method, as described in detail previously (Bonde-Petersen et al. 1980; Clemensen et al. 1994) with a gas mixture of 1 % SF6, 5 % N2O and 50 % O2 in N2 and a gas volume of 30 % of the calculated vital capacity (Berglund et al. 1963). TPR and stroke volume (SV) were calculated from MAPp/CO and CO/HR, respectively, using MAPp and HR values during the rebreathing manoeuvres. Room temperature was kept between 24.0 and 26.6°C and humidity between 38 and 66 %.

Results are given as means ±s.e.m. An analysis of variance (ANOVA; Statgraphics plus for Windows, version 3.0; Manugistics Inc.) for repeated measures, with the variable as main variate and time and subject as factors, was used to evaluate the effects on a variable over time within each series of experiments. Differences between values of the initial 5 min and those of the subsequent intervals during each series of experiments were evaluated by a post hoc multiple range test (Newman-Keuls). Student's paired t test was used to detect whether means differed at similar points in time, comparing values of corresponding series (SEAT vs. SUP and OCCL-SEAT vs. OCCL-SUP). P < 0.05 was chosen as the level of significance.

RESULTS

During SUP and OCCL-SUP, MAP decreased similarly from 94 ± 3 to 84 ± 2 mmHg (P < 0.0001) and from 98 ± 2 to 90 ± 2 mmHg, respectively (P < 0.005; Fig. 1). MAP did not change significantly during SEAT, whereas it increased during OCCL-SEAT from 98 ± 3 to 101 ± 2 mmHg (P < 0.01; Fig. 1). Systolic and diastolic arterial pressures are depicted in Table 1.

Figure 1.

Figure 1

Open in a new tab

Mean arterial pressure (MAP; top) and total peripheral vascular resistance (TPR; bottom) during SUP (5 min in the seated position, 5 min supine, and 5 min in seated position again; filled symbols) and SEAT (15 min of seated control; open symbols). Left panels depict sessions without and right panels sessions with arterial thigh occlusion (OCCL) during the whole 15 min experimental period. Values are means ±s.e.m.; n = 10 for MAP and n = 8 for TPR. * Significant difference compared with values of initial 5 min in the seated position (P < 0.05 or less, see text). † Significant difference compared with value at the same experimental point in time of the other session (P < 0.05).

Table 1.

Arterial variables and left atrial diameters during SUP, SEAT, OCCL-SUP and OCCL-SEAT

Supine
1.0 min 2.5 min 5 min 6.0 min 7.5 min 10 min 11.0 min 12.5 min 15 min
SAP (mmHg)
 SUP — 119 ± 4 120 ± 4 — 114 ± 3*† 114 ± 3*† — 118 ± 3 118 ± 4
 SEAT — 120 ± 3 120 ± 4 — 119 ± 3 120 ± 3 — 118 ± 3 118 ± 3
 OCCL-SUP — 122 ± 3 122 ± 3 — 117 ± 3*‡ 116 ± 3*‡ — 124 ± 3 124 ± 3
 OCCL-SEAT — 125 ± 5 124 ± 5 — 126 ± 5 126 ± 5 — 27 ± 5 127 ± 4
DAP (mmHg)
 SUP — 79 ± 2 81 ± 2 — 69 ± 2*† 70 ± 1*† — 78 ± 3 79 ± 2
 SEAT — 78 ± 1 78 ± 2 — 77 ± 2 78 ± 2 — 78 ± 2 79 ± 2
 OCCL-SUP — 83 ± 2 86 ± 2 — 76 ± 2*‡ 78 ± 2*‡ — 87 ± 2 88 ± 2
 OCCL-SEAT — 85 ± 2 85 ± 2 — 87 ± 2 89 ± 2* — 88 ± 3* 89 ± 2*
HR (beats min−1)
 SUP 58 ± 3 58 ± 3 60 ± 3 54 ± 3*† 53 ± 2*† 53 ± 2*† 58 ± 3 58 ± 3 58 ± 3
 SEAT 60 ± 3 62 ± 3 61 ± 3 62 ± 3 59 ± 3 60 ± 3 63 ± 3 60 ± 3 60 ± 3
 OCCL-SUP 57 ± 3 59 ± 3 64 ± 3 60 ± 3‡ 60 ± 3‡ 61 ± 3‡ 71 ± 3* 72 ± 2* 74 ± 3*
 OCCL-SEAT 57 ± 3 57 ± 3 62 ± 4 67 ± 3* 69 ± 3* 71 ± 4* 71 ± 3* 71 ± 3* 72 ± 3*
CO (l min−1)
 SUP — — 5.9 ± 0.4 — — 6.3 ± 0.4† — — 5.2 ± 0.3*
 SEAT — — 6.0 ± 0.3 — — 5.6 ± 0.3* — — 5.2 ± 0.3*
 OCCL-SUP — — 5.6 ± 0.4 — — 5.4 ± 0.4 — — 4.9 ± 0.3*
 OCCL-SEAT — — 5.9 ± 0.3 — — 5.2 ± 0.3* — — 4.8 ± 0.3*
SV (ml)
 SUP — — 95 ± 8 — — 112 ± 8*† — — 86 ± 6
 SEAT — — 94 ± 5 — — 90 ± 4 — — 84 ± 6*
 OCCL-SUP — — 81 ± 6 — — 85 ± 6 — — 67 ± 4*
 OCCL-SEAT — — 88 ± 7 — — 75 ± 6* — — 67 ± 5*
LAD (mm)
 SUP — 31 ± 1 30 ± 1 — 34 ± 1*† 33 ± 1*† — 30 ± 1 31 ± 1
 SEAT — 30 ± 1 31 ± 1 — 31 ± 1 31 ± 1 — 31 ± 1 30 ± 1
 OCCL-SUP — 31 ± 1 30 ± 1 — 32 ± 1‡ 32 ± 1‡ — 29 ± 1 29 ± 1
 OCCL-SEAT — 31 ± 1 31 ± 1 — 30 ± 1* 29 ± 1* — 29 ± 1* 29 ± 1*
Open in a new tab

SUP, a posture change from seated to supine and back to seated; SEAT, 15 min of being seated; OCCL-SUP, a posture change as in SUP, but with simultaneous arterial occlusion of the legs by thigh cuffs; OCCL-SEAT, 15 min of being seated, but with simultaneous arterial occlusion of the legs by thigh cuffs. SAP, systolic arterial pressure; DAP, diastolic arterial pressure; HR, heart rate; CO, cardiac output; SV, stroke volume; LAD, left atrial diameter. Values are means ±s.e.m.; n = 10, except for CO and SV where n = 8.

*

*Significant difference (P < 0.05 or less, see text) compared with initial 5 min.

†

Significant difference (P < 0.05) compared with value at same experimental point in time of SEAT.

‡

Significant difference (P < 0.05) compared with value at same experimental point in time of OCCL-SEAT.

Peripheral MAP (MAPp) exhibited a pattern very similar to that of MAP, with a decrease during SUP from 91 ± 3 to 80 ± 2 mmHg and during OCCL-SUP from 101 ± 3 to 87 ± 2 mmHg (P < 0.0001). MAPp did not change significantly during SEAT and OCCL-SEAT, varying between 93 ± 4 and 97 ± 5 mmHg and between 100 ± 3 and 105 ± 5 mmHg, respectively.

CO decreased significantly throughout SEAT and OCCL-SEAT from 6.0 ± 0.3 to 5.2 ± 0.3 l min−1 and from 5.9 ± 0.3 to 4.8 ± 0.3 l min−1, respectively (P < 0.005; Table 1). During SUP and OCCL-SUP, CO did not change significantly, but a decrease was observed in the 5 min period after SUP (P < 0.05; Table 1). Values during SEAT and SUP differed significantly (Table 1). SV increased during SUP from 95 ± 8 to 112 ± 8 ml (P < 0.005), whereas it was unchanged during OCCL-SUP (Table 1).

During SUP and OCCL-SUP, respectively, TPR decreased by 15 ± 4 %, from 0.94 ± 0.05 to 0.79 ± 0.05 mmHg s ml−1 (P < 0.001), and by 14 ± 3 %, from 1.15 ± 0.10 to 0.98 ± 0.07 mmHg s ml−1 (P < 0.01; Fig. 1). TPR increased during SEAT and OCCL-SEAT, from 0.95 ± 0.08 to 1.09 ± 0.08 mmHg s ml−1 and from 1.06 ± 0.09 to 1.30 ± 0.09 mmHg s ml−1, respectively (P < 0.05).

HR decreased promptly during SUP from 60 ± 3 beats min−1 to a nadir of 53 ± 2 beats min−1 (P < 0.01; Table 1). During OCCL-SEAT, HR increased, and during OCCL-SUP it was unchanged, but an increase was observed in the 5 min period after OCCL-SUP (Table 1).

During SUP, LAD increased from 31 ± 1 mm to a maximum of 34 ± 1 mm (P < 0.0001) and then returned to the initial level (Table 1). During SEAT, no significant changes in LAD occurred. During OCCL-SUP, LAD did not increase significantly, but the values were significantly above those during OCCL-SEAT (P < 0.05; Table 1). The differences between values of SUP and SEAT at similar points in time, however, were very similar to those between OCCL-SEAT and OCCL-SUP. Left atrial diameter measured from an apical view (LADa) exhibited a pattern very similar to that of LAD with an increase during SUP from 32 ± 2 to 36 ± 2 mm (P < 0.0001) and during OCCL-SUP from 33 ± 2 to 35 ± 2 mm (P < 0.05). During SEAT and OCCL-SEAT, there were no significant changes in LADa. Therefore, since the increase in LAD was similar in two different planes, it was probably not caused by a geometrical artefact.

DISCUSSION

The results of this study show that intact vascular beds of the legs are not pivotal for hypotensive effects to occur during a moderate antiorthostatic manoeuvre in humans. When the vascular beds of the legs are separated from the central circulation by arterial occlusion, the decreases in MAP and TPR during a posture change from upright seated to supine are very similar to those during a posture change without occlusion. This is in contrast to the effects of water immersion, where vasodilatation in the legs is necessary to prevent MAP from increasing (Johansen et al. 1997).

We have observed previously that during a posture change from SEAT to SUP, with a subsequent stimulation of arterial high- and cardiopulmonary low-pressure receptors, MAP decreases (Pump et al. 1997). Since the splanchnic region accounts for some 30 %, and skin and muscles for some 40 %, of the increase in TPR during orthostasis (Rowell, 1993), we expected that dilatation in both of these vascular beds would be pivotal to inducing a decrease in MAP during a moderate antiorthostatic posture change. In the present study, however, MAP and TPR decreased similarly with and without arterial occlusion of the legs. Thus, excluding the vascular bed of the legs by arterial occlusion did not attenuate the hypotensive response to the antiorthostatic manoeuvre.

Thus, vasodilatation in regions other than the legs (e.g. the abdomen) apparently compensates for the lack of effects of vasodilatation in the occluded legs during the posture change. Therefore, investigations on changes in peripheral vascular resistances and peripheral cardiovascular reflexes during ortho- and antiorthostatic manoeuvres in humans should consider changes in the vascular resistances in more central regions than those of the limbs.

During an antiorthostatic posture change, carotid baroreceptors and low-pressure receptors are stimulated simultaneously (but to different degrees) whether occlusion is applied or not. During seated water immersion, low-pressure receptors are clearly stimulated, whereas, due to maintenance of the hydrostatic gradient from head to heart and an unchanged MAP (Epstein, 1992; Johansen et al. 1997), carotid baroreceptors are only slightly, or not at all, stimulated. The discrepant effects on MAP of occlusion during water immersion (an increase; Johansen et al. 1997) and of OCCL-SUP (a decrease) can therefore theoretically be explained by this difference in carotid baroreceptor stimulation. Therefore, on comparing the results obtained from our previous water immersion study (Johansen et al. 1997) with those of the present study, stimulation of carotid baroreceptors appears to be important for vasodilatation in the more central regions. Other investigators using other approaches have reached a similar conclusion (Abboud et al. 1979).

During occlusion without the posture change (OCCL-SEAT) we, like others, observed an increase in HR, MAP and TPR over time (Korner, 1952; Stegemann, 1963; Bonde-Petersen et al. 1978). This increase could theoretically have been due to either stimulation of chemoreflexes in the legs or to discomfort. That it could have been caused by an incomplete arterial occlusion is unlikely, because the cuff pressure was 10 mmHg higher than the systolic arterial pressure at mid-thigh level. The discomfort and stimulation of chemoreflexes must in any case have been similar during OCCL-SEAT and OCCL-SUP. Therefore, the effects of excluding the vascular bed of the legs from the circulation in the seated and supine position, respectively, are comparable, even if the thigh cuffs caused the mentioned side effects. Despite an apparently increased sympathetic nervous activity with a subsequent increased MAP and TPR during occlusion, the decreases in these variables during the antiorthostatic posture change were similar when compared with those without occlusion. This observation indicates that the effects of even a moderate antiorthostatic manoeuvre can override the effects of an otherwise induced increase in sympathetic nervous activity.

Several investigators have measured vascular resistance in skin and muscle in the limbs during upright tilting (Skagen, 1983; Sander-Jensen et al. 1986; Kassis, 1989; Breit et al. 1993). The present results suggest, however, that changes in limb vascular resistances are not always representative of changes in TPR. Because TPR is an important variable in understanding the regulation of arterial pressures and heart function in health and disease, future investigations should focus more on CO and MAP than on local muscle and skin blood flows.

Possible limitations in interpreting the results

In this study we did not measure central venous pressure. Therefore, since central venous pressure in the seated position is a few millimetres of mercury below that in the supine position (Foldager et al. 1996), the differences in TPR between SEAT and SUP, and between OCCL-SEAT and OCCL-SUP, were underestimated by a few per cent. The underestimation of the decrease in TPR was probably very similar on comparing values of SUP with those of OCCL-SUP. Therefore, we believe it is unlikely that had central venous pressure been measured, it would have changed the conclusion of this study.

Furthermore, it cannot be excluded totally that factors other than altered baroreceptor stimulation modulated the arterial pressures. An altered wave reflection within the arterial tree due to the bending of the vasculature at groin level in the seated position might theoretically have contributed to the decrease in MAP during the antiorthostatic posture change. This notion, however, needs further investigation.

In conclusion, an intact vascular bed of the legs is not pivotal for hypotensive effects to occur during a moderate antiorthostatic manoeuvre in humans. Because the decreases in MAP and TPR during the posture change were very similar with and without arterial thigh occlusion, we suggest that, for the hypotensive effects to occur, vasodilatation in the more central vascular beds (e.g. abdomen) is more important than in those of the legs. This should be taken into account in future studies on peripheral vascular resistances and heart function in health and disease.

Acknowledgments

This study was supported by grant no. 9602455 from the Danish Research Council.

References

  1. Abboud FM, Eckberg DL, Johannsen UJ, Mark AL. Carotid and cardiopulmonary baroreceptor control of splanchnic and forearm vascular resistance during venous pooling in man. The Journal of Physiology. 1979;286:173–184. doi: 10.1113/jphysiol.1979.sp012612. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Berglund E, Birath G, Bjure J, Grimby G, Kjellmer I, Sandqvist L, Söderholm B. Spirometric studies in normal subjects. I. Forced expirograms in subjects between 7 and 70 years of age. Acta Medica Scandinavica. 1963;173:185–191. fasc.2. [PubMed] [Google Scholar]
  3. Bonde-Petersen F, Norsk P, Suzuki Y. A comparison between freon and acetylene rebreathing for measuring cardiac output. Aviation Space and Environmental Medicine. 1980;51:1214–1221. [PubMed] [Google Scholar]
  4. Bonde-Petersen F, Rowell LB, Murray RG, Blomqvist GG, White R, Karlsson E, Campbell W, Mitchell JH. Role of cardiac output in the pressure responses to graded muscle ischemia in man. Journal of Applied Physiology. 1978;45:574–580. doi: 10.1152/jappl.1978.45.4.574. [DOI] [PubMed] [Google Scholar]
  5. Breit GA, Watenpaugh DE, Ballard RE, Hargens AR. Acute cutaneous microvascular flow responses to whole-body tilting in humans. Microvasular Research. 1993;46:351–358. doi: 10.1006/mvre.1993.1058. [DOI] [PubMed] [Google Scholar]
  6. Clemensen P, Christensen P, Norsk P, Grønlund J. A modified photo- and magnetoacoustic multigas analyzer applied in gas exchange measurements. Journal of Applied Physiology. 1994;76:2832–2839. doi: 10.1152/jappl.1994.76.6.2832. [DOI] [PubMed] [Google Scholar]
  7. Epstein M. Renal effects of head-out water immersion in humans: a 15-year update. Physiological Reviews. 1992;72:563–621. doi: 10.1152/physrev.1992.72.3.563. [DOI] [PubMed] [Google Scholar]
  8. Foldager N, Andersen TAE, Jessen FB, Ellegaard P, Stadeager C, Videbæk R, Norsk P. Central venous pressure in humans during microgravity. Journal of Applied Physiology. 1996;81:408–412. doi: 10.1152/jappl.1996.81.1.408. [DOI] [PubMed] [Google Scholar]
  9. Johansen LB, Jensen TUS, Pump B, Norsk P. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. Journal of Applied Physiology. 1997;83:695–699. doi: 10.1152/jappl.1997.83.3.695. [DOI] [PubMed] [Google Scholar]
  10. Kassis E. Baroreflex control of the circulation in patients with congestive heart failure. Danish Medical Bulletin. 1989;36:195–211. [PubMed] [Google Scholar]
  11. Korner PI. Reflex regulation of post-exercise blood pressure. Australian Journal of Experimental Biology and Medical Science. 1952;30:385–394. [PubMed] [Google Scholar]
  12. Öberg B. Effects of cardiovascular reflexes on net capillary fluid transfer. Acta Physiologica Scandinavica. 1964;62(suppl. 229):1–98. [PubMed] [Google Scholar]
  13. Pump B, Christensen NJ, Videbæk R, Warberg J, Hendriksen O, Norsk P. Left atrial distension and antiorthostatic decrease in arterial pressure and heart rate in humans. American Journal of Physiology. 1997;273:H2632–2638. doi: 10.1152/ajpheart.1997.273.6.H2632. [DOI] [PubMed] [Google Scholar]
  14. Rowell LB. Human Cardiovascular Control. New York: Oxford University Press; 1993. [Google Scholar]
  15. Sander-Jensen K, Secher NH, Astrup A, Christensen NJ, Giese J, Schwartz TW, Warberg J, Bie P. Hypotension induced by passive head-up tilt: endocrine and circulatory mechanisms. American Journal of Physiology. 1986;251:R742–748. doi: 10.1152/ajpregu.1986.251.4.R742. [DOI] [PubMed] [Google Scholar]
  16. Skagen K. Sympathetic reflex control of blood flow in human subcutaneous tissue during orthostatic maneuvres. Danish Medical Bulletin. 1983;30:229–241. [PubMed] [Google Scholar]
  17. Stegemann J. Zum Mechanismus der Pulsfrequenzeinstellung durch den Stoffwechsel. Pflügers Archiv. 1963;276:481–492. [Google Scholar]
  18. Stout S, Watenpaugh DE, Breit GA, Hargens AR. Simulated microgravity increases cutaneous blood flow in the head and leg of humans. Aviation Space and Environmental Medicine. 1995;66:872–875. [PubMed] [Google Scholar]

Articles from The Journal of Physiology are provided here courtesy of The Physiological Society

RESOURCES