Increased renal tubular sodium reabsorption during exercise-induced hypervolemia in humans

2001 ◽  
Vol 91 (3) ◽  
pp. 1229-1236 ◽  
Author(s):  
Kei Nagashima ◽  
Jauchia Wu ◽  
Stavros A. Kavouras ◽  
Gary W. Mack
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Tubular Reabsorption ◽  
Proximal Tubules ◽  
Plasma Volume Expansion ◽  
Saline Loading ◽  
Exercise Induced ◽  
Renal Tubular

We tested the hypothesis that renal tubular Na+ reabsorption increased during the first 24 h of exercise-induced plasma volume expansion. Renal function was assessed 1 day after no-exercise control (C) or intermittent cycle ergometer exercise (Ex, 85% of peak O2 uptake) for 2 h before and 3 h after saline loading (12.5 ml/kg over 30 min) in seven subjects. Ex reduced renal blood flow ( p-aminohippurate clearance) compared with C (0.83 ± 0.12 vs. 1.49 ± 0.24 l/min, P < 0.05) but did not influence glomerular filtration rates (97 ± 10 ml/min, inulin clearance). Fractional tubular reabsorption of Na+ in the proximal tubules was higher in Ex than in C ( P < 0.05). Saline loading decreased fractional tubular reabsorption of Na+ from 99.1 ± 0.1 to 98.7 ± 0.1% ( P < 0.05) in C but not in Ex (99.3 ± 0.1 to 99.4 ± 0.1%). Saline loading reduced plasma renin activity and plasma arginine vasopressin levels in C and Ex, although the magnitude of decrease was greater in C ( P < 0.05). These results indicate that, during the acute phase of exercise-induced plasma volume expansion, increased tubular Na+ reabsorption is directed primarily to the proximal tubules and is associated with a decrease in renal blood flow. In addition, saline infusion caused a smaller reduction in fluid-regulating hormones in Ex. The attenuated volume-regulatory response acts to preserve distal tubular Na+ reabsorption during saline infusion 24 h after exercise.

Mechanism for the posture-specific plasma volume increase after a single intense exercise protocol

1999 ◽  
Vol 86 (3) ◽  
pp. 867-873 ◽  
Author(s):  
Kei Nagashima ◽  
Gary W. Mack ◽  
Andrew Haskell ◽  
Takeshi Nishiyasu ◽  
Ethan R. Nadel
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Urine Volume ◽  
Peak Oxygen Consumption ◽  
Plasma Volume Expansion ◽  
Plasma Albumin ◽  
Postural Changes ◽  
Albumin Content ◽  
Exercise Induced

To test the hypothesis that exercise-induced hypervolemia is a posture-dependent process, we measured plasma volume, plasma albumin content, and renal function in seven healthy subjects for 22 h after single upright (Up) or supine (Sup) intense (85% peak oxygen consumption rate) exercise. This posture was maintained for 5 h after exercise. Plasma volume decreased during exercise but returned to control levels by 5 h of recovery in both postures. By 22 h of recovery, plasma volume increased 2.4 ± 0.8 ml/kg in Up but decreased 2.1 ± 0.8 ml/kg in Sup. The plasma volume expansion in Up was accompanied by an increase in plasma albumin content (0.11 ± 0.04 g/kg; P < 0.05). Plasma albumin content was unchanged in Sup. Urine volume and sodium clearance were lower in Up than Sup ( P < 0.05) by 5 h of recovery. These data suggest that increased plasma albumin content contributes to the acute phase of exercise-induced hypervolemia. More importantly, the mechanism by which exercise influences the distribution of albumin between extra- and intravascular stores after exercise is altered by posture and is unknown. We speculate that factors associated with postural changes (e.g., central venous pressure) modify the increase in plasma albumin content and the plasma volume expansion after exercise.

Hemodynamics and interstitial fluid pressure in the rat tail

1984 ◽  
Vol 247 (1) ◽  
pp. H80-H87 ◽  
Author(s):  
K. Aukland ◽  
H. Wiig
Keyword(s):  
Blood Flow ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Interstitial Fluid ◽  
Cuff Pressure ◽  
Subcutaneous Tissue ◽  
Fluid Pressure ◽  
Interstitial Fluid Pressure ◽  
Venous Stasis ◽  
Plasma Volume Expansion

Blood flow in the rat was measured during pentobarbital anesthesia by plethysmographic and thermometric techniques. Tail arterial and venous pressures (Pa and Pv) were measured by glass micropipettes and interstitial fluid pressure (PIF) by wick-in-needle technique. Large pressure gradients were measured along the tail, Pa decreasing and Pv increasing toward the tip. In the vasoconstricted tail, distal arterial and venous pressures (Pad and Pvd, respectively, 10 cm from the tail root) were 55 and 11% of aortic pressure (PA), while PIF was 0-2 mmHg. Plasma volume expansion increased blood flow by a factor of 10 to 35. Pad rose to 74% and Pvd to 20% of PA. PIF increased to 15 mmHg, in parallel with Pv. Venous stasis (cuff pressure 14.7 mmHg) increased PIF and Pv by 3.5 and 9 mmHg, respectively, while tail volume increased by 0.4 to 1.2%. In conclusion, the large flow increase induced by plasma volume expansion depends strongly on dilation of the tail artery, with two- to threefold increase in internal radius. Simultaneously the tail veins relax and expand. Subcutaneous tissue is compressed between the expanding vessels and the tight skin, and PIF increases almost sufficiently to prevent a rise in net capillary filtration pressure. This immediate edema-preventing mechanism is less efficient during venous stasis, which presumably does not induce "active" dilation of the tail vessels. Similar mechanisms probably exist in other "encapsulated" tissues.

Operation Everest III: role of plasma volume expansion onV˙o2 max during prolonged high-altitude exposure

2000 ◽  
Vol 89 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Paul Robach ◽  
Michèle Déchaux ◽  
Sébastien Jarrot ◽  
Jenny Vaysse ◽  
Jean-Christophe Schneider ◽  
...  
Keyword(s):  
High Altitude ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Plasma Renin ◽  
Plasma Volume Expansion ◽  
Exercise Induced ◽  
Male Subjects ◽  
Increased Activity ◽  
Volume Decrease

We hypothesize that plasma volume decrease (ΔPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O2 uptake (V˙o2 max) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219–292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6,000 m after 10–12 days) and after return to SL (RSL, 1–3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% ( P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced ΔPV was reduced both by PVX and HA ( P < 0.05). Compared with SL, V˙o2 max was decreased by 58 and 11% at HA and RSL, respectively.V˙o2 max was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the moreV˙o2 max was improved by PVX ( P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation ofV˙o2 max during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery ofV˙o2 max.

Effect of acute plasma volume expansion on peripheral arteriolar tone in healthy subjects

1992 ◽  
Vol 83 (5) ◽  
pp. 541-547 ◽  
Author(s):  
Alison Calver ◽  
Joe Collier ◽  
Daniel Green ◽  
Patrick Vallance
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Plasma Volume ◽  
Healthy Subjects ◽  
Volume Expansion ◽  
Forearm Blood Flow ◽  
Plasma Volume Expansion ◽  
Arterial Infusion ◽  
Vasodilator Response ◽  
Flow Response

1. Using venous occlusion plethysmography, we have investigated the forearm blood flow response in healthy subjects to the acute plasma volume expansion caused by a rapid intravenous infusion of saline. The contribution made to this response by nitric oxide has been investigated using local intra-arterial infusions of the nitric oxide synthase inhibitor NG-monomethyl-l-arginine. 2. The infusion of 1000 ml of saline over 25 min caused plasma volume to increase by about 7%, and resulted in a rise in forearm blood flow, with no change in arterial blood pressure. The onset of the blood flow response occurred within 10 min and blood flow remained elevated above baseline 20 mm after the end of the saline infusion. 3. Local intra-arterial infusion of NG-monomethyl-l-arginine alone caused a reduction in forearm blood flow which was maximal at the end of the infusion and gradually recovered to baseline levels over 40 min. 4. When local intra-arterial infusion of NG-monomethyl-l-arginine was followed by plasma volume expansion, the calculated effect of NG-monomethyl-l-arginine was such as to abolish the vasodilator response to saline. 5. The effect of local intra-arterial infusion of NG-monomethyl-l-arginine on forearm blood flow was greater when the drug was given after volume expansion had occurred, than when it was given before the administration of saline. However, in control experiments the vasoconstrictor response to noradrenaline was also enhanced after the administration of the volume load in comparison with the response to noradrenaline given alone. 6. These results are consistent with the possibility that increased local synthesis of nitric oxide contributes to the vasodilator response to volume expansion.

Effect of volume expansion on papillary blood flow and sodium excretion

1991 ◽  
Vol 260 (6) ◽  
pp. F813-F822 ◽  
Author(s):  
F. J. Fenoy ◽  
R. J. Roman
Keyword(s):  
Blood Flow ◽  
Laser Doppler Flowmetry ◽  
Plasma Volume ◽  
Intravenous Infusion ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Oncotic Pressure ◽  
Plasma Volume Expansion ◽  
Doppler Flowmetry ◽  
Vasa Recta

The present study examined whether changes in plasma oncotic pressure or hematocrit play a role in the redistribution of renal blood flow and the natriuretic response to extracellular fluid volume (ECFV) expansion with saline. Intravenous infusion of saline produced a 46% increase in the flow of red blood cells (RBCs) in the papilla of Inactin-anesthetized euvolemic Munich-Wistar rats (n = 6). This was primarily due to an increase in the number of functional capillaries perfused with moving RBCs, as indicated both by laser-Doppler flowmetry and videomicroscopy. The velocity of RBCs in ascending or descending vasa recta was not significantly altered by the infusion of saline. Plasma volume expansion with a 6% solution of albumin (n = 6) did not increase papillary RBC flow, whereas volume expansion with whole blood produced a 17% increase in the flow of RBCs in the papilla. Sodium excretion after ECFV expansion with saline (n = 6) was greater than that seen after plasma volume expansion with a 6% solution of albumin (n = 5). The results indicate that the rise in papillary RBC flow after ECFV expansion with saline is due to an increase in the number of perfused vasa recta capillaries. The failure of plasma volume expansion to alter papillary RBC flow suggests that changes in plasma oncotic pressure and/or renal interstitial pressure may signal the rise in papillary RBC flow after intravenous infusion of saline. The present study also indicates that laser-Doppler flowmetry is a useful technique to monitor changes in the flow, velocity, and concentration of moving RBCs in tissue.

Mechanism for inhibition of renin release by acute plasma volume expansion in the dog

1985 ◽  
Vol 248 (2) ◽  
pp. F206-F211 ◽  
Author(s):  
M. W. Roy ◽  
C. E. Ott ◽  
W. J. Welch ◽  
J. H. Downs ◽  
T. A. Kotchen
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Renin Secretion ◽  
Renin Release ◽  
Renal Nerves ◽  
Plasma Volume Expansion ◽  
Renal Nerve ◽  
Albumin Infusion ◽  
Renal Tubular

Plasma volume expansion alters renal tubular sodium chloride transport and renal nerve activity. The purpose of this study was to determine the mechanism(s) for inhibition of renin secretion by acute volume expansion with albumin in the anesthetized dog. In dogs with a single intact kidney, albumin infusion decreased renin release by 86% and significantly increased renal blood flow, glomerular filtration rate, and sodium excretion. Albumin volume expansion inhibited renin secretion to a lesser extent in dogs with denervated filtering kidneys and in dogs with innervated nonfiltering kidneys. In dogs with denervated nonfiltering kidneys, albumin infusion did not change renin secretion. Comparable volume expansion was produced in all groups. Thus, inhibition of renin release by acute plasma volume expansion is dependent on both a renal tubular mechanism and the integrity of the renal nerves. Partial inhibition of renin release was observed with interruption of either one of the mechanisms, whereas interruption of both mechanisms totally abolished the effect of acute plasma volume expansion on renin secretion.

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