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.

Effects of Long-term Nitric Oxide Synthesis Inhibition on Plasma Volume Expansion and Fetal Growth in the Pregnant Rat

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1019-1023 ◽  
Author(s):  
Sofía P. Salas ◽  
Fernando Altermatt ◽  
Mauricio Campos ◽  
Andrea Giacaman ◽  
Pedro Rosso
Keyword(s):  
Nitric Oxide ◽  
Fetal Growth ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Nitric Oxide Synthesis ◽  
Plasma Volume Expansion ◽  
Pregnant Rat ◽  
Synthesis Inhibition

scholarly journals Parathyroid Hormone's Acute Effect on Vasodilatory Function

2010 ◽  
Vol 3 ◽  
pp. CMED.S4650 ◽  
Author(s):  
P. Farahnak ◽  
L. Lind ◽  
K. Mattala ◽  
I-L. Nilsson
Keyword(s):  
Cardiovascular Disease ◽  
Blood Flow ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Acute Effect ◽  
Venous Occlusion ◽  
Arterial Infusion ◽  
Resistance Vessels ◽  
Vasodilatory Function ◽  
Pth Level

Parathyroid hormone (PTH) seems to affect the risk of cardiovascular disease. The aim of the present study was to investigate PTH's acute effect on endothelial vasodilatory function in forearm resistance vessels. Ten healthy subjects underwent forearm venous occlusion plethysmography. We measured forearm blood flow at baseline and at a stable, locally increased PTH level after intra-arterial infusion of metacholine and nitroprusside. The contralateral arm served as a control. Ionized calcium (Ca++) and PTH values were normal in all subjects at baseline (1.26 ± 0.02 mM/L, 3.6 ± 1.2 pM/L). After 30 minutes of PTH infusion, the PTH level increased in the active arm (13.8 ± 4.0 pM/L P < 0.01), while the Ca++ level was unchanged (1.25 ± 0.04; mM/L). Both the PTH and the Ca++ level in the contralateral arm remained unchanged, which indicates no systemic influence. The endothelial-dependent vasodilation was inversely correlated to the Ca++ level at baseline (r = −0.75, P < 0.05) and after PTH infusion (r = −0.68, P < 0.05). The vasodilatory function was not affected during PTH-infusion.

Endothelium-derived nitric oxide mediates hypoxic vasodilation of resistance vessels in humans

1996 ◽  
Vol 271 (3) ◽  
pp. H1182-H1185 ◽  
Author(s):  
M. L. Blitzer ◽  
S. D. Lee ◽  
M. A. Creager
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Vasodilator Response ◽  
Healthy Humans ◽  
Resistance Vessels ◽  
Oxide Synthase ◽  
Forearm Vascular Resistance

Endothelium-derived nitric oxide (EDNO) contributes to basal systemic vascular resistance under normoxic conditions. The purpose of this investigation was to determine whether EDNO contributes to the regulation of limb vascular resistance during hypoxia in healthy humans. Forearm blood flow was assessed by venous occlusion plethysmography. Hypoxia was induced by delivering a mixture of N2 and O2 via a gas blender adjusted to reduce the PO2 to 50 mmHg. During hypoxia, forearm blood flow increased from 2.4 +/- 0.2 to 3.0 +/- 0.3 ml.100 ml-1.min-1 (P < 0.001), and forearm vascular resistance decreased from 38 +/- 3 to 29 +/- 3 units (P < 0.001). The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 2,000 micrograms/min intra-arterially) was administered to eight subjects. The percent increase in forearm vascular resistance after administration of L-NMMA was greater during hypoxia than normoxia (67 +/- 14 vs. 39 +/- 15%, P < 0.05). L-NMMA reduced the forearm vasodilator response to hypoxia from 27 +/- 3 to 11 +/- 5% (P = 0.01). To exclude the possibility that this attenuated response to hypoxia was a consequence of vasoconstriction and not specific for nitric oxide synthase inhibition, six subjects received intra-arterial phenylephrine. Phenylephrine did not affect the vasodilator response to hypoxia (17 +/- 3 vs. 21 +/- 6%, P = NS). It is concluded that EDNO contributes to hypoxia-induced vasodilation in the forearm resistance vessels in healthy humans.

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.

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.

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.

Modification of forearm resistance vessels by exercise training in young men

1994 ◽  
Vol 77 (4) ◽  
pp. 1829-1833 ◽  
Author(s):  
D. J. Green ◽  
N. T. Cable ◽  
C. Fox ◽  
J. M. Rankin ◽  
R. R. Taylor
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Exercise Training ◽  
Training Program ◽  
Forearm Blood Flow ◽  
Intervention Period ◽  
Flow Response ◽  
Resistance Vessels ◽  
Human Forearm ◽  
Forearm Exercise

The aim of this study was to determine whether a 4-wk handgrip training program would elicit changes in endothelium-dependent and endothelium-independent vasodilatation in resistance vessels of the human forearm. Minimum vascular resistance after a 10-min ischemic stimulus, an index of peak vasodilator capacity, was also determined. Forearm blood flow response to the endothelium-dependent vasodilator methacholine chloride did not change over the 4-wk-intervention period either in the group undertaking training (n = 11) or in control subjects (n = 6). Similarly, the response to sodium nitroprusside was not influenced by the handgrip training program. Peak vasodilator capacity of the trained forearms significantly increased, whereas no change was evident in the untrained limbs. These results suggest that 4 wk of forearm exercise training enhances peak vasodilator capacity of the vasculature without influencing stimulated activity of the nitric oxide dilator system.

scholarly journals Increased susceptibility of db/db mice to rosiglitazone-induced plasma volume expansion: role of dysregulation of renal water transporters

2013 ◽  
Vol 305 (10) ◽  
pp. F1491-F1497 ◽  
Author(s):  
Li Zhou ◽  
Gang Liu ◽  
Zhanjun Jia ◽  
Kevin T. Yang ◽  
Ying Sun ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Underlying Mechanism ◽  
Fluid Retention ◽  
Receptor Subtype ◽  
Fluorescent Nanoparticles ◽  
Peroxisome Proliferator ◽  
Plasma Volume Expansion

Thiazolidinediones (TZDs), which are synthetic peroxisome proliferator-activated receptor subtype-γ (PPARγ), agonists are highly effective for treatment of type 2 diabetes. However, the side effect of fluid retention has significantly limited their application. Most of the previous studies addressing TZD-induced fluid retention employed healthy animals. The underlying mechanism of this phenomenon is still incompletely understood, particularly in the setting of disease state. The present study was undertaken to examine rosiglitazone (RGZ)-induced fluid retention in db/db mice and to further investigate the underlying mechanism. In response to RGZ treatment, db/db mice exhibited an accelerated plasma volume expansion as assessed by hematocrit (Hct) and fluorescent nanoparticles, in parallel with a greater increase in body weight, compared with lean controls. In response to RGZ-induced fluid retention, urinary Na+ excretion and urine volume were significantly increased in lean mice. In contrast, the natriuretic and diuretic responses were significantly blunted in db/db mice. RGZ db/db mice exhibited a parallel decrease in plasma Na+ concentration and plasma osmolality, contrasting to unchanged levels in lean controls. Imunoblotting analysis showed downregulation of renal aquaporin (AQP) 2 expression in response to RGZ treatment in lean mice but not in db/db mice. Renal AQP3 protein expression was unaffected by RGZ treatment in lean mice but was elevated in db/db mice. In contrast, the expression of Na+/H+ exchanger-3 (NHE3) and NKCC2 was unchanged in either mouse strain. Together these results suggest that compared with the lean controls, db/db mice exhibited accelerated plasma volume expansion that was in part due to the inappropriate response of renal water transporters.

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