Capillary permeability: atrial peptide action is independent of "protein effect"

1990 ◽  
Vol 259 (5) ◽  
pp. H1351-H1356 ◽  
Author(s):  
V. H. Huxley ◽  
D. J. Meyer
Keyword(s):  
Hydraulic Conductivity ◽  
Bovine Serum Albumin ◽  
Atrial Natriuretic Peptide ◽  
Rana Pipiens ◽  
Capillary Permeability ◽  
Barrier Properties ◽  
Effective Area ◽  
Small Rise ◽  
Mesenteric Microvessels ◽  
Exchange Vessel

Perfusion of exchange microvessels with the vasoactive hormone, atrial natriuretic peptide (AP), acutely and reversibly elevates hydraulic conductivity (Lp) by mechanisms that are, as yet, unknown. This, the first of two studies to characterize AP responses when perfusate composition was altered, specifically focuses on the action of AP when perfusate albumin was lowered to change the transcapillary barrier properties for water by passive mechanisms (protein effect). Perfusion of frog (Rana pipiens) mesenteric microvessels with 1 nM AP in 10 mg/ml bovine serum albumin (BSA) elevated Lp by a median 2.1-fold (range 1.2-2.7, n = 13) from control levels (10 mg/ml BSA). Reduction of perfusate albumin from 10 to 1 mg/ml elicited a small rise in Lp (1.8-fold, n = 10); Lp rose a further 2.1-fold (n = 6) when 1 nM AP was added to 1 mg/ml BSA. Likewise, protein-free perfusion elevated Lp from a median 2.2 to 5.1 X 10(-7) cm.s-1.cmH2O-1 (n = 11); 1 nM AP in protein-free perfusate elevated Lp a further 2.1-fold (n = 8). Thus, regardless of protein content, the response to the peptide was a consistent, twofold increase in exchange vessel Lp (n = 27). These data are consistent with the suggestion that the AP-activated rise in Lp (twofold) occurs via an increase in the effective area of the transcapillary pathway for water without influencing the selectivity properties of the paracellular, albumin-sensitive portion of the barrier.

Capillary permeability: an albumin component attenuates active changes in Lp

1990 ◽  
Vol 259 (5) ◽  
pp. H1357-H1364 ◽  
Author(s):  
V. H. Huxley ◽  
D. J. Meyer
Keyword(s):  
Hydraulic Conductivity ◽  
Bovine Serum Albumin ◽  
Atrial Natriuretic Peptide ◽  
Bovine Serum ◽  
Rana Pipiens ◽  
Capillary Permeability ◽  
Fold Increase ◽  
Vessel Permeability ◽  
Per Se ◽  
Exchange Vessel

The mechanisms whereby atrial natriuretic peptide (AP) acutely and reversibly elevates hydraulic conductivity (Lp) are not known. This is the second of two studies of the influence of perfusate albumin composition on AP alterations in capillary Lp. In this study, we investigated the effect of dialysis of the perfusate albumin. A 2.2-fold increase in frog (Rana pipiens) mesenteric microvessel Lp occurred when 100 nM AP was added to the control perfusate containing dialyzed, crystallized bovine serum albumin (DXL-BSA 10 mg/ml; n = 20). By contrast, Lp was unchanged by 100 nM AP in 10 mg/ml untreated, crystallized BSA (XL-BSA; n = 8). The response to AP was unaltered at DXL-BSA contents of 10, 20, or 30 mg/ml (2.4-, 2.2-, and 3.1-fold, respectively; n = 8). Dialysis of the albumin, per se, did not influence control Lp (LpXL-BSA/LpDXL-BSA = 1.0; n = 5). The receptor-independent nitrovasodilator, sodium nitroprusside (SNP; 1 microM) elevated Lp by 1.7-fold in DXL-BSA (n = 30). The response was abolished in XL-BSA (n = 8). We conclude that small hydrophilic albumin-associated substances antagonize AP- and SNP-induced elevations of exchange microvessel hydraulic conductance without interfering with albumin's role in the maintenance of normal exchange vessel permeability.

ANP increases capillary permeability to protein independent of perfusate protein composition

1995 ◽  
Vol 268 (3) ◽  
pp. H1139-H1148 ◽  
Author(s):  
M. K. McKay ◽  
V. H. Huxley
Keyword(s):  
Hydraulic Conductivity ◽  
Bovine Serum Albumin ◽  
Hormonal Regulation ◽  
Rana Pipiens ◽  
Capillary Permeability ◽  
Transport Coefficients ◽  
Protein Composition ◽  
Similar Magnitude ◽  
Capillary Barrier

In further studying hormonal regulation of microvascular exchange, we tested two hypotheses: 1) atrial natriuretic peptide (ANP) would increase capillary permeability to protein and 2) the actions of ANP on capillary permeability would be independent of the perfusate protein composition. These hypotheses were tested by assessing in situ capillary transport coefficients: hydraulic conductivity (Lp), apparent and diffusive permeabilities (Ps and Psd, respectively) to the protein alpha-lactalbumine, and convective coupling [Lp(1-sigma)] in mesenteric capillaries in cerebrally pithed frogs (Rana pipiens). The transport coefficients were determined in the absence and presence of frog ANP (fANP) during perfusion with either frog plasma or bovine serum albumin (BSA). Control Lp was 1.8-fold greater in vessels perfused with BSA compared with plasma. In the presence of 10 or 100 nM fANP, Lp was increased by approximately 3.5-fold in plasma-perfused vessels and approximately 2-fold in BSA-perfused vessels from their respective controls. Control Ps was 4.2-fold higher in vessels perfused with BSA compared with plasma. Despite the differences in control permeability, the increase in Ps by fANP was of similar magnitude (2- to 3-fold) for both protein perfusates. Analysis of the pressure-dependent alpha-lactalbumin flux suggested that the increase in capillary permeability induced by fANP is consistent with fANP increasing permeability without altering the selectivity of the capillary barrier.

Albumin modulation of capillary permeability: role of endothelial cell [Ca2+]i

1993 ◽  
Vol 265 (1) ◽  
pp. H74-H82 ◽  
Author(s):  
P. He ◽  
F. E. Curry
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Calcium Concentration ◽  
Capillary Permeability ◽  
Common Mechanism ◽  
Cytoplasmic Calcium ◽  
Adsorption Model ◽  
Endothelial Cell Surface ◽  
Mesenteric Microvessels

Albumin is required in vascular perfusates to maintain the normal permeability of microvessel walls. The most common mechanism proposed for action of albumin involves binding to the endothelial cell surface to increase the resistance to water and solute flows through hydraulic pathways across the capillary wall. The results of the present experiments do not conform to this simple adsorption model. Ringer perfusion increased the hydraulic conductivity (Lp) of the wall of single perfused frog mesenteric microvessels by 4.0 +/- 0.5-fold. The increase in Lp was associated with an increase of cytoplasmic calcium concentration ([Ca2+]i) from 59 +/- 5 nM when albumin was in the perfusate to a transient peak of 181 +/- 13 nM, 1–2 min after Ringer perfusion. [Ca2+]i then fell back to close to 100 nM. Processes that reduced Ca2+ influx into endothelial cells (removal of extracellular Ca2+, membrane depolarization) reduced Ca2+ influx and attenuated the increase in [Ca2+]i. The same processes abolished the increase in Lp after Ringer perfusion and restored Lp to close to control values during Ringer perfusion. Thus Ca2+ entry into endothelial cells is required to initiate and maintain the increased permeability during Ringer perfusion.

Effects of hyperoncotic albumin on endothelial barrier properties of rat lung

1993 ◽  
Vol 265 (1) ◽  
pp. H198-H204 ◽  
Author(s):  
R. L. Qiao ◽  
X. Ying ◽  
J. Bhattacharya
Keyword(s):  
Blood Flow ◽  
Hydraulic Conductivity ◽  
Barrier Properties ◽  
Rat Plasma ◽  
Endothelial Barrier ◽  
Rat Lung ◽  
Inflation Pressure ◽  
Sprague Dawley ◽  
Pentobarbital Sodium ◽  
Drop Technique

We have determined the effect of concentrated albumin on lung endothelial hydraulic conductivity (Lp) by our split-drop technique. We anesthetized 39 rats (2% halothane and pentobarbital sodium, 30 mg/kg ip; Sprague-Dawley, 500 g), then isolated and blood perfused their lungs. At constant inflation pressure (5 cmH2O) and stopped blood flow, we viewed subpleural venules (diameter, 20 microns) by microscopy and video. By micropuncture, we first microinfused a venule for 6 min with albumin that was either isoncotic (4 g/dl) or hyperoncotic (6 g/dl) with respect to rat plasma. In the same venule we then injected and split an oil drop with 4 g/dl albumin. From the rates of movement of the split oil drop at different vascular pressures, we determined Lp for 4 g/dl albumin. In venules that were previously microinfused for 6 min with 4 g/dl albumin, Lp for 4 g/dl albumin did not differ from that of noninfused controls (5.4 +/- 0.8 x 10(-7) ml.cm-2.s-1.cmH2O-1). However, after a similar microinfusion of 6 g/dl albumin, the Lp immediately increased more than two times above baseline (P < 0.01) but returned to baseline after 15 min. Lp for 4 g/dl albumin was not affected by hyperoncotic preinfusions of either neutral dextran or immunoglobulin G. We conclude that concentrated albumin caused a reversible increase of the lung endothelial barrier conductivity.

Role of endothelial Ca2+ stores in the regulation of hydraulic conductivity of Rana microvessels in vivo

2003 ◽  
Vol 284 (4) ◽  
pp. H1468-H1478 ◽  
Author(s):  
C. A. Glass ◽  
D. O. Bates
Keyword(s):  
Hydraulic Conductivity ◽  
Vascular Permeability ◽  
Store Depletion ◽  
Plasmic Reticulum ◽  
Permeability Increase ◽  
Mesenteric Microvessels ◽  
The Relationship ◽  
Serca Inhibition

Vascular permeability is regulated by endothelial cytosolic Ca2+concentration ([Ca2+]i). To determine whether vascular permeability is dependent on extracellular Ca2+influx or release of Ca2+ from stores, hydraulic conductivity ( L p) was measured in single perfused frog mesenteric microvessels in the presence and absence of Ca2+ influx and store depletion. Prevention of Ca2+ reuptake into stores by sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) inhibition increased L p in the absence of extracellular Ca2+ influx. L p was further increased when Ca2+ influx was restored. Depletion of the Ca2+ stores with ionomycin and SERCA inhibition increased L p in the presence and the absence of extracellular Ca2+ influx. However, store depletion in itself did not significantly increase L p in the absence of active Ca2+ release from stores into the cytoplasm. There was a significant positive correlation between baseline permeability and the magnitude of the responses to both Ca2+ store release and Ca2+ influx, indicating that the Ca2+ regulating properties of the endothelial cells may regulate the baseline L p. To investigate the role of Ca2+ stores in regulation of L p, the relationship between SERCA inhibition and store release was studied. The magnitude of the L p increase during SERCA inhibition significantly and inversely correlated with that during store release by Ca2+ ionophore, implying that the degree of store depletion regulates the size of the increase on L p. These data show that microvascular permeability in vivo can be increased by agents that release Ca2+ from stores in the absence of Ca2+ influx. They also show that capacitative Ca2+ entry results in increased L p and that the size of the permeability increase can be regulated by the degree of Ca2+ release.

VEGF and ATP act by different mechanisms to increase microvascular permeability and endothelial [Ca2+]i

2000 ◽  
Vol 279 (4) ◽  
pp. H1625-H1634 ◽  
Author(s):  
T. M. Pocock ◽  
B. Williams ◽  
F. E. Curry ◽  
D. O. Bates
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Hydraulic Conductivity ◽  
Vascular Endothelial ◽  
Store Depletion ◽  
Independent Mechanism ◽  
Intracellular Ca ◽  
Mesenteric Microvessels ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) increases hydraulic conductivity ( L p) by stimulating Ca2+ influx into endothelial cells. To determine whether VEGF-mediated Ca2+ influx is stimulated by release of Ca2+ from intracellular stores, we measured the effect of Ca2+ store depletion on VEGF-mediated increased L p and endothelial intracellular Ca2+ concentration ([Ca2+]i) of frog mesenteric microvessels. Inhibition of Ca2+ influx by perfusion with NiCl2 significantly attenuated VEGF-mediated increased [Ca2+]i. Depletion of Ca2+ stores by perfusion of vessels with thapsigargin did not affect the VEGF-mediated increased [Ca2+]i or the increase in L p. In contrast, ATP-mediated increases in both [Ca2+]i and L p were inhibited by thapsigargin perfusion, demonstrating that ATP stimulated store-mediated Ca2+ influx. VEGF also increased Mn2+ influx after perfusion with thapsigargin, whereas ATP did not. These data showed that VEGF increased [Ca2+]i and L p even when Ca2+ stores were depleted and under conditions that prevented ATP-mediated increases in [Ca2+]iand L p. This suggests that VEGF acts through a Ca2+ store-independent mechanism, whereas ATP acts through Ca2+ store-mediated Ca2+ influx.

Bradykinin-induced elevations of hydraulic conductivity display spatial and temporal variations in frog capillaries

1993 ◽  
Vol 264 (5) ◽  
pp. H1575-H1581 ◽  
Author(s):  
D. A. Williams ◽  
V. H. Huxley
Keyword(s):  
Hydraulic Conductivity ◽  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Bovine Serum ◽  
Water Flux ◽  
Temporal Variations ◽  
Time Dependent ◽  
Microvascular Networks ◽  
Microvascular Network

Bradykinin, a vasodilator, increases permeability to macromolecules in postcapillary venules. Recent studies indicate that vasodilators elevate water flux from frog mesenteric capillaries. Thus we hypothesized that bradykinin would also increase transcapillary water flux. Arteriolar (ac), true (tc), and venular (vc) capillaries were identified within the microvascular network of frog mesentery. Each capillary was cannulated in situ and perfused with control (frog Ringer and 10 mg/ml bovine serum albumin) and then bradykinin test (10(-7) M) solutions. Hydraulic conductivity (Lp) increased across the network (1.8, 5.3, and 11.0 x 10(-7) cm.s-1.cmH2O-1 for ac, tc, and vc, respectively). Bradykinin test Lp normalized to control (LpBKN/LPC) was elevated threefold (n = 37). Lp for ac (n = 12) was elevated 3.5-fold and oscillated with time. Lp for tc (n = 13) increased fivefold within the first 5 min of exposure and then dropped. Lp for vc (n = 12) was not different from control. Location- and time-dependent responses of Lp indicate that capillaries forming microvascular networks have individual responses to bradykinin.

Regulation of capillary hydraulic conductivity in response to an acute change in shear

2005 ◽  
Vol 289 (5) ◽  
pp. H2126-H2135 ◽  
Author(s):  
Min-ho Kim ◽  
Norman R. Harris ◽  
John M. Tarbell
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Hydraulic Conductivity ◽  
Flow Shear ◽  
Fluid Filtration ◽  
Acute Change ◽  
Acute Changes ◽  
Mesenteric Microvessels

The effects of mechanical perturbations (shear stress, pressure) on microvascular permeability primarily have been examined in micropipette-cannulated vessels or in endothelial monolayers in vitro. The objective of this study is to determine whether acute changes in blood flow shear stress might influence measurements of hydraulic conductivity ( Lp) in autoperfused microvessels in vivo. Rat mesenteric microvessels were observed via intravital microscopy. Occlusion of a third-order arteriole with a micropipette was used to divert and increase flow through a nonoccluded capillary or fourth-order arteriolar branch. Transvascular fluid filtration rate in the branching vessel was measured with a Landis technique. Flow (shear)-induced increases in Lp disappeared within 20–30 s of the removal of the shear and could be eliminated with nitric oxide synthase inhibition. The shear-induced increase in Lp was greater in capillaries compared with terminal arterioles. An acute change in shear may regulate Lp by a nitric oxide-dependent mechanism that displays heterogeneity within a microvascular network.

scholarly journals The role of atrial natriuretic peptide to attenuate inflammation in a mouse skin wound and individually perfused rat mesenteric microvessels

2016 ◽  
Vol 4 (18) ◽  
pp. e12968 ◽  
Author(s):  
Fitz-Roy E. Curry ◽  
Joyce F. Clark ◽  
Yanyan Jiang ◽  
Min-Ho Kim ◽  
Roger H. Adamson ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mouse Skin ◽  
Skin Wound ◽  
Mesenteric Microvessels ◽  
Atrial Natriuretic
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