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F E Curry

Publications and source records attributed to F E Curry.

At least 55 records · Page 3Linked to original sources
PubMed1994

Quantitative laser scanning confocal microscopy on single capillaries: permeability measurement.

OBJECTIVE: We tested the hypothesis that there is significant solute loss to the superfusate during microvessel solute permeability measurement in frog mesentery which leads to underestimation of permeability coefficient. This is the first application of laser-scanning confocal microscopy to measure microvessel permeability. METHODS: Microvessel permeability to sodium fluorescein (0.5 mg/ml, MW 376) was measured in the presence of bovine serum albumin (10 mg/ml) in Ringer's solution. Every 11-12s an optical section transverse to the vessel axis (x-z section) was collected. The images were corrected for fluorescence attenuation in the z direction and nonuniformity of light collection (shading) in the x direction by comparison to a fluorescent standard. Extravascular fluorescence, which increased linearly with time, and the step increase in fluorescence intensity of the vessel lumen were used to calculate an apparent permeability. Measurements were made first with the tissue superfused with Ringer and second after changing the superfusate to mineral oil in order to retain solute potentially lost to Ringer superfusate. RESULTS: The permeability to fluorescein measured with Ringer superfusate (5.0 +/- SD 2.6 x 10(-5) cm/s; n = 3) was not different from that measured with mineral oil covering the upper mesothelial surface (4.5 +/- 1.9). CONCLUSIONS: Therefore, the loss of sodium fluorescein through the upper mesothelium does not significantly alter permeability under these conditions. These techniques enable detailed analysis of solute concentration gradients surrounding microvessels.

Animals↗
PubMed1993

Differential action of plasma and albumin on transcapillary exchange of anionic solute.

We tested two hypotheses to account for the reduction in coupling of anionic solute to water flow (solvent drag) in microvessels during perfusion with plasma compared with albumin. Solvent drag is determined by both hydraulic conductivity (Lp) and solute reflection coefficient (sigma). Accordingly, decreased solvent drag during plasma perfusion must be the result of an increase in sigma (hypothesis 1) or reduction of Lp (hypothesis 2) or some combination of both mechanisms. These hypotheses were assessed by measuring Lp, sigma, and diffusive solute permeability (Psd) to the anionic protein alpha-lactalbumin in frog mesenteric exchange microvessels during plasma or albumin perfusion. The solute permeability coefficient to alpha-lactalbumin (Ps alpha-lactalbumin) was lower during exposure to plasma than bovine serum albumin (BSA) [(Ps alpha-lactalbumin)plasma/(Ps alpha-lactalbumin)BSA = 0.31 +/- 0.11 (means +/- SE, n = 9)]. Solute reflection coefficient to alpha-lactalbumin (sigma alpha-lactalbumin) was 0.69 +/- 0.02 in plasma and 0.34 +/- 0.03 in BSA (n = 7). Lp was not significantly influenced by perfusate protein composition (Lp plasma/Lp BSA = 1.02 +/- 0.11; n = 20). These data lead to the conclusion that the actions of plasma are to confer charge selectivity for anionic solute and, to a lesser extent, modify the porous pathways of the microvessel wall. Taken together, these results indicate that porous pathways contribute significantly to macromolecular flux in plasma-perfused vessels.

Animals↗
PubMed1993

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

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.

Animals↗
PubMed1993

Differential actions of cAMP on endothelial [Ca2+]i and permeability in microvessels exposed to ATP.

We investigated the hypothesis that one of the actions of adenosine 3',5'-cyclic monophosphate (cAMP) to attenuate agonist-induced increase in microvessel permeability is to reduce the initial increase in endothelial cell cytoplasmic Ca2+ concentration ([Ca2+]i). ATP (10 microM) was used to increase hydraulic conductivity (Lp) and [Ca2+]i in venular microvessel in frog mesentery. The cAMP analogue, 8-bromo-cAMP (8-BrcAMP, 2 mM) significantly attenuated the initial increase in Lp (from a peak increase of 7.1 +/- 2.4 times control with ATP alone to 1.2 +/- 0.34 times control with ATP and cAMP). In contrast, cAMP did not significantly change the magnitude or time course of the biphasic increase in [Ca2+]i, which increased from 54 +/- 5 nM to peak of 187 +/- 48 nM with ATP alone, and from 55 +/- 8 nM to 190 +/- 28 nM with ATP and cAMP. Thus the action of cAMP to attenuate microvessel permeability increase in the presence of ATP does not involve modification of the initial Ca2+ transient in endothelial cells. Our results enable alternative hypotheses, such as the suggestion that cAMP might modulate a Ca(2+)-calmodulin-dependent actin-myosin cascade, to be investigated without the added complications of having to account for the modulation of initial changes in [Ca2+]i. Our data also demonstrate, for the first time in the endothelial cells of intact microvessels, that an increase in [Ca2+]i is not always associated with an increase in microvessel permeability.

Adenosine Triphosphate↗
PubMed1992

A three-dimensional junction-pore-matrix model for capillary permeability.

A three-dimensional model is presented for the hydraulic conductivity and diffusive permeability of capillary endothelial clefts with a junctional strand with discrete pores and a fiber matrix in its wide parts. The model attempts to provide new insight into long-standing issues concerning the relative importance of open junction discontinuities, restricted slit regions, and matrix components in determining the permeability and selectivity of the capillary wall. The predictions drawn from the model are used to formulate new experiments to test two hypotheses concerning the molecular organization of the junction strand and the location of matrix structures in the wide part of the cleft. Using the three-dimensional theoretical approach recently developed by Tsay, Weinbaum, and Pfeffer (Chem. Eng. Comm. 82, 67-102, 1989), the model first explores the behavior of three different molecular models for the junctional strand discontinuities: (i) a more frequent circular pore of 5.5-nm radius formed by isolated missing junction proteins; (ii) a restricted rectangular slit of four to eight missing proteins and 8-nm gap height; and (iii) larger more infrequent breaks of four to eight missing proteins with a gap height of 22 nm, equal to the width of the wide part of the cleft. For the circular and 8-nm gap height pores the primary molecular sieve can be located at the level of the junction strand, whereas for the 22-nm gap height pores, matrix components must be present in at least some portion of the cleft to provide the molecular filter. The water flow through the cross-bridging fibers in the wide part of the cleft is described either by a new exact three-dimensional theory (Tsay and Weinbaum, J. Fluid Mech. 226, 125-148, 1991) for an ordered periodic array or by a new approximate theory for a random array of perpendicular fibers. Both this theory and the new approximate theory for diffusion presented herein take into account for the first time the interaction between the fibers and plasmalemma boundaries. The principal predictions of the model are that (i) infrequent larger breaks are most likely required to account for small solute permeability; (ii) these larger breaks must be accompanied by a sieving matrix, but this matrix probably occupies only a small portion of the depth of the cleft and/or its entrance at the luminal surface; (iii) neither junctional pore, restricted slit, or fiber matrix models can by themselves satisfy permeability and selectivity data; and (iv) one-dimensional models are a poor description of a cleft with infrequent larger breaks since the solute will be confined to small wakelike regions on the downstream side of the junction strand discontinuities and thus not fill the wide part of the cleft.

Capillary Permeability↗
PubMed1992

Modulation of venular microvessel permeability by calcium influx into endothelial cells.

It has been proposed that calcium ion influx into endothelial cells modulates the permeability of venular microvessels via a calcium-dependent contractile process. The results of recent investigations using permeabilized endothelial cell monolayers conform to this hypothesis by demonstrating a calcium-dependent interaction of endothelial actin and myosin during the retraction of adjacent endothelial cells exposed to inflammatory agents. Little is known about the pathway for calcium influx into endothelial cells after exposure to mediators of inflammation, but evidence suggests that the properties of the calcium entry pathways are similar to the calcium entry pathways that regulate the release of endothelium-derived relaxing factor (EDRF). Substances that stimulate EDRF release from arterial endothelium also increase venular microvessel permeability. Recently developed methods to measure cytoplasmic calcium concentration in the endothelial cells forming the walls of individually perfused microvessels enable a direct investigation of the modulation of the permeability of venular microvessels by calcium influx. These experiments demonstrate that the magnitude of the initial increase in the permeability of microvessels after exposure to an agent that increases permeability, such as a calcium ionophore, is determined by the magnitude of calcium ion influx into the endothelial cells. Furthermore, the magnitude of the calcium influx into endothelial cells is modulated by the membrane potential of the endothelial cells. Depolarization of the endothelial cell membrane reduces calcium influx and attenuates increases in permeability whereas hyperpolarization of the endothelial membrane increases calcium influx and potentiates increases in permeability. These data conform to the hypothesis that a passive conductance channel for calcium is a major pathway for calcium ion flux responsible to eliciting an increase in the permeability of the endothelial barrier in microvessels.

Animals↗
PubMed1991

Differential actions of albumin and plasma on capillary solute permeability.

We tested the hypothesis that albumin regulates the solute permeability coefficients (Ps) of individually perfused exchange microvessels of the frog mesentery by mechanisms similar to those described for hydraulic conductivity. Using unbound Evans blue dye (T-1824, mol wt 960, 1.3 nm radius) as a test solute, we demonstrated a hysteresis of PT-1824s on luminal albumin content as perfusate albumin concentration was first reduced in three steps from 1 mg/ml to zero and then returned to 1 mg/ml. PT-1824 s did not return to initial control values. The same result was found with tetramethylrhodamine isothiocyanate-alpha-lactalbumin (mol wt 14,176; 2.0 nm radius) even when the perfusate albumin concentration was increased by 10-fold to 10 mg/ml. In contrast, frog plasma at the same total protein concentration restored P alpha-lactalbumin s to values below those measured with control albumin perfusates before Ringer perfusion. Our results conform to the hypothesis that a plasma factor (possibly orosomucoid) that modifies the charge selectivity of the microvessel wall is removed from the microvessel membrane during protein-free Ringer perfusion and is not restored by reperfusion with albumin alone.

Animals↗
PubMed1991

Depolarization modulates endothelial cell calcium influx and microvessel permeability.

We investigated the mechanisms whereby high-potassium (57.9 mM) Ringer solutions attenuate the increase in permeability caused when microvessels are exposed to the calcium ionophores ionomycin and A23187 (5 microM). In single perfused microvessels we measured cytoplasmic calcium concentration, [Ca2+]i, in the cells forming the microvessel wall and the hydraulic conductivity, Lp, to follow changes in the permeability of the microvessel walls. In normal Ringer solution, [Ca2+]i was increased to an initial peak value of 226 +/- 12 nM after exposure to calcium ionophores; the corresponding increase in microvessel Lp was 10.3 +/- 2.6 times control. With high-potassium solutions, the peak value of [Ca2+]i was 133 +/- 12 nM and Lp was increased to only 2.5 +/- 0.7 times control. Increasing extracellular calcium from 1.1 to 5 mM with high potassium restored the initial peak value of [Ca2+]i to 303 +/- 38 nM. The increases in both [Ca2+]i and Lp were abolished in calcium-free solutions. If high-potassium solutions depolarize the cells forming the microvessel wall as indicated by the membrane potential-sensitive dye bisoxonol, then the magnitude of the initial increase in [Ca2+]i could be accounted for by changes in the electrochemical driving force through conductive channels for calcium ion. Our results conform to the hypothesis that the permeability properties of microvessels are modulated by changes in the membrane potential of the endothelial cells and/or pericytes forming the microvessel wall.

Animals↗
PubMed1990

Graded modulation of frog microvessel permeability to albumin using ionophore A23187.

We investigated the exchange of water and macromolecules across venular microvessels after permeability was increased. Quantitative fluorescence microscopy was used to measure albumin permeability coefficients in individually perfused microvessels of decerebrate frogs. Control permeability coefficient was 2.3 +/- 0.25 X 10(-7) cm/s. Solvent drag increased the apparent solute permeability coefficient (Ps) by 0.57 +/- 0.05 X 10(-7) cm/s for each cmH2O increase in microvessel pressure. The divalent cation ionophore A23187 (0.1-5 microM) produced a transient increase in Ps to a peak value (within 1-3 min), followed (after 4-8 min) by a sustained increase in permeability (16-34% of peak values). Peak values of Ps were 13 and 80 times control for 0.1 and 5 microM A23187, respectively. Both diffusion and solvent drag contributed to the sustained increase in Ps. The equivalent pore radius of the structures determining diffusion and solvent drag was less than or equal to 25 nm during the sustained increase in permeability, smaller than observed gaps between adjacent endothelial cells. The basement membrane and a fibrous matrix secreted by endothelial cells into the gaps may offer resistance to exchange in the high permeability state.

Animals↗
PubMed1990

Measurement of cytoplasmic calcium in single microvessels with increased permeability.

We investigated the hypothesis that an increase in cytoplasmic calcium ion concentration, [Ca2+]i, is one of the mechanisms responsible for increased microvessel permeability. We loaded the cells forming the walls of individually perfused microvessels in frog mesentery with fura-2 and measured [Ca2+]i in the control state and after adding the Ca2+ ionophore ionomycin to the perfusate. [Ca2+]i in the control state was 65 +/- 6 nM and increased to an initial peak of 285 +/- 29 nM after 1-3 min. After 4, 6, and 10 min, [Ca2+]i was 199 +/- 18, 163 +/- 16, and 129 +/- 9 nM, respectively. [Ca2+]i fell back to 77 +/- 7 nM after ionophore was removed. In similar experiments, hydraulic conductivity (Lp) increased to a peak of 9.5 times control after 1-3 min, then fell to 2.0 times control after 6 min. Lp remained elevated at this level for as long as ionophore was present in the perfusate. [Ca2+]i modulates the initial and sustained phases of the permeability increase. Both processes depend on external Ca2+ influx. Our experiments provide the first direct measurement of [Ca2+]i during a change in the permeability of an intact microvessel.

Animals↗
PubMed1989

Modulation of microvessel wall charge by plasma glycoprotein orosomucoid.

Haraldsson and Rippe suggested that the circulating glycoprotein orosomucoid (alpha 1-acid glycoprotein) contributes to the net charge on microvessel walls (Acta Physiol. Scand. 129: 127-135, 1987). We tested their hypothesis in individually perfused microvessels of frog mesentery by measuring solute permeability coefficients of two globular proteins (alpha-lactalbumin and ribonuclease) having approximately the same size (Stokes radius, 2 nm) but different charge (-11 and +3, respectively). In vessels perfused with orosomucoid (0.1 and 1 mg/ml) in a Ringer-albumin perfusate, the solute permeability coefficient of alpha-lactalbumin decreased to one-half [0.47 +/- 0.25 (SD)] the value in the absence of orosomucoid, and the solute permeability coefficient of ribonuclease was close to six times as large as alpha-lactalbumin permeability. Both results may be accounted for if orosomucoid increases the net negative charge on microvessel walls in frog mesentery from 11.2 to 28 meq/l. A similar change in microvessel charge would be more than sufficient to account for the decrease in albumin clearance in the presence of orosomucoid reported by Haraldsson and Rippe in rat muscle microvessels.

Animals↗
PubMed1988

Single capillary permeability to proteins having similar size but different charge.

We investigated the hypothesis that solute charge modulates transcapillary exchange in microvessels with continuous endothelium. Two globular proteins, alpha-lactalbumin and ribonuclease, having approximately the same size (mol wt 14,176 and 13,683, respectively) but different net charge (-10 and +4, respectively) were test solutes. Each solute was labeled with the fluorescent probe tetramethylrhodamine isothiocyanate. Labeling did not significantly change solute size, but increased negative charge on each solute by one valency unit. An in vivo fluorescent microscope technique [Huxley et. al., Am. J. Physiol. 252 (Heart Circ. Physiol. 21): H188-H197, 1987] was used to measure solute permeability coefficients (P) in single microvessels of frog mesentery at 14-16 degrees C. The mean P for alpha-lactalbumin, measured when capillary pressure was 10 cmH2O, was 2.1 X 10(-6) cm/s and the mean P for ribonuclease was 4.3 X 10(-6) cm/s. Our results conform to the hypothesis that the transcapillary pathways of frog mesenteric microvessels are negatively charged. With the use of a Donnan-type model for electrostatic partitioning, charge density in the pathway is estimated as 11.4 meq/l. Comparison of measured Ps with those for small solutes in frog mesenteric microvessels indicates that molecular size is a proportionally more significant determinant of solute permeability in continuous capillaries than is solute charge.

Algorithms↗
PubMed1987

Effect of albumin on the osmotic pressure exerted by myoglobin across capillary walls in frog mesentery.

1. Individual capillaries in mesenteries of pithed frogs were perfused sequentially with two frog Ringer solutions containing myoglobin at a concentration of 70 mg/ml. The first perfusate solution contained bovine serum albumin at a concentration of 10 mg/ml. The second perfusate contained no albumin. The modified Landis micro-occlusion technique (Michel, Mason, Curry & Tooke, 1974) was used to measure the capillary hydraulic conductivity and the effective osmotic pressure of the myoglobin solution across the capillary wall under conditions where the transcapillary concentration difference was established by steady-state ultrafiltration. 2. In six capillaries the effective osmotic pressure of the myoglobin solution at 20-22 degrees C was 15.9 +/- 2.2 (S.E. of mean) cmH2O when albumin was in the perfusate and 10.1 +/- 1.1 cmH2O after albumin was removed from the perfusate. 3. The hydraulic conductivity of the capillary wall increased from a mean value of 6.5 +/- 1.4 X 10(-7) cm/(s cmH2O) when albumin was in the perfusate to 15.6 +/- 3.8 X 10(-7) cm/(s cmH2O) during perfusion with Ringer solution containing myoglobin alone. 4. Control experiments to measure steady-state filtration rates at pressures 10-30 cmH2O were carried out to check the assumption in the method that the reduction in the measured osmotic pressure of myoglobin was the result of changes in the properties of the molecular sieve within the capillary wall and was not simply the result of solute accumulation on the tissue side of the capillary wall. 5. The measured reduction in the effective osmotic pressure of myoglobin when albumin was removed from the perfusate does not conform to the hypothesis (Crone, 1984) that the tight segment of the intercellular junction is the principal molecular filter for myoglobin in the wall of frog mesenteric capillaries. 6. Our results do conform to the hypothesis that a network of fibrous molecules, reinforced by adsorbed albumin, forms the principal molecular filter at the capillary wall in frog mesenteric capillaries.

Albumins↗
PubMed1987

Quantitative fluorescence microscopy on single capillaries: alpha-lactalbumin transport.

We have extended the use of a microscope densitometric technique [Am. J. Physiol. 245 (Heart Circ. Physiol. 14): H495-H505, 1983] to measure the solute permeability coefficients (Pa) of fluorescently labeled solutes in single perfused capillaries of frog mesentery. The method enables the transcapillary flux of solutes larger than 10,000 mol wt to be measured under conditions where the forces that determine both solute and water flows across the capillary wall are known. The Pa for alpha-lactalbumin (mol wt 14,176, Stokes radius 2.02 nm) increased from a mean value of 2.1 X 10(-6) cm/s when capillary pressure was 3.0 cmH2O (no net filtration) to greater than 4.0 X 10(-6) cm/s when capillary pressure was 15 cmH2O. Taking a value of 0.35 for the solvent drag reflection coefficient for alpha-lactalbumin, we conclude that the increased solute flux represents solvent drag through a water pathway with a hydraulic conductivity of 3.6 X 10(-7) cm X s-1 X cmH2O-1. Our data conforms to the hypothesis that alpha-lactalbumin is transported across the capillary wall by restricted diffusion and solvent drag in a pathway that carries 90% of the transcapillary water flow (the principle water pathway). In vitro and in vivo calibration experiments have been carried out to test the assumption that the measured fluorescent light intensity is proportional to the number of fluorescent molecules in the measuring window of the photometer.

Animals↗
PubMed1987

Effect of superfusate albumin on single capillary hydraulic conductivity.

It has been proposed that albumin interacts with the endothelial cell surface to form part of the molecular filter at the capillary wall. Previous investigations of the "protein effect" have been limited to sites accessible to albumin from the capillary lumen. We tested for a specific interaction of albumin with the ablumenal surface of the capillary wall. The hydraulic conductivity (Lp) of single capillaries in frog mesentery, perfused initially with albumin-free Ringer, was reduced when albumin (concentration greater than 1 mg/ml) was added to the superfusate (mean fractional reduction 0.56 +/- 0.05 SE, n = 15). A similar reduction was measured when the mesothelial barrier to water and solute flows between the superfusate and the albuminal surface of the capillary was destroyed. When the albumin was extensively dialyzed against Ringer to remove small vasoactive molecules, no change in the fractional reduction of Lp was observed. Lp was reduced to a minimum value in any capillary when the albumin concentration on both sides of the capillary wall was greater than 1 mg/ml. Our data conform to the hypothesis that albumin modifies structures throughout the capillary wall to maintain normal permeability. We predict that extravascular albumin reduces the ability of a Ringer perfusate to increase permeability in many isolated perfused organs.

Albumins↗
PubMed1985

Albumin modulation of capillary permeability: test of an adsorption mechanism.

We investigated further the mechanism whereby albumin interacts with the walls of capillary blood vessels to maintain normal permeability properties. In individually perfused capillaries of frog mesentery, hydraulic conductivity was measured as the albumin perfusate concentration was first reduced in three steps from 0.1 to 0 g/dl (intermediate concns 0.01 and 0.001 g/dl), then increased in up to four steps to 1 g/dl (intermediate concns 0.001, 0.01, and 0.1 g/dl). The albumin concentration required to return hydraulic conductivity toward control values, following Ringer perfusion, was at least an order of magnitude larger than that required to maintain permeability close to control values prior to Ringer perfusion. The experiments indicate that the affinity of albumin for binding sites on the capillary wall following Ringer perfusion is less than the albumin affinity for binding sites after the capillary has been perfused with solutions containing 0.1 g/dl albumin. Before the hysteresis of hydraulic conductivity on albumin concentration can be understood, the factors determining the transport of albumin into the membrane must be investigated further.

Adsorption↗
PubMed1984

Water flow across the walls of single muscle capillaries in the frog, Rana pipiens.

Individual capillaries of the transilluminated frog muscle cutaneous pectoris were perfused with suspensions of human red cells in frog Ringer solution containing 1 g/dl bovine serum albumin. The modified Landis technique (Michel, Mason, Curry & Tooke, 1974) was used to measure hydraulic conductivities of the capillary wall. Sucrose osmotic reflexion coefficients of the capillary wall were measured in four capillaries when the superfusate contained 100 mM-sucrose. All experiments were made at 22-24 degrees C. The hydraulic conductivity of arterial capillaries varied from 0.3 to 1.26 X 10(-7) cm/(s cmH2O) with a mean of 0.79 X 10(-7) cm/(s cmH2O) (six capillaries). The hydraulic conductivities of mid-capillaries varied from 0.43 to 1.86 X 10(-7) cm/(s cmH2O) with a mean value of 0.72 X 10(-7) cm/(s cmH2O) (six capillaries). The mean reflexion coefficient to sucrose was 0.12 +/- 0.05 (S.D.). The measured reflexion coefficients to sucrose conform to the hypothesis that 90% of the transcapillary water flow crosses the capillary wall via the principal hydrophilic pathway. The remaining 10% crosses via an exclusive water pathway. The distribution of water flow is similar to that previously described in frog mesenteric capillaries. The mean value of the hydraulic conductivity of frog muscle capillaries is about one-seventh the mean value of the hydraulic conductivity of frog mesenteric capillaries measured at the same temperature. The result conforms to the hypothesis that only a small fraction (mean 10%) of the area of junctional contact between adjacent endothelial cells is available for water and solute exchange in frog muscle capillaries. The hydraulic and diffusional conductances per unit length of open junction appear to be very similar when muscle capillaries are compared to mesenteric capillaries in the frog. Our results lead us to speculate that structures within the intercellular junctions determine the extent of open junction and may modulate the hydraulic conductivity of both the principal water pathway and the exclusive water pathway.

Animals↗