Atrial natriuretic peptide: Direct effects on human red blood cell dynamics

Zamir, Nadav; Tuvia, Shmuel; Riven-Kreitman, Rivka; Levin, Shlomo; Korenstein, Rafi

doi:10.1016/0006-291x(92)91331-j

Cited by 12 publications

(6 citation statements)

References 22 publications

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“…The present study shows that β‐adrenergic agonists are potent in elevating both CMFs and filterability of RBCs. Such a positive correlation between CMFs and filterability of RBCs has already been reported for human erythrocytes when exposed to hyper‐ and hyposmotic media (Tuvia et al 1992 a ) or following exposure to atrial natriuretic peptide and cGMP (Zamir et al 1992). Moreover, a similar correlation has been established in metastatic and non‐metastatic lines of T lymphocytes (Mittelman et al 1994).…”

Section: Discussionsupporting

confidence: 65%

“…1992). A direct correlation between CMF amplitude and RBC filterability was found to exist both in erythrocytes (Tuvia et al 1992 a ; Zamir et al 1992) and in lymphoid cell lines possessing a different metastatic potential (Mittelman et al 1994).…”

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confidence: 99%

“…These effects and their underlying mechanisms are still unresolved. Recently, we demonstrated an increase in CMFs and cell filterability following the exposure of RBCs to atrial natriuretic peptide which was found to exert its effect via a cGMP‐dependent pathway (Zamir et al . 1992).…”

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confidence: 99%

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β‐Adrenergic agonists regulate cell membrane fluctuations of human erythrocytes

Tuvia

Moses

Gulayev

et al. 1999

The Journal of Physiology

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Mechanical fluctuations of the cell membrane (CMFs) in human erythrocytes reflect the bending deformability of the membrane‐skeleton complex. These fluctuations were monitored by time‐dependent light scattering from a small area (≈0.25 μm2) of the cell surface by a method based on point dark field microscopy. Exposure of red blood cells (RBCs) to adrenaline (epinephrine) and isoproterenol (isoprenaline) resulted in up to a 45 % increase in the maximal fluctuation amplitude and up to a 35 % increase in the half‐width of the amplitude distribution. The power spectra of membrane fluctuations of control and treated cells revealed that adrenaline stimulated only the low frequency component (0.3‐3 Hz). Analysis of the dose‐response curves of β‐adrenergic agonists yielded an EC50 of 5 × 10−9 and 1 × 10−11 M for adrenaline and isoproterenol, respectively. Propranolol had an inhibitory effect on the stimulatory effect of isoproterenol. These findings show a potency order of propranolol > isoproterenol > adrenaline. The stimulatory effect of adrenaline was a temporal one, reaching its maximal level after 20‐30 min but being abolished after 60 min. However, in the presence of 3‐isobutyl‐1‐methylxanthine, a partial stimulatory effect was maintained even after 60 min. Pentoxifylline and 8‐bromo‐cAMP elevated CMFs. However, exposure of ATP‐depleted erythrocytes to adrenaline or 8‐bromo‐cAMP did not yield any elevation in CMFs. These findings suggest that the β‐agonist effect on CMFs is transduced via a cAMP‐dependent pathway. Deoxygenation decreased CMFs and filterability of erythrocytes by ≈30 %. The stimulatory effect of isoproterenol on CMFs was 2.2‐fold higher in deoxygenated RBCs than in oxygenated cells. Exposure of RBCs to adrenaline resulted in a concentration‐dependent increase in RBC filterability, demonstrating a linear relationship between CMFs and filterability, under the same exposure conditions to adrenaline. These findings suggest that β‐adrenergic agonists may improve passage of erythrocytes through microvasculature, enhancing oxygen delivery to tissues, especially under situations of reduced oxygen tension for periods longer than 20 min.

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Section: Discussionsupporting

confidence: 65%

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β‐Adrenergic agonists regulate cell membrane fluctuations of human erythrocytes

Tuvia

Moses

Gulayev

et al. 1999

The Journal of Physiology

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“…It has been previously shown that RBC filterability, a major determinant in microcirculation, is directly related to CMF (29,30). Thus, in addition to altering vascular flow resistance, elevated plasma viscosity may influence the microcirculation by decreasing RBCs ability to pass through narrow pores.…”

Section: Resultsmentioning

confidence: 99%

Cell membrane fluctuations are regulated by medium macroviscosity: Evidence for a metabolic driving force

Tuvia

Almagor

Bitler

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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115

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Extracellular f luid macroviscosity (EFM), modified by macromolecular cosolvents as occurs in body f luids, has been shown to affect cell membrane protein activities but not isolated proteins. In search for the mechanism of this phenomenon, we examined the effect of EFM on mechanical f luctuations of the cell membrane of human erythrocytes. The macroviscosity of the external medium was varied by adding to it various macromolecules [dextrans (70, 500, and 2,000 kDa), polyethylene glycol (20 kDa), and carboxymethyl-cellulose (100 kDa)], which differ in size, chemical nature, and in their capacity to increase f luid viscosity. The parameters of cell membrane f luctuations (maximal amplitude and half-width of amplitude distribution) were diminished with the elevation of solvent macroviscosity, regardless of the cosolvent used to increase EFM. Because thermally driven membrane f luctuations cannot be damped by elevation of EFM, the existence of a metabolic driving force is suggested. This is supported by the finding that in ATPdepleted red blood cells elevation of EMF did not affect cell membrane f luctuations. This study demonstrates that (i) EFM is a regulator of membrane dynamics, providing a possible mechanism by which EFM affects cell membrane activities; and (ii) cell membrane f luctuations are driven by a metabolic driving force in addition to the thermal one.The viscosity of body fluids is determined by the level of macromolecules consisting of proteins, lipoproteins, and polysacharides (1). Accordingly, elevated plasma viscosity has been observed in various diseases associated with increased levels of proteins and lipoproteins, such as diabetes, hyperlipidemia, macroglobulinemia, multiple myeloma, nephrosis, and others (1-5). Various studies have shown that solvent viscosity affects protein dynamics and reactions (6-10). However, in these studies the solvent viscosity was modified by the addition of high concentrations of small cosolvents such as glycerol and sucrose, producing relatively high viscosity levels. This is incompatible with physiological and pathological states, where fluid viscosity is altered by small concentrations of large macromolecules (1). Other studies, in which the viscosity was elevated by macromolecular cosolvents, have shown that extracellular fluid macroviscosity (EFM) is a regulator of cellular processes, such as secretion of renin (11) and lipoproteins (12), phospholipase A 2 activity at the cell membrane (13, 14), and ganglioside metabolism (15). In search of the mechanism of this phenomenon, the effect of macroviscosity, as modified by macromolecules, on isolated proteins in aqueous solutions was examined (16,17). It was found that the effect of solvent viscosity decreases with increasing molecular weight of the cosolvent and is practically diminished when the cosolvent molecular weight exceeds that of the protein. Because the activity of cell membrane enzymes is known to be sensitive to the physical properties of the membrane (18), we considered the possibility that the...

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“…However, NO decreases rat RBC deformability in sepsis [167]. Activation of the cGMP-dependent pathway by atrial natriuretic peptide also increases filterability of RBCs [168]. is a well-known signalling ion and the interactions between NO-and Ca 2+ -dependent signalling are briefly discussed below.…”

Section: Possible Implications Of Nomentioning

confidence: 99%

Erythrocyte Signal Transduction Pathways, their Oxygenation Dependence and Functional Significance

Barvitenko

Adragna

Weber³

2005

Cell Physiol Biochem

135

104

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Erythrocytes play a key role in human and vertebrate metabolism. Tissue O₂ supply is regulated by both hemoglobin (Hb)-O₂ affinity and erythrocyte rheology, a key determinant of tissue perfusion. Oxygenation-deoxygenation transitions of Hb may lead to re-organization of the cytoskeleton and signalling pathways activation/deactivation in an O₂-dependent manner. Deoxygenated Hb binds to the cytoplasmic domain of the anion exchanger band 3, which is anchored to the cytoskeleton, and is considered a major mechanism underlying the oxygenation-dependence of several erythrocyte functions. This work discusses the multiple modes of Hb-cytoskeleton interactions. In addition, it reviews the effects of Mg²⁺, 2,3-diphosphoglycerate, NO, shear stress and Ca²⁺, all factors accompanying the oxygenation-deoxygenation cycle in circulating red cells. Due to the extensive literature on the subject, the data discussed here, pertain mainly to human erythrocytes whose O₂ affinity is modulated by 2,3-diphosphoglycerate, ectothermic vertebrate erythrocytes that use ATP, and to bird erythrocytes that use inositol pentaphosphate.

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Atrial natriuretic peptide: Direct effects on human red blood cell dynamics

Cited by 12 publications

References 22 publications

β‐Adrenergic agonists regulate cell membrane fluctuations of human erythrocytes

β‐Adrenergic agonists regulate cell membrane fluctuations of human erythrocytes

Cell membrane fluctuations are regulated by medium macroviscosity: Evidence for a metabolic driving force

Erythrocyte Signal Transduction Pathways, their Oxygenation Dependence and Functional Significance

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