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Biomedical subjects

R Garay

Publications and source records attributed to R Garay.

At least 73 records · Page 4Linked to original sources
PubMed1985

Ion transport regulation by prostaglandins in mouse macrophages.

Although the prostaglandins PGE1, PGE2 and PGF2 alpha had no effect on ion transport in isolated human erythrocytes, they modulated ion transport in isolated mouse macrophages, apparently through the mediation of cAMP, by inhibiting the NA+, K+ cotransport system, stimulating the Na+, K+ pump, and stimulating the Na+: Ca++ exchange mechanism.

Alprostadil↗
PubMed1984

Ion transport characteristics in rhesus monkey erythrocytes: relationship to age and blood pressure.

Erythrocyte (RBC) ion transport characteristics were examined in six young Rhesus monkeys (RM) age 3.3 +/- .3 (means +/- S.D.) years and seven mature RM 15.4 +/- 1 (means +/- S.D.) years. It was found that the older RM when compared to the younger RM demonstrated significantly elevated mean arterial pressures (MAP) (96 +/- 15 versus 75 +/- 11 mmHg), RBC intracellular sodiums (RBC Nai) (16.2 +/- 4 versus 11 +/- 3 mEq/liter RBC) and NaK ATPase pump rates per RBC (PR) (PR = ouabain sensitive K uptake divided by ouabain binding sites per RBC) (104 +/- 18 versus 83 +/- 18 K+ ions/sec/pump unit). However, it was also found that when the data from both groups were pooled and collectively analyzed a significantly positive correlation could be found between MAP and RBC Nai (p less than .001, r = .82), MAP and PR (p less than .01, r = .67) as well as PR and RBC Nai (p less than .001, r = .76). The fact that positive correlations exist among these parameters, independent of age, would suggest that while MAP, RBC Nai and PR tend to be elevated with advancing age, these abberations are not invariable consequences of age and best reflect the pivotal abberration of rising Nai. While insufficient data exist to account for the rise in Nai and no cause-effect relationship can be established it is clear that rising MAP and PR correlate best with rising Nai.

Age Factors↗
PubMed1984

Ion transport, prostaglandins, and essential hypertension.

Prostaglandins (including PGE1, PGE2 and PGI2) showed little or no effect on Na+ and K+ transport across human red cell membranes. Conversely, they were able to: i) inhibit Na+, K+ cotransport system, ii) stimulate Na+, K+-pump and iii) stimulate Na+, Ca2+ exchange in mouse macrophages. These effects which seem to be mediated by cyclic AMP, provoke a more rapid extrusion of a cell Na+ -load. This may counterbalance the abnormal cell Na+ regulation that appears to be associated with essential hypertension.

Animals↗
PubMed1983

Modulation of Na+ transport systems in Wistar rat erythrocytes by excess dietary Na+ intake.

Plasma Na+, erythrocyte Na+ content and the activity of Na+ transport systems of red cells were measured in Wistar rat fed a normal or high Na+ diet. Net Na+ and K+ fluxes of erythrocytes were also measured in the presence of plasma of rats fed with excess Na+. Na+-K+ cotransport and passive Na+ permeability were increased. Erythrocyte Na+ content was increased after 2 months but not after 8 days of high Na+ intake. No significant difference in plasma Na+ and pump activity could be detected after such a diet. No factor acting in Na+ extrusion was found to be present in plasma of salt loaded rats. These results indicate that Na+ intake may modulate Na+ transport systems, namely passive permeability and Na+-K+ cotransport and that increased Na+ erythrocyte content is not a causative factor.

Animals↗
PubMed1983

Erythrocyte Na+ and K+ transport systems in children with Bartter syndrome: increase in passive sodium permeability.

Na+ and K+ intracellular content was studied in five children with Bartter syndrome and their age and race-paired controls. Na+ and K+ pump (ouabain sensitive) fluxes, Na+-K+ co-transport (furosemide sensitive), and rate constants of passive Na+ and K+ permeability were determined in each patient and control and also in six parents. The results show that in Bartter syndrome, there is a significant increase in the rate constant of passive Na+ permeability without any change in passive K+ permeability. This increase in the rate constant of passive permeability might explain at least partially the increased intracellular Na+ concentration also found in these patients. Moreover, the maximal rate of ouabain sensitive Na+ efflux was increased slightly, and co-transport fluxes were variable. Parents of patients had normal erythrocyte fluxes.

Adolescent↗
PubMed1983

The effect of cyclic nucleotides and icosanoids on Na+ and K+ transport in human red cells.

Cyclic AMP inhibits the bumetanide-sensitive Na+,K+ cotransport system in human red cells. The cotransport inhibition is enhanced by addition of phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine to the incubation medium. The cyclic AMP concentration giving half-maximal cotransport inhibition showed a wide variation among different individuals (from 0.1 to 5 mM external cyclic AMP concentration). In contrast to cyclic AMP, cyclic GMP showed little effect on the cotransport system. The ouabain-sensitive Na+,K+ pump was almost unaffected by cyclic nucleotides. Prostacyclin was the only tested prostaglandin showing an effect on Na+ and K+ transport in human red cells. In some individuals, this icosanoid stimulated the Na+,K+ cotransport system. Leukotriene B4 stimulated K+ fluxes.

1-Methyl-3-isobutylxanthine↗
PubMed1981

Outward sodium and potassium cotransport in human red cells.

This paper reports some kinetic properties of Na-K cotransport in human red cells. All fluxes were measured in the presence of 10(-4) M ouabain. We measured Na and K efflux from cells loaded by the PCMBS method to contain different concentrations of these ions into a medium that contained neither Na nor K (MgCl2-sucrose substitution) in the absence and presence of furosemide. Furosemide inhibited 30-60% of the total efflux depending on the internal ion concentration and the individual subject. We took the furosemide-sensitive fluxes to be a measure of Na-K cotransport. The ratio of Na to K cotransport was 1 over the entire range of internal Na and K concentrations studied. When Na was substituted for K as the only internal cation, cotransport was maximally activated when the Na and K concentrations were between 20 and 90 mmol/liter cells. The concentration of internal Na required to produce half-maximal cotransport was about 13 +/- 4 mmol/liter cells (n = 4), while the comparable concentration of K was somewhat lower. The activation curve was definitely sigmoid in character, suggesting that at least two Na ions are involved in the transport process. The maximum of Na-K cotransport was about 0.5 +/- 0.15 mmol/liter cells x hr (n = 5); it had a flat maximum in the medium at about pH 7.0, decreasing in both the acid and alkaline sides. Furosemide-resistant effluxes were found to be linear functions of internal Na and K concentrations and to yield rate coefficients of 0.019 +/- 0.002 hr-1 and 0.014 +/- 0.002 hr-1 (n=7), respectively. These values are of the same order of magnitude expected of ions moving across phospholipid bilayers.

Biological Transport, Active↗
PubMed1981

Evidence for imbalanced furosemide-sensitive Na+, K+ cotransport in hereditary stomatocytosis.

The red cells from 5 related patients with hereditary stomatocytosis were investigated. Maximal rate constant of Na+ passive permeability was increased while that of K+ passive permeability was nearly normal. Ouabain-sensitive Na+ efflux was elevated. The Na+ component of furosemide-sensitive Na+, K+ cotransport was also increased. However, its K+ component, determined in 2 patients, remained within normal limits, thus departing from the strict 1:1 stoichiometry of the Na+, K+ cotransport system. Yet, intracellular Na+ and K+ concentrations displayed limited and inconstant changes. A variety of abnormally-shaped cells, including stomatocytes, were observed in scanning electron micrographs. Upon differential centrifugation, reticulocytes usually concentrated in the most dense region of the gradient. Red cell deformability, as studied by ektacytometry, was reduced. Membrane phosphatidylcholines and sphingomyelins were increased and decreased, respectively, where-as fatty acid distribution was unchanged. Membrane microviscosity was normal.

Cations↗
PubMed1981

Na countertransport and cotransport in human red cells: function, dysfunction, and genes in essential hypertension.

We describe in this paper studies on the modes of operation of ouabain-insensitive sodium transport systems in red cells of normotensive and hypertensive patients. We have extensively investigated the properties of Na countertransport and cotransport in order to clarify whether they are two different proteins or one transport protein with two modes of operation. Several criteria of discrimination between the two pathways are described: They differ in their affinity for Na and Li, sensitivity to several inhibitors, changes in cell volume, and chloride replacement by nitrate. We propose that there are two different transport systems. We have found elevated countertransport in red cells of hypertensive patients in France and in the United States. However, the cotransport system was found elevated in patients in Boston but reduced in patients in Paris. Studies of the modes of operation of the Na-K cotransport system indicate that it can promote K accumulation using an inward sodium gradient. This mode might be more efficient than Na extrusion at the physiological level of Na and K gradients. We interpret our findings of elevated Na-K cotransport in American hypertensive patients as an increased number of transport units functioning as K accumulators. It remains to be determined whether the reduced affinity for internal sodium of the outward cotransport is a defective outward cotransport or else a modulation of this transport system to favor K accumulation.

4-Chloromercuribenzenesulfonate↗
PubMed1981

Furosemide and bumetanide-sensitive Na+ fluxes in erythrocytes from genetically hypertensive rats (SHR).

Na+ and K+ fluxes from erythrocytes of SHR and WKY control rats have been studied. Fluxes were measured in both fresh and sodium-loaded (after exposure to ouabain or PCMBS) erythrocytes. Pump activity appears higher and furosemide or bumetanide sensitive Na+ efflux lower in SHR compared to WKY suggesting a similar abnormality in SHR genetic hypertension as in human hypertension.

4-Chloromercuribenzenesulfonate↗