Red cell sodium-proton exchange is increased in Dahl salt-sensitive hypertensive rats.

To investigate the relationship between red blood cell Na+/H+ exchange (EXC) and genetic factors in hypertension, we studied the maximal rate of the antiporter (mmol/liter cell x hr; flux units = FU) in three strains of genetically hypertensive rats. Salt-resistant Dahl rats (DR) were normotensive under low (0.02%) and high (8%) NaCl diets, while salt-sensitive Dahl rats (DS) became markedly hypertensive after four weeks on the high-NaCl diet.

Kinetic abnormalities of the red blood cell sodium-proton exchange in hypertensive patients.

The present study was designed to examine the kinetics of Na(+)-H+ exchange in red blood cells of normotensive and hypertensive subjects and its relation to the previously reported abnormalities in Na(+)-Li+ exchange. The Na(+)-H+ antiporter activation kinetics were studied by varying cell pH and measuring net Na+ influx (mmol/l cell x hr = units) driven by an outward H+ gradient. The Na(+)-Li+ exchange was determined at pH 7.

Kinetics and stoichiometry of the human red cell Na+/H+ exchanger.

We have investigated the kinetic properties of the human red blood cell Na+/H+ exchanger to provide a tool to study the role of genetic, hormonal and environmental factors in its expression as well as its functional properties in several clinical conditions. The present study reports its stoichiometry and the kinetic effects of internal H+ (Hi) and external Na+ (Nao) in red blood cells of normal subjects. Red blood cells with different cell Na+ (Nai) and pH (pHi) were prepared by nystatin and DIDS treatment of acid-loaded cells.

Charybdotoxin blocks with high affinity the Ca-activated K+ channel of Hb A and Hb S red cells: individual differences in the number of channels.

We have investigated the effect of a purified preparation of Charybdotoxin (CTX) on the Ca-activated K+ (Ca-K) channel of human red cells (RBC). Cytosolic Ca2+ was increased either by ATP depletion or by the Ca ionophore A23187 and incubation in Na+ media containing CaCl2. The Ca-K efflux activated by metabolic depletion was partially (77%) inhibited from 15.

Na-K-C1 cotransport and Na pump in red cells of young blacks and blood pressure response to salt loading.

The functional operation of Na and K fluxes, mediated by the furosemide-sensitive (FS) Na-K-C1 cotransport and the ouabain-sensitive Na pump, was studied in a representative young (18-22 years) black population. Cation fluxes (mumol/L cell X hour = FU) were studied prior to salt loading; results were compared with the blood pressure response to chronic oral salt loading. All subjects (n = 26) took 10 g/day NaC1 plus their usual diets for 14 days.

Volume-dependent and NEM-stimulated K+,Cl- transport is elevated in oxygenated SS, SC and CC human red cells.

Mechanisms involved in cell volume regulation are important in SS, SC cells as they might be involved in determining the extent of sickling and the generation of dense cells and irreversibly sickled cells. We have studied in these cells the response to cell swelling of the K+,Cl- transporter. We found that Hb SS, SC and CC red cells have higher values of a ouabain-resistant, chloride-dependent and NEM-stimulated K+ efflux than AA red cells.

Red cell sodium countertransport and cotransport in normotensive and hypertensive blacks.

We have previously described elevated Lii -Nao countertransport (CT) and Na-K cotransport (CO) in red cells of Caucasian patients from Boston. In this study, we report both transport systems in black patients from Philadelphia. The maximal rate (Vmax) of CT was assayed by measuring the Nao-stimulated Li efflux from cells containing +/- 6 mmol Li/liter.

Family history of hypertension and red cell cation transport in high school students.

High school students who had at least one parent with hypertension (n = 22) were compared to schoolmates of the same age with a negative family history of hypertension in the parents (n = 21). We investigated in both groups the maximal rate of the ouabain-sensitive Na pump and the Na-K cotransport in nystatin-loaded cells and the Lii-Nao countertransport in lithium-loaded cells. The two groups were significantly different only in the sum of net Na transport mediated by the Na-K pump and Na-K cotransport.