Intracellular Chloride in Essential Hypertension

Abstract

In 25 patients with untreated essential hypertension and 25 healthy controls, erythrocyte intracellular Cl- concentration and activity as well as Na+ activity were measured. Intracellular Cl- concentration in essential hypertensive patients was 70.6 +/- 11.3 as compared with 84.4 +/- 9.5 mmol/l in the controls (P less than 0.001). Intracellular Cl- activity was 77.5 +/- 13.0 mmol/l of cell water in hypertensive patients, the control value being 100.8 +/- 11.0 mmol/l of cell water (P less than 0.001). In the hypertensive group intracellular Na+ activity was 14.3 +/- 4.1 as compared with 7.1 +/- 1.8 mmol/l of cell water in the normotensive group (P less than 0.01). From these results it is suggested that in essential hypertension not only disturbances of cation metabolism, but also of anion metabolism, occur. Possibly the Cl- changes reflect a decreased Cl- inward transport due to an altered Na-K cotransport.

Influence of race, sex, and blood pressure on erythrocyte sodium transport in humans.

“…39 The group mean for neither [Na]j nor the number of sites/RBC was significantly different for essential hypertensive subjects in comparison to values for normal subjects. This finding contrasts with previously reported higher 8 ? and lower 10 concentrations.…”

Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl−

“…Also, in essential hypertension there may be a relationship between intracellular Cl − and Na + /Mg 2+ antiport. In essential hypertension, [Cl − ] i in erythrocytes was found to be reduced from 84.4 mmol/l to 70.6 mmol/l [36]. On the other hand, in 45% of patients with essential hypertension, Na + /Mg 2+ antiport was increased [37,38].…”

A laser Raman tweezers study of eryptosis

“…Therefore, the activation of the cation channels can hyperpolarise the cell membrane, which leads to membrane shrinkage. Hyperpolarisation further causes Cl − loss, which occurs through AE1 (in RBCs cytosolic Cl − concentration [80 mM] is known to be less than the extracellular Cl − concentration). The membrane resting potential, E Cl , is around −10 mV .…”

“…Any hyperpolarisation above −10 mV will drive Cl − anions out of the cell. Hyperpolarisation of the membrane can be thought of as increasing the electric driving force for expulsion of negatively charged Cl − . The Ca 2+ ‐sensitive K + channels—also referred to as Gardos channels —can mediate K + loss, which is higher by two orders of magnitude compared with standard K + efflux .…”