Abnormal Na<sup>+</sup>K<sup>+</sup> cotransport function in a group of patients with essential hypertension

Garay, Ricardo P.; Nazaret, Corinne; Hannaert, Patrick; Price, Matt D.

doi:10.1111/j.1365-2362.1983.tb00106.x

Cited by 76 publications

(44 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ferret red cells thus provide an excellent system in which to examine factors which might control the activity of the co-transport system. Recent theories assign key roles to the cotransport system in the activation of secretion in epithelia (Petersen & Maruyama, 1984) and in the genesis of some types of essential hypertension (see, for instance, Garay, Dagher, Pernollet, Devynck & Meyer, 1980;Garay, Nazaret, Hannaert & Price, 1983). Alterations in intracellular ionized calcium concentration are central to these theories (see also Blaustein, Lang & James-Kracke, 1981).…”

Section: Introductionmentioning

confidence: 99%

The effects of calcium on potassium transport in ferret red cells.

Flatman

1987

The Journal of Physiology

View full text Add to dashboard Cite

1. The effects of changes in the concentration of intracellular calcium on potassium transport were investigated in ferret red cells. Bumetanide was used to divide potassium transport into three components: total, bumetanide sensitive and bumetanide resistant. The bumetanide‐sensitive component is equivalent to sodium‐potassium‐chloride co‐transport. 2. Internal calcium concentration was controlled with the ionophore A23187 which was present throughout the experiments. 3. Changes in internal ionized calcium over the range 5 X 10(‐10) M to 7 X 10(‐7) M did not affect any component of potassium uptake. 4. Increasing the internal ionized calcium concentration above 10(‐6) M stimulated bumetanide‐resistant potassium transport. Half‐maximal stimulation of this system was achieved with 3 X 10(‐6) M‐internal calcium. The system spontaneously inactivated after the initial activation by calcium and ionophore. Transport was inhibited by 1 mM‐quinine. 5. Increasing the internal ionized calcium concentration to 10(‐5) M had no effect on bumetanide‐sensitive transport. 6. Concentrations of intracellular ionized calcium above 10(‐5) M inhibited all three components of transport. Inhibition of the bumetanide‐sensitive component was only slightly reversed when internal calcium concentration was reduced to normal. 7. Physiological changes in internal ionized calcium concentration do not affect sodium‐potassium‐chloride co‐transport in ferret red cells. Very high concentrations of calcium inhibit transport, probably by an indirect mechanism. 8. In the course of the experiments the concentration of ionized intracellular magnesium in oxygenated ferret red cells was found to be about 0.65 mM.

show abstract

Section: Introductionmentioning

confidence: 99%

The effects of calcium on potassium transport in ferret red cells.

Flatman

1987

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…Regarding ion transport in erythrocytes, the total population of patients with essential hypertension is heterogeneous and includes a subgroup of higher Na + -Li + CT flux with normal Na + -K + cotransport (COT) function and one of abnormal Na + -K + COT function with normal Na + -Li + CT flux (36). In hypertensive patients, Na…”

Section: Ion Exchangersmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (K ATP ) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as K ATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs.

show abstract

“…These observations subsequent-ly were confirmed in some laboratories, 13 but other investigators 14 " 17 using different methodology found normal inward cotransport or increased values of outward cotransport in RBCs from their hypertensive populations. Garay and co-workers 18 ' l9 later extended their original observations to examine the kinetics of RBC Na + -K + cotransport in hypertensive patients by Na; activation of Na and K efflux in RBCs loaded at several concentrations of Na,. A substantial portion of their hypertensive study population had decreased apparent affinity (increased K 05 ) for internal Na in activating outward Na + -K + cotransport.…”

mentioning

confidence: 99%

Kinetic analysis of erythrocyte Na+-K+ pump and cotransport in essential hypertension.

Tuck¹,

Corry²,

Maxwell³

et al. 1987

Hypertension

View full text Add to dashboard Cite

SUMMARY Alterations in red blood cell (RBC) Na + -K + pump and Na + -K + cotransport have been described in essential hypertension. We evaluated Na + -K + pump and cotransport in 30 hypertensive and 26 normotensive subjects subdivided by race and family history of hypertension using an improved method to examine the kinetics of Na and K effluxes. RBCs were Na-loaded by the nystatin method to five different levels of internal Na with pump determined as ouabain-sensitive Na efflux and cotransport as furosemide-sensitive Na and K efflux. Two kinetic parameters were determined for both transport systems: the apparent affinity for Na (K 0 . s ) and the velocity of efflux at saturating internal Na concentration (V max ). Mean intracellular Na content in fresh RBCs (mniol/L cells) was higher in black hypertensive (12.6 ± 1.8 mmol/L cells) and normotensive subjects (10.9 ± 1.2 mmol/L cells) than in white hypertensive (8.7 ± 1.0 mmol/L cells) or normotensive subjects (8.5 ± 0.8 mmol/L cells). The V mai and K 0 .s for pump were not significantly different between study groups. The V max for cotransport was elevated in white hypertensive compared with normotensive subjects, but the K 0 .s values were similar. Black normotensive and hypertensive subjects displayed a lower V max and increased K 0 _ s for cotransport compared with the white groups. A family history of hypertension had no influence on cotransport kinetics in blacks but did predict white normotensive and hypertensive subjects with low cotransport. The reduction in intracellular Na affinity for cotransport in black subjects may explain their higher intracellular Na in fresh RBCs. The wide range of cotransport V max with normal K os in white hypertensive subjects suggests an abnormality in cotransport activity in this population that differs from that in blacks. This study also demonstrates that the RBC pump, as evaluated by cation flux methodology, functions normally over a wide range of intracellular Na in the hypertensive population. (Hypertension 10: 204-211, 1987)

show abstract

Abnormal Na⁺K⁺ cotransport function in a group of patients with essential hypertension

Cited by 76 publications

References 30 publications

The effects of calcium on potassium transport in ferret red cells.

The effects of calcium on potassium transport in ferret red cells.

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Kinetic analysis of erythrocyte Na+-K+ pump and cotransport in essential hypertension.

Contact Info

Product

Resources

About

Abnormal Na+K+ cotransport function in a group of patients with essential hypertension

Cited by 76 publications

References 30 publications

The effects of calcium on potassium transport in ferret red cells.

The effects of calcium on potassium transport in ferret red cells.

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Kinetic analysis of erythrocyte Na+-K+ pump and cotransport in essential hypertension.

Contact Info

Product

Resources

About

Abnormal Na⁺K⁺ cotransport function in a group of patients with essential hypertension