Potential role of Cl-HCO3 exchange in regulating vascular tone.

Karniski, Lawrence P.

doi:10.1161/01.hyp.15.1.104

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…This is further supported by previous suggestions that this transport mechanism could be an important factor in maintaining vascular tone 47 and in transducing growth factor signals. 48 In conclusion, we have confirmed that cell pH is diminished and the Na + -H + exchanger is increased in erythrocytes of essential hypertensive patients.…”

supporting

confidence: 87%

Erythrocyte anion exchanger activity and intracellular pH in essential hypertension.

et al. 1993

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The present study was designed to examine the activity of the sodium-independent chloride-bicarbonate anion exchanger and the sodium-proton exchanger in erythrocytes of 30 normotensive and 35 hypertensive subjects and its relation to the previously reported decrease in erythrocyte pH. Erythrocyte cytosolic pH was measured by the pH-sensitive fluorescent probe 2'-7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The activity of the anion exchanger was determined by acidifying cell pH and measuring the initial rate of the net sodium-independent, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid-sensitive, bicarbonate influx driven by an outward proton gradient. The activity of the sodium-proton exchanger was determined by acidifying cell pH and measuring the initial rate of the net sodium-dependent proton efflux driven by an outward proton gradient. The activity of the anion exchanger was higher in hypertensive than control individuals (

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confidence: 87%

Erythrocyte anion exchanger activity and intracellular pH in essential hypertension.

et al. 1993

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“…Changes in ion conductance may in turn be linked to regulation of intracellular pH and changes in calcium disposition. An imbalance between HCO3-Cl exchange in either direction can affect vascular tone (Karniski, 1990) and thus could account for the non-specific effect of alterations in chloride on vasoactivity. Similarly, the integral role of calcium in smooth muscle contraction as well as in intracellular signalling mechanisms (Khalil et al, 1990) and the capacity for chloride to increase intracellular levels of free calcium (Okuda et al, 1986) could also underlie the generalized depression of the vascular responsiveness of the rat kidney to the three agonists when chloride was lowered.…”

Section: Discussionmentioning

confidence: 99%

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Quilley

Lin

McGiff

1993

British J Pharmacology

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“…114 To our knowledge, neither the Na + -dependent C1"-HCO 3 " exchanger nor the Na + -independent CI~-HCO 3~ exchanger has been studied in experimental models of hypertension. As emphasized by Karniski,23 if intracellular pH or the Na + -H + exchanger is to be implicated in the pathogenesis of hypertension, then HCO 3~-dependent transport processes cannot be ignored. By design, whenever the external medium lacks HCO 3 -CO 2 , the operation of all HCO 3~-dependent transporters is eliminated and the role of the Na + -H + exchanger in pH, regulation is overestimated.…”

Section: Discussionmentioning

confidence: 99%

“…22 Alterations in the control of any or all of these processes could in various ways be involved in the pathogenesis of hypertension. 2 -3910 - 23 Exploration of the activity and kinetic properties of the various pH, regulatory transporters therefore seems a logical step in the evaluation of pH r regulating mechanisms in cells from hypertensive subjects. Two distinct bicarbonate transporters have been identified in various cell systems, including an electroneutraJ Na + -independent C1~-HCO 3~ exchanger and an electroneutraJ Na + -dependent Cr-HCO 3 " exchanger.…”

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confidence: 99%

Regulation of intracellular pH in the spontaneously hypertensive rat. Role of bicarbonate-dependent transporters.

Redón

Batlle

1994

Hypertension

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Previous studies that have evaluated the Na + -H + antiporter in cells from hypertensive subjects were generally performed under conditions in which HCO 3 -CO 2 , the physiological buffer system, was absent from the assay media. The objective of this study was to evaluate the activity of the Na + -H + antiporter and that of the Na + -dependent and Na + -independent Cr-HCO 3 " exchangers in cells assayed in the presence of HCO3-CO2 in the media. Lymphocytes from 6-to 8-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats were obtained from the thymus gland and assayed immediately after isolation. The activity of the Na + -H + antiporter after stimulation by cell acidification (pH, approximately 6.4) was similar in SHR and WKY rats (18.67+1.03 and 16.12±0.92 mmol H + /L per minute, respectively). Recovery from cell alkalinization was effected by an Na + -independent C1~-HCO 3~ exchanger, with maximal activity at an alkaline pH, (approximately 7.7). The stimulated activity of this Na + -independent Cr-HCO 3 " exchanger was also not different between SHR and WKY cells (2.65±0.25 and 2.55±0.32 mmol H + /Lper minute, respectively). Acute chloride removal produced a rise in pH, that was Na + -dependent and sensitive to 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) but resistant to ethylisopropylamiloride (EIPA), reflecting the activity of an Na + -dependent C1~-HCO 3~ ex-O ver the last several years the investigation of intracellular proton concentration and the Na + -H + antiporter in experimental 16 and clinical 7 " 14 hypertension has received increasing attention. Previous studies that have evaluated the Na + -H + antiporter in cells from hypertensive subjects were performed under conditions in which bicarbonate-carbon dioxide (HCO 3 -CO 2 ), the physiological buffer system, was absent from the assay media. This, by design, results in an overestimation of the role of the Na + -H + antiporter in the regulation of intracellular pH (pH|) and ignores the existence of other HCO 3~-dependent transporters that contribute not only to the regulation of pH| 15 -17 but also to the regulation of cell volume, 1819 cell growth, 2021 and intracellular sodium. 22 Alterations in the control of any or all of these processes could in various ways be involved in the pathogenesis of hypertension. 2 - 3910 -23 Received September 10, 1993; accepted in revised form December 21, 1993.From Northwestern University Medical School and Lakeside Veterans Administration Hospital, Chicago, Illinois.Correspondence to Daniel Batlle, MD, Division of Nephrology and Hypertension, Northwestern University Medical School, 310 E Superior, Morton Bldg 3-615, Chicago, IL 60611.changer. Unlike the Na + -H + exchanger and the Na + -independent C1"-HCO 3 " exchanger, which had their highest activities at extremes of pH, (low pH|, Na + -H + exchanger, and high pH, Na + -independent C1"-HCO 3 " exchanger), the Na + -dependent G~-HCO 3~ exchanger had its maximal activity near steady-state pH, (approximately...

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Potential role of Cl-HCO3 exchange in regulating vascular tone.

Cited by 4 publications

References 19 publications

Erythrocyte anion exchanger activity and intracellular pH in essential hypertension.

Erythrocyte anion exchanger activity and intracellular pH in essential hypertension.

Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents

Regulation of intracellular pH in the spontaneously hypertensive rat. Role of bicarbonate-dependent transporters.

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