Changes in potassium content and membrane potassium channels in circulating cells from normal volunteers treated with cromakalim

Lijnen, Paul; Tan, Weiping; Fagard, Robert; Staessen, Jan A.; Améry, A

doi:10.1097/00004872-198905000-00009

Cited by 5 publications

(2 citation statements)

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“…5,6 Ciclazindol, which abolishes EDHF relaxation in the presence of apamin, inhibits IK Ca in RBC 4 and cromakalim, a known K + channel activator with vasodilator properties, opens IK Ca in RBC. 7 Our data show that increased K + efflux occurs in RBC treated with 8Br-cGMP (Delgado et al, 2002, unpublished data) probably by activation of IK Ca as it occurs in VSMC. 8 Therefore, it is reasonable to suppose that K + changes occurring in RBC are reflecting K + changes in the VSMC or in the endothelium.…”

Section: Introductionsupporting

confidence: 54%

“…33 Red blood cells, although lacking a nucleus, are useful models for membrane transport studies 34,35 and share membrane properties related to VSMC and the endothelium. RBC, which are equipped with IK Ca and inducible nitric oxide synthase, 36,37 respond to K Ca activators producing vasodilatation 7 or to 8Br-cGMP (Delgado et al, 2002, unpublished data) in a manner similar to the VSMC with the activation of K Ca and the efflux of K + . 8 Consequently, K + changes in RBC could be a marker for K + changes in other cells such as VSMC and the endothelium.…”

Section: Discussionmentioning

confidence: 99%

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Red blood cell K+ could be a marker of K+ changes in other cells involved in blood pressure regulation

Delgado

Delgado-Almeida

2003

J Hum Hypertens

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The aim of this study is to determine whether red blood cell K + content (RBC Ki ) is associated with blood pressure levels and, if so, could RBC Ki be a marker of potassium changes in other cells involved in blood pressure regulation. The study was performed on 50 untreated hypertensives, 32 of their offspring and 50 age-and sex-matched controls. Systolic (SBP) and diastolic (DBP) blood pressures, height, weight, plasma, urine and red blood cell electrolytes were measured in all subjects. RBC Ki was significantly lower in hypertensives than in offspring of hypertensives and normotensive controls. Offspring of hypertensives had significantly lower RBC Ki than normotensive controls. Plasma K + was significantly lower both in hypertensives and offspring of hypertensives when compared to normotensive controls. A significant negative correlation was found in hypertensives between RBC Ki and DBP (r ¼ À0.27, P ¼ 0.04) and in offspring of hypertensives between RBC Ki and DBP (r ¼ À0.43, P ¼ 0.02). A significant correlation was found in hypertensives between RBC Ki and plasma K + (r ¼ 0.3, P ¼ 0.02). A positive correlation with borderline significance was found in hypertensives between RBC Ki and ionized Ca 2+ (r ¼ 0.2, P ¼ 0.1). In conclusion, our results support the hypothesis that RBC Ki is associated with blood pressure levels and that the measurement of RBC Ki levels may represent a biochemical marker for K + changes in other cells involved in blood pressure regulation. Further studies are necessary to explain the exact mechanisms of reduced RBC Ki levels in hypertensive patients and their offspring.

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