Decreased calcium pump adenosine triphosphatase in red blood cells of hypertensive subjects.

Vincenzi, Frank F.; Morris, Cynthia D.; Kinsel, Laura B.; Kenny, Margaret A.; McCarron, David A.

doi:10.1161/01.hyp.8.11.1058

Cited by 65 publications

(15 citation statements)

References 48 publications

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“…The basis for increased Ca, accumulation in hypertension and diabetes is unknown, but decreased cell membrane calcium ATPase activity has been described in hypertension. 16 Similarly, workers in Detroit reported increases in red cell total calcium in hypertensives with diabetes specifically associated with suppressed calcium ATPase pump activity. 17 Suppressed Mg, levels characterized NIDDM subjects, with or without hypertension, and also were present in all hypertensive groups.…”

Section: Ob-hibp (N-23)mentioning

confidence: 98%

Cellular ions in hypertension, diabetes, and obesity. A nuclear magnetic resonance spectroscopic study.

et al. 1991

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To investigate the cellular basis linking hypertension, non-insulin-dependent diabetes melllrus (NIDDM), and obesity, we used 31 P and "F nuclear magnetic resonance spectroscopy to measure intracellular pH (pHJ, free magnesium (M&), and cytosolic free calcium (Ca,) in erythrocytes of obese and NIDDM subjects with and without hypertension. Compared with nonnotensive, nondiabetic controls (Ca^ 25.2 ±1.4 nM; Mg,, 232 ±8 fiM), Cat was elevated in both nonnotensive (36.8±2.7 nM, sig=0.005) and hypertensive (43.4±2.9 nM, sig=0.001) NIDDM subjects, and Mg, was concomitantly suppressed (nonnotensive: 206±ll juM, sig=0.05; hypertensive: 196±8 fiM, sig=0.001). Similar but less striking changes were noted in obese subjects. Values of pH, were significantly lower (sig=0.05) in all hypertensive groups compared with their nonnotensive controls. Continuous relations were observed for all subjects between Ca, and diastolic blood pressure (r=0.649,/7<0.001) and body mass index (r=0-565,p<0.001), between Mg, and diastolic blood pressure (r=-0.563, p<0.001) and fasting blood glucose (r=-0.580, p<0.001), and in diabetics, between pH, and diastolic blood pressure (r= -0.680, p<0.001). Thus, the constellation of elevated Ca, and suppressed Mg, and pH, levels is characteristic of the hypertensive state. These abnormalities of cellular ion handling in whole or in part common to hypertension, diabetes, and obesity may contribute to the pathophysiology of these syndromes and may help to explain their frequent clinical coexistence. (Hypertension 1991;17:951-957) T he long-recognized association of hypertension, obesity, and non-insulin-dependent diabetes mellitus (NIDDM) has received increasing attention.1 In particular, it has been suggested that the insulin resistance and concomitant hyperinsulinemia present in these disease states may represent a metabolic link mediating their increased clinical coincidence. -3At the cellular level, we previously have reported that levels of intracellular free magnesium (Mgi) are closely related to the height of the blood pressure and to the insulinemic response to glucose loading; the lower the Mg^ the higher the pressure and the greater the peripheral insulin resistance. -7 Similarly, we found that lower intracellular pH (pHj) values strongly correlated with both blood pressure and hyperinsulinemia. 58 We hypothesized that these

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Section: Ob-hibp (N-23)mentioning

confidence: 98%

Cellular ions in hypertension, diabetes, and obesity. A nuclear magnetic resonance spectroscopic study.

et al. 1991

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“…There are also a large number of studies suggesting that PMCA play a role in several different types of pathophysiologies (Lehotsky et al 2002), however, there are discrepancies in the literature. As an example, a decreased ATP-dependent Ca 2+ uptake has been shown to occur in PM vesicles isolated from hypertensive rat arterial smooth muscle (Kwan et al , 1980a(Kwan et al , 1980b, and in erythrocytes from animal and human models of hypertension (de la Sierra et al 1990;Vincenzi et al 1986;Postnov and Orlov 1983), and yet cultured hypertensive vascular smooth muscle cells show an increase in the levels of mRNA for PMCA (Monteith et al 1997). This matter is further confused by the observation that PMCA pump protein solubilized from erythrocytes and incorporated into liposomes has been shown to act under conditions like B-type Ca 2+ channels (Pinet et al 2002) that had been earlier reported in cardiac myocytes (Antoine et al 2001).…”

Section: Studies Using Transgenic Micementioning

confidence: 99%

Plasma membrane calcium pumps in smooth muscle: from fictional molecules to novel inhibitors

Pande

Grover²

2005

Can. J. Physiol. Pharmacol.

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Plasma membrane Ca2+ pumps (PMCA pumps) are Ca2+-Mg2+ ATPases that expel Ca2+ from the cytosol to extracellular space and are pivotal to cell survival and function. PMCA pumps are encoded by the genes PMCA1, -2, -3, and -4. Alternative splicing results in a large number of isoforms that differ in their kinetics and activation by calmodulin and protein kinases A and C. Expression by 4 genes and a multifactorial regulation provide redundancy to allow for animal survival despite genetic defects. Heterozygous mice with ablation of any of the PMCA genes survive and only the homozygous mice with PMCA1 ablation are embryolethal. Some PMCA isoforms may also be involved in other cell functions. Biochemical and biophysical studies of PMCA pumps have been limited by their low levels of expression. Delineation of the exact physiological roles of PMCA pumps has been difficult since most cells also express sarco/endoplasmic reticulum Ca2+ pumps and a Na+-Ca2+-exchanger, both of which can lower cytosolic Ca2+. A major limitation in the field has been the lack of specific inhibitors of PMCA pumps. More recently, a class of inhibitors named caloxins have emerged, and these may aid in delineating the roles of PMCA pumps.

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“…We have reported (2) a survey of 15 recent publications that quantified intracellular cal- (33) found that the basal pump activity in red blood cells from patients with essential hypertension was significantly less than that from normotensive control subjects. Although this pump has been demonstrated in vascular smooth muscle, these authors could not extrapolate their finding of its deficient activity in hypertension to this more relevant tissue.…”

Section: Calciummentioning

confidence: 99%

Plasma Membrane in Hypertension: Microviscosity and Calcium Stabilization.

1994

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Over the past decade the possibility of membrane abnormalities in hypertension has been studied very extensively. These studies reflect the putative significance of membrane abnormalities in the pathogenesis of this disease, and the need for resolution of the great divergence of the results that have been reported. Nevertheless, two sound generalizations have emerged from studies of the plasma membrane in hypertension:1) The microviscosity of the plasma membrane is elevated (fluidity is decreased). However, genetic studies have cast doubt on the possibility that the decreased fluidity of the plasma membrane plays a role in the cause of experimental hypertension.2) The stabilizing influence of calcium is diminished. The roles, if any, of these two abnormalities in the pathogenesis of hypertension require further study. Specific abnormalities, such as that of the Na/Li countertransport or Na/H exchange activity, may be useful phenotypic markers of subgroups of patients with essential hypertension. (Hypertens Res 1994; 17: 79-86) Key Words: cell membrane, membrane microviscosity, ion transport, lipid bilayer, calcium, spontaneously hypertensive rat Plasma membrane abnormalities have been associated with both experimental and clinical hypertension (1,2). The aim of this review is to summarize observations that characterize these abnormalities. It will be evident that the findings do not yet permit comfortable generalizations about the role, if any, played by the membrane abnormalities as a cause of hypertension. Furthermore, current literature includes serious controversies about the characterizations of the membrane abnormalities. Sodium Plasma membrane transport systems for sodium in hypertension received early attention. This interest followed recognition that the blood pressure in hypertension could be manipulated by changes in sodium intake (3) . It was also known that the hypertensive patient responded to a sodium load with an exaggerated natriuresis (4). Something seemed different about sodium metabolism in hypertension.Since it was also recognized that the blood pressure elevation resulted from vasoconstriction that increased total peripheral resistance (TPR), initial studies dealing with an abnormality in sodium metabolism were carried out on vascular smooth muscle in experimental hypertension. Forty years ago Tobian and Binion (5) studying renal and mineralocorticoid hypertension in rats observed an increase in sodium and water in the arteries of these animals. They introduced the concept of water-logging of the vessel wall as contributing to the increase in total peripheral resistance. Definitive studies were then carried out in the tail artery by Friedman (6) and the rat aorta by Jones (7). These studies (7) indicated that the permeability of the plasma membrane of vascular smooth muscle to sodium is increased in mineralocorticoid hypertension and in spontaneously hypertensive rats (SHR).New dimensions of interest arose in the membrane permeability to sodium when Postnov (8) reported that this param...

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Decreased calcium pump adenosine triphosphatase in red blood cells of hypertensive subjects.

Cited by 65 publications

References 48 publications

Cellular ions in hypertension, diabetes, and obesity. A nuclear magnetic resonance spectroscopic study.

Cellular ions in hypertension, diabetes, and obesity. A nuclear magnetic resonance spectroscopic study.

Plasma membrane calcium pumps in smooth muscle: from fictional molecules to novel inhibitors

Plasma Membrane in Hypertension: Microviscosity and Calcium Stabilization.

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