Cyclic nucleotides attenuate thrombin-evoked alterations in parameters of platelet Na/H antiport. The role of cytosolic Ca.

Kimura, Masayuki; Lasker, Norman; Aviv, Abraham

doi:10.1172/jci115692

Cited by 30 publications

(22 citation statements)

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“…3), whereas it does not influence the Na+/H+-exchange rate in platelets (Kimura et al, 1992) and in LLC-PK1 cultured renal cell line (Cantiello and Ausiello, 1986). In contrast to platelets (Kimura et al, 1992), LLC-PKI renal cell line (Cantiello and Ausiello, 1986) and erythrocytes (Fig. 3), 8-Br-cGMP inhibits the Na+/H+-exchange rate in chicken enterocytes (Semrad et a].., 1990) by increasing the cytoplasmic Ca" concentration.…”

Section: Discussionmentioning

confidence: 99%

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na⁺/H⁺ exchange

Petrov

Améry

Lijnen

1994

European Journal of Biochemistry

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Human atrial natriuretic peptide (ANP) fragments ANP-(127-150) or ANP-I11 and ANP-(127-149) or ANP-I1 activate Na+/H+ exchange in human erythrocytes at concentrations as low as 1 pM. Both ANP-(127-147) or ANP-I and ANP-(129-150) or des-Ser5, Ser6-ANP-I11 have no effect on erythrocyte Na+/H+ exchange. ANP-I11 also produces a time-dependent increase of intraerythrocyte guanosine 3',5'-phosphate (cGMP) Concentration. M&B 22,948, a specific inhibitor of cGMP phosphodiesterase, increases Na+/H+ exchange and the intracellular concentration of cGMP. Both 8-bromoguanosine 3',5'-phosphate (8-Br-cGMP) and dibutyryl-cGMP mimic the effect of ANP-I11 on erythrocyte Na+/H+ exchange. Our data suggest that human erythrocytes possess guanylate-cyclase activity stimulated by ANP-I11 and that activation of Na+/H+ exchange by this peptide is mediated by cGMP. Human erythrocytes display a high degree of sensitivity to ANP-I11 or ANP-I1 and a specificity for ANP-fragment structures just as cells with established ANP-specific receptors.Atrial natriuretic peptides (ANP) act on the Na+/H+-exchange rate in cells, which contain specific ANP receptors, through the elevation of intracellular guanosine 3',5'-phosphate (cGMP) concentration (Semrad et al., 1990) or via a cGMP-independent pathway (Gupta et al., 1989). Semrad et al. (1990) have reported a cGMP-mediated inhibition of the Na+/H+-exchange rate by ANP in chicken enterocytes, whereas Gupta et al. (1989) found a cGMP-independent stimulation of the Na+/H+-exchange rate in rabbit aorta segments.Specific receptors for ANP fragments in human erythrocytes have not been determined. There is also controversy whether or not intracellular cGMP synthesis occurs. Indeed, cholinergic agonists stimulate (Tang et al., 1984) or do not affect (Sekar and Hokin, 1986) cGMP production, and guanylate-cyclase activity has not been determined (Bohme et al., 1974) in human erythrocytes. Basal intraerythrocyte cGMP concentration is attributed to its passive uptake (deBari and Bennun, 1982). In the present study we report that human (h)ANP-I11 increases both Na+/H+ exchange and intracellular cGMP concentration in human erythrocytes. Its effect is mimicked by 8-Br-cGMP or dibutyryl-cGMP. The effects of other hANP fragments (ANP-11, ANP-I, des-Ser5, Ser6-ANP-111) on the Na+/H+ exchange depend on their molecular structures.Correspondence to P. Lijnen, Hypertension Unit, Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, BelgiumAbbreviations. ANP, atrial natriuretic peptide ; cGMP, guanosine 3',S'-phosphate; iBuMeXan, 3-isobutyl-I-methylxanthine; M&B 22,948, 2-O-propoxyphenyl-8-azapurin-6-one; 8-Br-cGMP, 8-bromo-guanosine 3',5'-phosphate; ANF, atrial natriuretic factor; h, human. MATERIALS AND METHODS Erythrocyte preparationBlood from healthy donors was drawn into heparinized tubes and centrifuged at 2000 g for 7 min at 4°C. The plasma and buffy coat were removed by aspiration, and the erythrocytes were then washed four times with an ice-cold solution consisting of 150 mM KC1,0.15 mM MgC1, and 10 mM glucose. The ...

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Section: Discussionmentioning

confidence: 99%

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na⁺/H⁺ exchange

Petrov

Améry

Lijnen

1994

European Journal of Biochemistry

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“…Activation of platelets by a variety of agonists (i.e., thrombin and ADP) is associated with stimulation of the Na + /H + exchanger [35]. This mode of activation of the Na + /H + exchanger usually induces a rise in cytosolic Ca 2+ , granule secretion, stimulation of shape change, and aggregation [35].…”

Section: Discussionmentioning

confidence: 99%

“…This mode of activation of the Na + /H + exchanger usually induces a rise in cytosolic Ca 2+ , granule secretion, stimulation of shape change, and aggregation [35]. Basal pHi is normally maintained within a narrow range, and even small changes in pHi may have significant effects on platelet activity.…”

Section: Discussionmentioning

confidence: 99%

“…In many cell types (i.e., smooth muscle cells), Na + /H + exchange activity is regulated by [Ca 2+ ]i [36]. Furthermore, Kimura et al [35] reported that cyclic nucleotides (i.e., cyclic AMP) modulate Na + /H + exchange in human platelets. Inhibition of Na + /H + exchange by cyclic AMP has also been demonstrated in other cells, such as epithelia of the urinary system and in osteoblast-like cells [37].…”

Section: Discussionmentioning

confidence: 99%

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Inhibitory mechanisms of low concentrations of oxidized low-density lipoprotein on platelet aggregation

et al. 2005

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SummaryThe intracellular mechanisms underlying oxidized low-density lipoprotein (oxLDL)-signaling pathways in platelets are not yet completely understood. Therefore, the aim of this study was to further examine the effects of oxLDL in prevention of platelet aggregation. In this study, oxLDL concentration-dependently (40-120 lg/ml) inhibited platelet aggregation in human platelet-rich plasma stimulated by agonists. Moreover, oxLDL (40 and 80 lg/ml) markedly decreased the fluorescence intensity of platelet membranes tagged with diphenylhexatriene. Rapid phosphorylation of a protein of Mr 47,000 (P47), a marker of protein kinase C activation, was triggered by PDBu (150 nM). This phosphorylation was markedly inhibited by oxLDL (40 and 80 lg/ml) in phosphorus-32-labeled platelets. In addition, oxLDL (40 and 80 lg/ml) markedly increased levels of cyclic AMP and cyclic AMP-induced vasodilator-stimulated phosphoprotein (VASP) Ser 157 phosphorylation. The thrombin-evoked increase in pHi was inhibited in the presence of oxLDL (40 and 80 lg/ml). These results indicate that the antiplatelet activity of oxLDL may involve the following pathways. (1) oxLDL may initially induce conformational changes in platelet membranes, leading to inhibition of the activation of protein kinase C, followed by inhibition of P47 protein phosphorylation, and intracellular Ca 2+ mobilization. (2) oxLDL also activated formation of cyclic AMP and cyclic AMP-induced VASP Ser 157 phosphorylation, resulting in inhibition of the Na + /H + exchanger; this leads to reduced intracellular Ca 2+ mobilization, and ultimately to inhibition of platelet aggregation. This study further provides new insights concerning the effects of low concentrations of oxLDL on platelet aggregation.

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“…20 - 21 Platelet hyperactrvity is frequently associated with a rise in Ca<; the resulting increase in metabolic activity and the stimulation of the plasma membrane Ca-ATPase (an exchanger of cellular calcium for extracellular proton) would promote cellular acidification. Coupled with an increase in the Z,, an alkaline shift in the X; could therefore serve to attenuate this tendency for cytosolic acidification.…”

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confidence: 99%

Platelet sodium-hydrogen antiport in obese and diabetic black women.

Zentay¹,

Reddi²,

Raguwanshi³

et al. 1992

Hypertension

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In this investigation we correlated platelet Na-H antiport parameters with blood pressure and serum lipids in a sample population of non-insulin-dependent diabetic obese, nondiabetic obese, and nondiabetic nonobese black women. Parameters of the Na-H antiport were examined in aspirin-treated platelets. These parameters were not altered in resting or in thrombin-stimulated platelets of diabetic patients. The activity index of platelet Na-H antiport after thrombin stimulation was positively correlated with the blood pressure (systolic blood pressure, r=0.5320 and p=0.0001; diastolic blood pressure, r=0-5123 and p=0.0017). Lower high density lipoprotein cholesterol levels were associated with an alkaline shift in the cytosolic pH set point for activation of the Na-H antiport. Highly significant correlations were also observed between the total cholesterol/high density lipoprotein cholesterol ratio and the cytosolic pH set point for activation of the Na-H antiport These correlations were independent of diabetes or the body mass index. Together, these observations indicate that parameters of platelet Na-H antiport are altered with an increase in blood pressure and a decrease in serum high density lipoprotein cholesterol. (Hypertension 1992^0:549-554) KEY WORDS • diabetes mellltus, non-insulin-dependent • lipoproteins, HDL • hypertension, essential N on-insulin-dependent diabetes mellitus(NIDDM) is frequently accompanied by elevated blood pressure, whereas essential hypertension is usually associated with insulin resistance.1 " 4 NIDDM and essential hypertension also share a tendency for accelerated atherosclerotic and thromboembolic complications, 5 " 8 which may arise from serum lipid abnormalities and platelet hyperactrvity 9 "12 that are commonly observed in these diseases.Recent studies have indicated that the activity of the Na-H antiport is increased in platelets of patients with essential hypertension, 13 -17 a process that may relate to platelet hyperactivity. Since NIDDM and essential hypertension appear to express common cellular perturbations, it is possible that these include altered platelet Na-H antiport activity. The present study was therefore designed to answer the following questions: are parameters of platelet Na-H antiport altered in NIDDM and obesity (two conditions commonly associated with essential hypertension) and are there any relations be-

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Cyclic nucleotides attenuate thrombin-evoked alterations in parameters of platelet Na/H antiport. The role of cytosolic Ca.

Cited by 30 publications

References 54 publications

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na⁺/H⁺ exchange

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na⁺/H⁺ exchange

Inhibitory mechanisms of low concentrations of oxidized low-density lipoprotein on platelet aggregation

Platelet sodium-hydrogen antiport in obese and diabetic black women.

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Cyclic nucleotides attenuate thrombin-evoked alterations in parameters of platelet Na/H antiport. The role of cytosolic Ca.

Cited by 30 publications

References 54 publications

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na+/H+ exchange

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na+/H+ exchange

Inhibitory mechanisms of low concentrations of oxidized low-density lipoprotein on platelet aggregation

Platelet sodium-hydrogen antiport in obese and diabetic black women.

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Product

Resources

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Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na⁺/H⁺ exchange

Role of cyclic GMP in atrial‐natriuretic‐peptide stimulation of erythrocyte Na⁺/H⁺ exchange