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Biomedical subjects

W Zidek

Publications and source records attributed to W Zidek.

At least 163 records · Page 9Linked to original sources
PubMed1995

The impact of lacidipine, a novel dihydropyridine calcium antagonist, on carbohydrate and lipid metabolism.

In an open, multicenter study, the calcium antagonist lacidipine was tested for efficacy and safety, particularly with respect to any influence on lipid and carbohydrate metabolism. The study was performed in 2,127 patients with essential hypertension. The patients were treated orally, with lacidipine in a dosage of 2-6 mg once daily for 48 weeks. Lacidipine significantly reduced both systolic and diastolic blood pressure by 20 +/- 17 mm Hg and 14 +/- 10 mm Hg, respectively, from baseline values (both p < 0.0001). Decreases in blood pressure were achieved without any adverse effects on lipid and carbohydrate metabolism, either in the total group or in subsets of diabetic or hyperlipidemic patients. It is concluded that lacidipine is a safe and effective drug in the long-term antihypertensive treatment of patients with essential hypertension and with concomitant metabolic disorders such as diabetes mellitus or dyslipidemia.

Calcium Channel Blockers↗
PubMed1995

Diadenosine polyphosphate-induced increase in cytosolic free calcium in vascular smooth muscle cells.

OBJECTIVE: To evaluate the effects of two new endogenous vasoconstricting substances, diadenosine pentaphosphate (AP5A) and diadenosine hexaphosphate (AP6A) on the cytosolic free calcium concentration in vascular smooth muscle cells. METHODS: Spectrofluorophotometric measurements of cytosolic Ca2+ were conducted in monolayers of cultured rat vascular smooth muscle cells using the calcium-sensitive fluorescent dye fura-2. RESULTS: The resting Ca2+ concentration in vascular smooth muscle cells was 80 +/- 5 nmol/l (mean +/- SEM; n = 39). The addition of 10 mu mol/l AP5A or AP6A significantly increased Ca2+ in vascular smooth muscle cells to 248 +/- 55 and 358 +/- 124 nmol/l, respectively. The sustained increase in Ca2+ after administration of AP5A or AP6A was 143 +/- 40 and 148 +/- 57 nmol/l, respectively. Diadenosine polyphosphates induce a transplasmamembrane calcium influx as detected by experiments in the absence of external calcium or by using the manganese quenching technique to report unidirectional calcium fluxes. The effects of diadenosine polyphosphates were compared to those of the well known vasoconstrictor angiotensin II, which increased Ca2+ in vascular smooth muscle cells by 1053 +/- 174 nmol/l. CONCLUSIONS: Diadenosine polyphosphates increase Ca2+ in vascular smooth muscle cells, thereby regulating the contractility of vascular smooth muscle and subsequently blood pressure.

Animals↗
PubMed1995

Different effects of hypertension, atherosclerosis and hyperlipidaemia on arterial distensibility.

OBJECTIVE: To investigate the different effects of hypertension, hyperlipidaemia and atherosclerosis on the visco-elastic properties of large arteries. DESIGN: Vessel wall properties were determined in patients who had been subjected for the first time to coronary arteriography. Normotensive patients with no coronary disease (n = 15), one-vessel disease (n = 15) or two- or three-vessel disease (n = 15), 15 treated hypertensive patients (mean +/- SEM duration of hypertension 9.6 +/- 1.7 years) with no coronary disease and normocholesterolaemia and 15 healthy controls were matched for blood pressure, age and sex. METHODS: Arterial distension of the common carotid artery was determined by using a multigate Doppler system. The blood pressure curve was recorded by finger plethysmography. RESULTS: The end-diastolic diameter was significantly higher in the hypertensives (P<0.05) but not significantly different in the normotensives compared with the controls. Arterial distensibility was significantly lower in the hypertensive group [(13.3 +/- 0.8) x 10(-3)/kPa] than in the controls [(19.1 +/- 1.5) x 10(-3)/kP; P<0.01), in the group with no coronary disease [(18.8 +/- 1.3) x 10(-3)/kPa; P<0.01] and in those with one-vessel disease [(17.7 +/- 1.4) x 10(-3)/kPa; P<0.05]. Arterial distensibility was not significantly lower in the hypertensives than in the group with two- or three-vessel disease [(15.0 +/- 1.0) x 10(-3)/kPa; NS). No significant correlation was found between cholesterol or lipoprotein(a) levels and arterial distensibility in the normotensive patients. CONCLUSIONS: Hypertension is the predominant factor affecting the visco-elastic properties of large arteries. Arterial compliance is significantly altered only in extensive atherosclerosis.

Arteriosclerosis↗
PubMed1994

Filling state of intracellular Ca2+ pools triggers trans plasma membrane Na+ and Ca2+ influx by a tyrosine kinase-dependent pathway.

The relations between the filling state of intracellular calcium stores that are regulated by the endoplasmic Ca(2+)-ATPase and trans plasma membrane sodium and calcium influx were investigated. The effects of specific inhibition of endoplasmic Ca(2+)-ATPase by thapsigargin, cyclopiazonic acid, and 2,5-di-(tert-butyl)-1,4-benzohydroquinone (BHQ) on cytosolic free sodium concentration ([Na+]i) and cytosolic free calcium concentration ([Ca2+]i) were evaluated in lymphocytes from healthy subjects using the fluorescent dyes sodium-binding benzofuran isophthalate and fura2. The specific inhibition of endoplasmic Ca(2+)-ATPase by thapsigargin, cyclopiazonic acid, or BHQ increased lymphocytic [Na+]i and [Ca2+]i. The thapsigargin-induced [Na+]i increase was abolished in the absence of external sodium, indicating that thapsigargin induced a trans plasma membrane sodium influx. In the absence of external calcium the thapsigargin-induced [Ca2+]i increase was significantly reduced, whereas the thapsigargin-induced [Na+]i increase remained the same. This finding indicates that the filling state of intracellular calcium pools rather than the elevation of [Ca2+]i per se regulates the plasma membrane permeability for sodium in lymphocytes. The inhibition of the tyrosine kinase by genistein inhibited the thapsigargin-induced increases of both [Na+]i and [Ca2+]i in lymphocytes. The present study shows that the filling state of intracellular thapsigargin-sensitive calcium pools regulates trans plasma membrane sodium and calcium influx via a tyrosine kinase-dependent pathway.

Calcium↗
PubMed1994

Thapsigargin-induced [Ca2+]i increase activates sodium influx in human platelets.

Using the fluorescent dyes sodium-binding-benzofuran-isophthalate and fura-2 cytosolic free sodium concentration ([Na+]i) and cytosolic free calcium concentration ([Ca2+]i) were investigated in intact human platelets in order to characterize the effect of elevated [Ca2+]i on [Na+]i. Spectrofluorometric studies of [Ca2+]i and [Na+]i in intact platelets were done after specific inhibition of endoplasmic Ca-ATPase by thapsigargin. Thapsigargin increased [Ca2+]i and [Na+]i in platelets. Addition of thapsigargin increased [Na+]i from 23.5 +/- 2.9 mM to 51.6 +/- 11.1 mM (mean +/- S.E., P < 0.05). The thapsigargin induced [Na+]i increase was also seen in the absence of extracellular calcium. In the absence of external sodium the thapsigargin induced [Na+]i increase was abolished, indicating that thapsigargin induced [Na+]i increase was due to sodium influx. Thapsigargin induced sodium influx was blocked after administration of NiCl2. The present results support the idea that the filling state of intracellular calcium stores regulate plasma permeability for sodium.

Blood Platelets↗
PubMed1994

Diadenosine phosphates and the physiological control of blood pressure.

Our understanding of the regulation of vascular tone has been extended since the identification of vasoactive agents such as the atrial natriuretic peptides, endothelial-derived relaxing factor and endothelin. Unidentified vasopressive agents have been found in platelets. Here we isolate these vasopressors and identify them as diadenosine pentaphosphate (AP5A) and diadenosine hexaphosphate (AP6A) by chromatography, mass spectrometry, ultraviolet spectroscopy and enzymatic cleavage. In the vasculature of isolated perfused rat kidney, both diadenosine phosphates were active at a concentration of 10(-9) M; in aortic rings, contractions were elicited at 10(-8) M. Intra-aortic injection in the rat caused a prolonged increase in blood pressure. We conclude that AP5A and AP6A may play a part in local vasoregulation and possibly in the regulation of blood pressure.

5'-Nucleotidase↗
PubMed1994

Early detection of distal symmetrical polyneuropathy during HIV infection by paired stimulation of sural nerve.

In 203 HIV infected patients in various clinical stages neurological examination, paired stimulation (LPSS), nerve conduction velocity (NCVS) and amplitude (AMPS) of the sural nerve, distal latency (DLP), nerve conduction velocity (NCVP), amplitude (AMPP) and F waves of the peroneal nerve were recorded. Neurological examination revealed symptoms and clinical signs of polyneuropathy in 67 (33%) (WR 1-6) of the patients. LPSS after paired stimulation was abnormal in 25.5%, NCVS in 14.2%, AMPS in 9.8%, NCVP in 11.8%, DLP in 11.2%, AMPP in 5.9% and FWP in 14.6%. Our findings indicate a high incidence of peripheral nerve system involvement during HIV infection. In 11.5% of all patients only LPSS proved polyneuropathy. Neurophysiological results from HIV infected patients with symptoms and clinical signs of polyneuropathy were statistically significantly different from HIV infected patients without symptoms and clinical signs of polyneuropathy. The delay of LPSS represents the most sensitive neurophysiological indicator of polyneuropathy during HIV infection and announces the onset of peripheral nerve disease even in early stages of infection, according to Walter Reed staging classification 1 and 2 (approx. 20%).

Adult↗
PubMed1994

Captopril inhibits the agonist-induced increase of cytosolic free Ca2+ in glomerular mesangial cells.

To evaluate the underlying mechanism of the putative renal protective effects of angiotensin converting enzyme (ACE) inhibitors, the modulatory action of captopril on the angiotensin II (Ang II) and platelet-derived growth factor (PDGF)-induced increase of cytosolic free calcium concentration ([Ca2+]i) was investigated in cultured glomerular mesangial cells (MC) from spontaneously hypertensive rats from the Münster strain (SHR) and normotensive Wistar-Kyoto rats (WKY). Resting [Ca2+]i was not affected by captopril in MC from either SHR or WKY. Captopril inhibited the Ang II-induced [Ca2+]i increase in MC from both SHR and WKY in a dose-dependent and time-dependent fashion. The preincubation of MC with 1 mumol/liter captopril for 40 minutes significantly reduced the Ang II-induced [Ca2+]i increase in SHR from 167 +/- 30 nmol/liter (N = 17) to 74 +/- 20 nmol/liter (N = 8, P < 0.05) and in WKY from 102 +/- 42 nmol/liter (N = 14) to 43 +/- 12 nmol/liter (N = 7, P < 0.05). After removal of external calcium there was no significant effect of captopril on the Ang II-induced [Ca2+]i increase. With the Mn2+ quenching technique, it was confirmed that captopril affects Ca2+ influx. Phospholipase C activity as estimated by diacylglycerol formation was not changed by captopril. The preincubation of MC with 1 mumol/liter captopril for 40 minutes significantly reduced the PDGF-induced [Ca2+]i increase in SHR from 166 +/-54 nmol/liter (N = 9) to 31 +/- 19 nmol/liter (N = 6, P < 0.01) and in WKY from 127 +/- 31 nmol/liter (N = 11) to 61 +/- 32 nmol/liter (N = 5, P < 0.05). Similarly captopril reduced the [Ca2+]i increase induced by endothelin and vasopressin. The results indicate that the actions of Ang II and PDGF on MC are modulated by captopril, probably resulting in the impairment of the calcium dependent contractile response of mesangial cells.

Angiotensin II↗
PubMed1994

Reduced cytosolic free sodium concentration in vascular smooth muscle cells from spontaneously hypertensive rats.

1. Cytosolic free sodium concentration and sodium transport systems were measured in intact cultured vascular smooth muscle cells from spontaneously hypertensive rats of the Münster strain and from normotensive Wistar-Kyoto rats using the sodium-sensitive fluorescent dye sodium-binding benzofuran isophthalate. 2. Resting cytosolic free sodium concentration was significantly lower in vascular smooth muscle cells from spontaneously hypertensive rats than from Wistar-Kyoto rats (10.2 +/- 1.5 mmol/l, n = 26, versus 19.4 +/- 2.5 mmol/l, n = 20, P < 0.01). 3. Inhibition of Na+, K(+)-ATPase by ouabain caused a dose-dependent increase in cytosolic free sodium concentration in spontaneously hypertensive rats and Wistar-Kyoto rats. 4. Activation of Na(+)-Ca2+ exchange by ionomycin increased cytosolic free sodium concentration in both strains. However, the ionomycin-induced increase in cytosolic free sodium concentrations was significantly higher in vascular smooth muscle cells from spontaneously hypertensive rats than from Wistar-Kyoto rats (220 +/- 35% of the resting cytosolic free sodium concentration versus 148 +/- 27%; P < 0.05). The ionomycin-induced increase in cytosolic free sodium concentration was prevented in the absence of external sodium or by inhibition of Na(+)-Ca2+ exchange by NiCl2. 5. Activation of Na(+)-H+ exchange by intracellular acidification of vascular smooth muscle cells with propionic acid increased cytosolic free sodium concentration in each strain (19.6 +/- 5.7 versus 16.3 +/- 3.2 mmol/l). 6. It is concluded that concepts concerning the role of cytosolic free sodium concentration in the pathogenesis of primary hypertension need to be reinvestigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cellular Ca2+ ATPase activity in diabetes mellitus.

Basal and maximal Ca2+ ATPase activity was studied in erythrocytes of 29 healthy controls, 15 patients with insulin-dependent diabetes mellitus (IDDM) and 22 patients with non-insulin-dependent diabetes mellitus (NIDDM). Basal and maximal Ca2+ ATPase activity was significantly decreased in insulin-dependent diabetes mellitus (8.4 +/- 0.5 and 22.5 +/- 1.1 pmol/10(6) RBC/min) and non-insulin-dependent diabetes mellitus (7.3 +/- 1.0 and 18.6 +/- 1.8 pmol/10(6) RBC/min) compared to healthy controls (9.3 +/- 1.0 and 24.6 +/- 1.1 pmol/10(6) RBC/min). Maximal Ca2+ ATPase activity showed a significant correlation to systolic blood pressure in both insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus. There was no significant correlation of maximal Ca2+ ATPase activity to fasting serum glucose concentration and to HbA1 levels. Maximal Ca2+ ATPase activity was significantly correlated to creatinine clearance in non-insulin-dependent diabetes mellitus, but not in insulin-dependent diabetes mellitus. It is concluded that a decreased cellular Ca2+ ATPase activity may predispose to the development of hypertension in diabetes mellitus.

Aged↗
PubMed1994

Albuminuria in HIV-infected patients.

Albumin excretion, Analysis of urinary proteins by polyacrylamide gel electrophoresis (PAGE), and clinical evaluation were performed in 90 HIV-infected patients to assess subclinical renal involvement in HIV infection. Thirteen percent of all patients showed an albumin excretion > 20 mg/liter. Seven of four homosexual patients had albuminuria. Albuminuria occurred exclusively with T4 cell counts below 200/mm3. Polyacrylamide gel electrophoresis indicated glomerular lesions and showed no tubular proteinuria in patients with increased albumin excretion. It is concluded that subclinical renal involvement is not uncommon in HIV infection with T4 cell counts > 200/mm3. HIV-associated nephropathy and heroin-associated nephropathy may not be the main causes of renal involvement. In some cases, opportunistic viral infections may be the cause of microalbuminuria.

Adolescent↗
PubMed1994

Role of Na(+)-Ca2+ exchange in agonist-induced changes in cytosolic Ca2+ in vascular smooth muscle cells.

Changes in cytosolic free calcium concentration ([Ca2+]i) induced by angiotensin II (ANG II), arginine vasopressin (AVP), angiotensin III (ANG III), norepinephrine (NE), or thapsigargin were investigated after inhibition of the Na(+)-Ca2+ exchange in vascular smooth muscle cells (VSMC) from Wistar-Kyoto rats by use of the fluorescent dye technique. The ANG II-induced peak [Ca2+]i increase was significantly enhanced after inhibition of Na(+)-Ca2+ exchange by NiCl2 or 1,3-dimethyl-2-thiourea (DMTU): control, 99 +/- 9 (SE) nM (n = 64); NiCl2, 181 +/- 23 nM (n = 23; P < 0.01); DMTU, 182 +/- 35 nM (n = 10; P < 0.05). In the absence of external calcium, the inhibition of the Na(+)-Ca2+ exchange by NiCl2 also enhanced the ANG II-induced [Ca2+]i increase. Inhibition of Na(+)-Ca2+ exchange by removal of external sodium, which was replaced by choline, augmented the ANG II-induced [Ca2+]i increase to 174 +/- 26 nM (n = 11; P < 0.05 compared with control). The inhibition of the protein kinase C activity by isoquinoline-sulfonyl-O-2-methylpiperazine blocked the enhancing effect of NiCl2 on ANG II-induced [Ca2+]i increase. The inhibition of the Na(+)-Ca2+ exchange did not enhance the increase in [Ca2+]i induced by ANG III, NE, or thapsigargin. The AVP-induced changes in [Ca2+]i were not significantly different in the presence or absence of NiCl2. It is concluded that the recovery of resting [Ca2+]i after stimulation by ANG II is mediated by calcium efflux via the Na(+)-Ca2+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1994

Differential effects of insulin-like growth factor I and platelet-derived growth factor on growth response, matrix formation, and cytosolic free calcium of glomerular mesangial cells of spontaneously hypertensive and normotensive rats.

In this study, we compared the cellular functions of cultured glomerular mesangial cells (MC) from spontaneously hypertensive rats (SHR) and from normotensive Wistar-Kyoto rats (WKY) in response to the growth factors insulin-like growth factor I (IGF-I) and platelet-derived growth factor (PDGF). IGF-I and PDGF at a concentration above 2 ng/ml and a combination of both tested growth factors exerted a highly elevated growth response of SHR MC versus WKY MC. The total RNA synthesis induced by IGF-I and PDGF was increased in SHR MC as compared with WKY MC, while the overall protein synthesis showed no differences between both strains. Analysis of cell-associated fibronectin accumulation and incorporation of proline into collagenous proteins revealed an enhanced basal and PDGF-stimulated matrix formation of SHR MC which was not dependent on the increased production of autocrine matrix-stimulatory mediators by SHR MC. Changes of cytosolic free calcium - [Ca2+]i - could not be correlated with the enhanced responsiveness of SHR MC to the tested growth factors. The described differences of cellular functions between SHR and WKY MC may contribute to pronounced glomerular alterations such as glomerulosclerosis seen in primary and secondary forms of hypertension.

Animals↗
PubMed1994

Effect of lisinopril and metoprolol on arterial distensibility.

Apart from lowering blood pressure, antihypertensive drugs may influence vessel wall function. In a randomized double-blind study, the effect of lisinopril and metoprolol on arterial distensibility was studied in 40 patients with essential hypertension. After a placebo run-in period, the patients were randomly treated with metoprolol (50, 100, or 200 mg) or lisinopril (5, 10, or 20 mg) for 10 weeks. In the lisinopril group, blood pressure decreased after 10 weeks of therapy from 173 +/- 10/102 +/- 5 to 155 +/- 10/85 +/- 3 mm Hg and in the metoprolol group from 167 +/- 12/102 +/- 4 to 153 +/- 8/84 +/- 3 mm Hg. Diameter (millimeters), relative change in diameter (percent), and distensibility (10(-3)/kPa) of the left common carotid artery were determined after the placebo run-in period and after 6 and 10 weeks of antihypertensive therapy. A multigate Doppler system was used to measure the vessel wall movements by Doppler analysis in M-mode; blood pressure was recorded by finger plethysmography (Finapres). Neither lisinopril nor metoprolol influenced the end-diastolic diameter of the common carotid artery after 6 and 10 weeks of treatment. In the lisinopril group, a significant increase of percent change in diameter (P < .05 compared with the baseline value; P < .05 compared with the metoprolol group) and distensibility (P < .01 compared with the baseline value; P < .05 compared with the metoprolol group) was observed. The results show that lisinopril but not metoprolol improves arterial distensibility in essential hypertension. Pressure-independent effects of angiotensin converting enzyme inhibitors may be important modulators of adaptive changes in the arterial wall.

Adult↗
PubMed1994

Increased cytosolic sodium and reduced Na,K-ATPase activity in transgenic rats.

The transgenic rat TGR(mRen2)27 is a new monogenetic model in hypertension research that develops fulminant hypertension after the mouse Ren-2d renin gene has been integrated into its genome. To evaluate the molecular mechanism of development of hypertension in this animal model, we measured cytosolic free sodium concentration in intact lymphocytes from seven transgenic rats and eight age-matched normotensive Sprague-Dawley rats using the novel sodium-sensitive fluorescent dye sodium-binding benzofuranisophthalate. Resting cytosolic sodium was significantly higher in transgenic rats compared with Sprague-Dawley rats (31.7 +/- 2.2 versus 18.2 +/- 0.4 mmol/L, mean +/- SEM, P < .001). Inhibition of Na,K-ATPase by 0.5 mmol/L ouabain for 5 minutes significantly increased lymphocytic cytosolic sodium in Sprague-Dawley rats to 36.5 +/- 3.4 mmol/L (P < .001 compared with resting value), whereas no significant change could be observed in transgenic rats (35.4 +/- 0.6 mmol/L), indicating that Na,K-ATPase is less responsive in transgenic rats. The Na,K-ATPase activity from erythrocytes was measured with an enzyme-linked assay. Na,K-ATPase activity was significantly reduced in transgenic rats compared with Sprague-Dawley rats (4.0 +/- 0.3 versus 8.1 +/- 0.6 U/L, P < .001). We concluded that reduced Na,K-ATPase activity leads to elevated cytosolic sodium in this model of genetic hypertension.

Animals↗
PubMed1994

Reduced sodium-proton exchange activity in lymphocytes from transgenic rats.

We investigated sodium-proton (Na(+)-H+) exchange activity in transgenic TGR(mRen-2)27 rats, a strain showing fulminant hypertension after the mouse Ren-2d renin gene has been integrated into its genome, in age-matched normotensive Sprague-Dawley (SD) rats, in spontaneously hypertensive rats (SHR) from the Münster strain, and in normotensive Wistar-Kyoto (WKY) rats. From each strain Na(+)-H+ exchange activity was determined in lymphocytes using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM) by measuring the recovery rate of cytosolic pH (pHi) after intracellular acidification. Resting pHi was not significantly different in transgenic rats (n = 10) compared with SD rats (n = 10) (7.305 +/- 0.038 versus 7.337 +/- 0.031; mean +/- SEM), but resting pHi was significantly lower in lymphocytes from SHR (n = 12) compared with their normotensive WKY counterparts (n = 12) (7.232 +/- 0.030 versus 7.377 +/- 0.022; P < .01). Na(+)-H+ exchange activity was significantly lower in lymphocytes from transgenic rats compared with SD rats (5.102 +/- 0.561 versus 7.385 +/- 0.491 x 10(-3) dpHi/s; P < .01), whereas Na(+)-H+ exchange was significantly enhanced in lymphocytes from SHR compared with WKY rats (5.564 +/- 0.432 versus 3.921 +/- 0.433 x 10(-3) dpHi/s; P < .05). The apparent half-maximal activation of Na(+)-H+ exchange was not significantly different in the strains tested. The present study indicates that hypertension in transgenic rats is not related to Na(+)-H+ exchange overactivity.

Animals↗
PubMed1994

Effect of magnesium on cytosolic free sodium in human lymphocytes.

Cytosolic free sodium concentration ([Na+]i) was measured in intact human lymphocytes using the novel sodium-sensitive fluorescent dye sodium-binding benzofuran-isophthalate. In the presence of 1 mmol/l external Mg2+ the resting [Na+]i was significantly lower compared to the value in the absence of external Mg2+ (22.7 +/- 1.1 mmol/l vs. 37.6 +/- 1.4 mmol/l; p < 0.0001). The thapsigargin induced [Na+]i increase was significantly lower in the presence of 1 mmol/l external Mg2+ compared to the value in the absence of external Mg2+ (73.4 +/- 6.0 mmol/l vs. 120.7 +/- 5.8 mmol/l; p < 0.001). Since Mg2+ is known to be a cofactor of the membrane Na+,K(+)-ATPase these measurements in intact lymphocytes indicate that deprivation of external Mg2+ causes an increase of [Na+]i.

Calcium-Transporting ATPases↗