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Biomedical subjects

M Barbagallo

Publications and source records attributed to M Barbagallo.

At least 19 recordsLinked to original sources

Bisphosphonates and atherosclerosis: why?

The increasing knowledge on bone calcification processes has revealed some similarities with vascular tissue, where calcifications of arteries and cardiac valves contribute to several cardiovascular problems, such as heart failure, systolic hypertension, and myocardial and peripheral ischemic disease. Bisphosphonates have been used extensively for over two decades for the treatment of diseases associated with excessive bone resorption, i.e., osteoporosis, osteolytic bone metastasis, hypercalcemia and Paget's disease, by blocking osteoclastic function. Etidronate, pamidronate and clodronate has been shown to inhibit the development of experimental atherosclerosis, and proposed mechanisms for this action include inhibition of arterial calcification and lipid accumulation, degradation of atherogenic LDL-cholesterol and reduced foam cell formation. Bisphosphonates inhibit various enzymes involved in cholesterol biosynthesis and suppress macrophages in atheromatous lesions. The possibility of pharmacological agents that effectively treat both osteoporosis and atherosclerosis is attractive, however, current evidence is not conclusive and further research is necessary to confirm these actions in the clinical setting.

Apoptosis↗

Safety of rofecoxib in subjects with a history of adverse cutaneous reactions to aspirin and/or non-steroidal anti-inflammatory drugs.

BACKGROUND: Adverse reactions to non-steroidal anti-inflammatory drugs (NSAID)s are frequent, and the need to identify a safe alternative drug is a common problem in clinical practice. OBJECTIVE: To assess the tolerability of rofecoxib, a drug that specifically inhibits COX-2, in a group of NSAID-sensitive patients. METHODS: One-hundred and four subjects (29 males and 75 females, mean age 35.6 +/- 14.1) were enrolled. All subjects had experienced one or more episode characterized by cutaneous symptoms (erythema, and/or urticaria angioedema) following the assumption of NSAIDs; 92 subjects experienced reactions to only one NSAID (single intolerance: SI) and 12 subjects had reactions to multiple NSAIDs (multiple intolerance: MI). Rofecoxib was challenged at the following dosages: 1/4 of 25 mg (6.25 mg), 1/4 of 25 mg, and 1/2 of 25 mg (12.5 mg), at intervals of 1 h if no symptoms had developed with the previous administration, in order to reach a cumulative dose of 25 mg. All subjects underwent two double-blind, placebo-controlled challenges in two consecutive days. RESULTS: No reactions against placebo were observed. Similarly, no reactions were observed in all subjects both after the first and after the second challenge to rofecoxib. CONCLUSIONS: The present study demonstrated that rofecoxib does not have cross-reactivity to NSAIDs. Rofecoxib is a safe alternative in subjects with previous adverse cutaneous reaction to NSAIDs.

Adult↗

Effects of drug therapy on cardiac arrhythmias and ischemia in hypertensives with LVH.

Left ventricular hypertrophy (LVH) in hypertensive subjects is associated with an increased prevalence of ventricular arrhythmias. To evaluate the effect of antihypertensive treatment on cardiac arrhythmias (CA) and transient episodes of myocardial ischemia (TEMI), we studied 46 hypertensive patients with LVH, divided into four groups randomly treated with enalapril, hydrochlorothiazide (HCTZ), atenolol, or verapamil (SR-V) for 6 months. Office blood pressure and office heart rate values were recorded, in basal conditions, after 1 and 6 months of treatment, and all patients underwent echocardiography, electrocardiographic Holter monitoring, and stress testing. All drugs significantly lowered blood pressure, whereas left ventricular mass index was reduced by atenolol, enalapril, and SR-V, but not by HCTZ. Treatment induced a significant reduction in the number of patients with supraventricular arrhythmias (35 v 15, P < .034, and 28 v 8, excluding patients treated with HCTZ, P < .008). The number of patients with ventricular arrhythmias was also reduced (32 v 16 considering all groups, P < .08, and 24 v 9, excluding patients treated with HCTZ, P < .04). The number of TEMI during Holter monitoring significantly decreased from 47 to 23 (P = .043) in all patients, and from 39 to 14 (P = .013) excluding patients treated with HCTZ. In all groups, irrespective of treatment, a reduction of blood pressure, heart rate, and systolic blood pressure/heart rate product measured by exercise stress test was observed. The present study shows that in hypertensive patients with LVH, antihypertensive treatment with atenolol, enalapril and SR-V reduces LVH and decreases the prevalence of CA and TEMI. Treatment with HCTZ during the 6-month study did not alter LVH and did not appear to reduce CA and TEMI.

Adult↗

Relation of cellular potassium to other mineral ions in hypertension and diabetes.

To investigate the role of intracellular potassium (K(i))and other ions in hypertension and diabetes, we utilized (39)K-, (23)Na-, (31)P-, and (19)F-nuclear magnetic resonance (NMR) spectroscopy to measure K(i), intracellular sodium (Na(i)), intracellular free magnesium (Mg(i)), and cytosolic free calcium (Ca(i)), respectively, in red blood cells of fasting normotensive nondiabetic control subjects (n=10), untreated (n=13) and treated (n=14) essential hypertensive subjects, and diabetic subjects (n=5). In 12 subjects (6 hypertensive and 6 normotensive controls), ions were also measured before and after the acute infusion of 1 L of normal saline. Compared with those in controls (K(i)=148+/-2.0 mmol/L), K(i) levels were significantly lower in hypertensive (132.2+/-2.9 mmol/L, sig=0.05) and in type 2 diabetic subjects (121.2+/-6.8 mmol/L, sig=0.05). K(i) was higher in treated hypertensives than in untreated hypertensives (139+/-3.1 mmol/L, sig=0.05) but was still lower than in normals. Although no significant relation was observed between basal K(i) and Na(i) values, saline infusion elevated Na(i) (P<0.01) and reciprocally suppressed K(i) levels (142+/-2.4 to 131+/-2.2 mmol/L, P<0.01). K(i) was strongly and inversely related to Ca(i) (r=-0.846, P<0.001), and was directly related to Mg(i) (r=0.664, P<0.001). We conclude that (1) K(i) depletion is a common feature of essential hypertension and type 2 diabetes, (2) treatment of hypertension at least partially restores K(i) levels toward normal, and (3) fasting steady-state K(i) levels are closely linked to Ca(i) and Mg(i) homeostasis. Altogether, these results emphasize the similar and coordinate nature of ionic defects in diabetes and hypertension and suggest that their interpretation requires an understanding of their interaction.

Aged↗

Insulin-mimetic action of vanadate: role of intracellular magnesium.

The insulin-mimetic effect of vanadate is well established, and vanadate has been shown to improve insulin sensitivity in diabetic rats and humans. Although the exact mechanism(s) remain undefined, we have previously demonstrated a direct relation of intracellular free magnesium (Mg(i)) levels to glucose disposal, to insulinemic responses following glucose loading, and to insulin-induced ionic effects. To investigate whether the insulin-mimetic effects of vanadate could similarly be mediated by Mg(i), we utilized (31)P-nuclear magnetic resonance spectroscopy to measure Mg(i) in erythrocytes from normal (NL, n=10) and hypertensive (HTN, n=12) subjects, before and after incubation with insulin and with different doses of sodium vanadate. In NL, vanadate elevated Mg(i) levels, with maximum efficacy at 50 7 micromol/L (186+/-6 to 222+/-6 7micromol/L, P>0.01), as did physiologically maximal doses of insulin, 200 7microU/mL (185+/-6 to 222+/-8 7micromol/L, P<0.01). In HTN, only vanadate, but not insulin, increased Mg(i) (insulin: 173+/-7 to 180+/-9 7micromol/L, P=NS; vanadate: 170+/-7 to 208+/-10 7micromol/L, P<0.01). Mg(i) responses to insulin (r=0.637, P<0.001), but not to vanadate (r=0.15, P=NS), were closely and directly related to basal Mg(i) levels. We conclude that (1) both vanadate and insulin stimulate erythrocyte Mg(i) levels; (2) cellular Mg(i) responses to insulin, but not to vanadate, depend on basal Mg(i) content-the lower the basal Mg(i), the less the Mg(i) response to insulin. As such, (3) Mg(i) responses to vanadate were equivalent among HTN and NL, whereas HTN cells exhibited blunted Mg(i) responses to insulin, and (4) the ability of vanadate to improve insulin sensitivity clinically may be mediated, at least in part, by its ability to increase Mg(i) levels, which in turn, helps to determine cellular insulin action.

Dose-Response Relationship, Drug↗

Altered cellular magnesium responsiveness to hyperglycemia in hypertensive subjects.

Previous studies by our group have identified ionic aspects of insulin resistance in hypertension, in which cellular responses to insulin were influenced by the basal intracellular ionic environment-the lower the cytosolic free magnesium (Mg(i)), the less Mg(i) increased following insulin stimulation. To investigate whether this ionic insulin resistance represents a more general abnormality of cellular responsiveness in hypertension, we studied Mg(i) responses to nonhormonal signals such as hyperglycemia (15 mmol/L) and used (31)P-nuclear magnetic resonance (NMR) spectroscopy to measure Mg(i) in erythrocytes from normal (NL, n=14) and hypertensive (HTN, n=12) subjects before and 30, 60, 120, and 180 minutes after in vitro glucose incubations. Basal Mg(i) levels were significantly lower in HTN subjects than in NL subjects (169+/-10 versus 205+/-8 micromol.L(-1), P<0.01). In NL cells, hyperglycemia significantly lowered Mg(i), from 205+/-8 micromol.L(-1) (basal, T=0) to 181+/-8, 162+/-6, 152+/-7, and 175+/-9 micromol.L(-1) (T=30, 60, 120, and 180, respectively; P<0.005 versus T=0 at all times). In HTN cells, maximal Mg(i) responses to hyperglycemia were blunted, from 169+/-10 micromol.L(-1) (basal, T=0) to 170+/-11, 179+/-12, 181+/-14, and 173+/-15 micromol.L(-1) (T=30, 60, 120, and 180, respectively; P=NS versus T=0 at all times). For all subjects, Mg(i) responses to hyperglycemia were closely related to basal Mg(i) levels: the higher the Mg(i), the greater the response (n=26, r=0.620, P<0.001). Thus, (1) erythrocytes from hypertensive vis-à-vis normotensive subjects are resistant to the ionic effects of extracellular hyperglycemia on Mg(i) levels, and (2) cellular ionic responses to glucose depend on the basal Mg(i) environment. Altogether, these data support a role for altered extracellular glucose levels in regulating cellular magnesium metabolism and also suggest the importance of ionic factors in determining cellular responsiveness to nonhormonal as well as hormonal signals.

Blood Glucose↗

Efficacy and tolerability of lercanidipine in monotherapy in elderly patients with isolated systolic hypertension.

To investigate the efficacy and tolerability of lercanidipine, used as monotherapy once a day, in elderly patients with isolated systolic hypertension (ISH), 83 patients were enrolled in this multicenter, double-blind, randomized, placebo-controlled study. All patients were older than 60 years, and their mean age was 66.7 +/- 5.4 years. ISH was defined as SBP > or = 160 mmHg, and DBP < 95 mmHg. After wash-out and placebo run-in periods, patients were randomly assigned to placebo or lercanidipine (10 mg once a day) treatment for 4 weeks. Non-responding patients of the lercanidipine-treated group were later treated with 20 mg of lercanidipine once a day for 4 additional weeks. At the end of the study, the reduction in systolic blood pressure was significantly larger in the lercanidipine-treated patients (-32.4 mmHg) compared to the fall observed in the placebo group (-9.6 mmHg). Diastolic blood pressure decreased slightly but significantly in the lercanidipine-treated patients only. At the end of lercanidipine treatment, 23 of 37 patients (62%) were normalized. Changes in heart rate, occurrence of orthostatic hypotension, and clinically relevant changes in electrocardiographic and laboratory findings were not observed in either group. Lercanidipine treatment was suspended in one patient because of epigastric pain. These data indicate that lercanidipine, used as monotherapy once a day, is effective in lowering elevated systolic blood pressure in elderly patients, and is well tolerated.

Aged↗

Effects of simvastatin and atorvastatin administration on insulin resistance and respiratory quotient in aged dyslipidemic non-insulin dependent diabetic patients.

One hundred and ninety-five aged (mean age: 67+/-4.8 years), non-insulin dependent diabetic patients underwent a randomised single-blind study for investigating the effect of statin administration on insulin resistance and respiratory quotient. After 4 weeks run-in period, all patients were randomised in three groups: placebo (n=67), simvastatin (10 mg/day) (n=61) and atorvastatin (5 mg/day) (n=67). Each treatment period lasted 8 weeks. At the beginning, after the run-in and at the end of the study, insulin resistance was assessed by homeostasis model assessment (HOMA) index, while respiratory quotient (Rq) was evaluated by indirect calorimetry. Statins versus placebo significantly lowered plasma total, LDL-, HDL-cholesterol and triglyceride concentrations and improved insulin resistance and Rq and metabolic control. Atorvastatin had a greater effect than simvastatin on plasma triglyceride concentration (-26.3+/-3.1 vs. -19.7+/-2.8%, P<0.03), HOMA index (-13.1+/-0.6 vs. -9.1+/-0.9%, P<0.05), Rq (5.9+/-0.4 vs. 3.1+/-0.5%, P<0.05) and glycosylated haemoglobin (-11.2+/-0.3 vs. -7. 1+/-0.4%, P<0.05). In the whole group of subjects (n=195) and at the end of the study, changes in plasma triglyceride concentrations were significantly correlated with the change in the HOMA index (r=0.44, P<0.001) and age and BMI adjusted-Rq (r=-0.32, P<0.005). Multivariate analyses demonstrated that decline in plasma triglyceride concentration was a significant determinant for explaining the effect of statin on insulin resistance and Rq. In conclusion our study demonstrates that statin administration is useful for controlling dyslipidemia in NIDDM patients and for improving the metabolic control. With regard to this latter aim, atorvastatin seems to be more powerful than simvastatin.

Aged↗

Cellular ionic alterations with age: relation to hypertension and diabetes.

BACKGROUND: Cytosolic free calcium (Cai) and magnesium (Mgi) are vital to cellular homeostasis and function. OBJECTIVE: To evaluate cellular divalent cations in normal subjects at different ages and their relationship to ion levels in essential hypertension and diabetes. DESIGN: A cross-sectional study. SETTING: A university hospital in New York. PARTICIPANTS: A total of 103 subjects (32 older, 71.1 +/- 1.2 y/o, and 71 young/middle aged subjects, 51.1 +/- 2.3 y/o). INTERVENTION: Oral glucose tolerance test. MEASUREMENTS: 19F and 31P NMR spectroscopy were used to measure Cai and Mgi levels in erythrocytes from normal (>65 y/o, n = 11; <65 y/o, n = 26), hypertensive (EH) (>65 y/o, n = 9; <65 y/o, n = 30), and type 2 diabetic (DM) (>65 y/o, n = 12; <65 y/o, n = 15) subjects; these levels were also compared with glucose and insulin levels before and after oral glucose loading. RESULTS: Fasting Mgi levels were lower (207 +/- 7.8 vs 236 +/- 7.5 microM; P < .05) and Cai higher (32.2 +/- 3.0 vs 20.3 +/- 1.8 nM; P < .05) in older than in younger normal subjects. For all normal subjects, the greater the age, the higher the Cai (r = 0.622, P = .004) and the lower the Mgi (r = -0.423; P = .011). However, no significant (P = NS) differences in Mgi or Cai levels were observed between older normal and young/middle-aged subjects with EH (Mgi = 189.7 +/- 5.9 vs 182.6 +/- 9.8 microM; Cai = 33.8 +/- 4.9 vs 35.6 +/- 4.0 nM) or DM (Mgi = 182.8 +/- 10.9 vs 180.8 +/- 8.1 microM; Cai = 33.6 +/- 4.3 vs 39.7 +/- 5.9 nM). Significant relationships were also found between cellular ion content, blood pressure, and glycemic indices. CONCLUSIONS: Aging is associated with the onset of altered Cai and Mgi levels, indistinguishable from those observed in hypertension and diabetes, independent of age. We suggest that these ionic changes may be clinically significant, underlying the predisposition of older subjects to cardiovascular and metabolic diseases.

Age Factors↗

Effects of glutathione on red blood cell intracellular magnesium: relation to glucose metabolism.

Recent evidence suggests that the endogenous antioxidant glutathione may play a protective role in cardiovascular disease. To directly investigate the role of glutathione in the regulation of glucose metabolism in hypertension, we studied the acute effects of in vivo infusions of this antioxidant (alone or in combination with insulin) on whole body glucose disposal (WBGD) using euglycemic glucose clamp and the effects on total red blood cell intracellular magnesium (RBC-Mg) in hypertensive (n=20) and normotensive (n=30) subjects. The relationships among WBGD, circulating reduced/oxidized glutathione (GSH/GSSG) levels, and RBC-Mg in both groups were evaluated. The in vitro effects of glutathione (100 micromol/L) on RBC free cytosolic magnesium (Mg(i)) were also studied. In vivo infusions of glutathione (15 mg/minx120 minutes) increased RBC-Mg in both normotensives and hypertensives (1.99+/-0.02 to 2.13+/-0.03 mmol/L, P<0.01, and 1.69+/-0.03 to 1.81+/-0.03 mmol/L, P<0.01, respectively). In vitro GSH but not GSSG increased Mg(i) (179+/-3 to 214+/-5 micromol/L, P<0.01). In basal conditions, RBC-Mg values were related to GSH/GSSG ratios (r=0.84, P<0.0001), and WBGD was directly, significantly, and independently related to both GSH/GSSG ratios (r=0.79, P<0.0001) and RBC-Mg (r=0.89, P<0.0001). This was also true when hypertensive and control groups were analyzed separately. On multivariate analysis, basal RBC-Mg (t=6.81, P<0.001), GSH/GSSG (t=3. 67, P<0.02), and blood pressure (t=2.89, P<0.05) were each independent determinants of WBGD, with RBC-Mg explaining 31% of the variability of WBGD. These data demonstrate a direct action of glutathione both in vivo and in vitro to enhance intracellular magnesium and a clinical linkage between cellular magnesium, GSH/GSSG ratios, and tissue glucose metabolism.

Adult↗

Effects of vitamin E and glutathione on glucose metabolism: role of magnesium.

Vitamin E is an antioxidant that has been demonstrated to improve insulin action. Glutathione, another natural antioxidant, may also be important in blood pressure and glucose homeostasis, consistent with the involvement of free radicals in both essential hypertension and diabetes mellitus. Our group has recently suggested that the effects of reduced glutathione on glucose metabolism may be mediated, at least in part, by intracellular magnesium levels (Mg([i])). Recent evidence suggests that vitamin E enhances glutathione levels and may play a protective role in magnesium deficiency-induced cardiac lesions. To directly investigate the effects of vitamin E supplementation on insulin sensitivity in hypertension, in relation to the effects on circulating levels of reduced (GSH) and oxidized (GSSG) glutathione and on Mg([i]), we performed a 4-week, double-blind, randomized study of vitamin E administration (600 mg/d) versus placebo in 24 hypertensive patients and measured whole-body glucose disposal (WBGD) by euglycemic glucose clamp, GSH/GSSG ratios, and Mg([i]) before and after intervention. The relationships among WBGD, GSH/GSSG, and Mg([i]) in both groups were evaluated. In hypertensive subjects, vitamin E administration significantly increased WBGD (25.56+/-0.61 to 31.75+/-0.53 micromol/kg of fat-free mass per minute; P<0.01), GSH/GSSG ratio (1.10+/-0.07 to 1.65+/-0.11; P<0.01), and Mg([i]) (1.71+/-0.042 to 1.99+/-0.049 mmol/L; P<0.01). In basal conditions, WBGD was significantly related to both GSH/GSSG ratios (r=0.58, P=0.047) and Mg([i]) (r=0.78, P=0.003). These data show a clinical link between vitamin E administration, cellular magnesium, GSH/GSSG ratio, and tissue glucose metabolism. Further studies are needed to explore the cellular mechanism(s) of this association.

Double-Blind Method↗

Effects of aging on serum ionized and cytosolic free calcium: relation to hypertension and diabetes.

Elevated cytosolic free calcium (Ca(i)) and reciprocally reduced, extracellular ionized calcium (Ca-ion) levels are observed in both hypertension and non-insulin-dependent diabetes mellitus (NIDDM). Because the changes of vascular function and insulin sensitivity in these conditions resemble the changes associated with "normal" aging, we wondered to what extent similar alterations in calcium metabolism occur with aging per se in the absence of overt hypertension or diabetes. We therefore measured platelet Ca(i) levels by spectrofluorometry and serum Ca-ion levels in normotensive, nondiabetic, healthy, normal, elderly (>65 years old) subjects, mean age +/-SEM, 72.2+/-1.5 years old (n=11); in healthy, normal, young (<65 years old) adults, 46.1+/-2.3 years old (n=12); in 10 young adult hypertensives, 48.6+/-1.9 years old; and in 10 normotensive NIDDM subjects, 49.2+/-1.6 years old. Platelet Ca(i) levels were higher (104.5+/-4.9 versus 80.2+/-1.8 nmol/L, P<0.01) and Ca-ion levels lower (1.212+/-0.010 versus 1.236+/-0.011 mmol/L, P<0.05) in normal elderly compared with young control subjects, but normal elderly Ca(i) and Ca-ion levels were indistinguishable from those in hypertensive (Ca(i) 107.5+/-3.6 nmol/L, Ca-ion 1.210+/-0.009 mmol/L) and NIDDM (Ca(i) 110.7+/-4.7 nmol/L, Ca-ion 1.204+/-0.014 mmol/L) subjects. In normal subjects, significant correlations were found between platelet Ca(i) levels and age (r=0.655, P<0.01) and between Ca(i) levels and systolic blood pressure (r=0.733, P<0.001). We conclude that aging is associated with alterations of Ca(i) and Ca-ion levels resembling those changes present at any age in hypertension and type 2 diabetes. We hypothesize that these alterations of calcium metabolism underlie the predisposition to the alterations of blood pressure and insulin sensitivity characteristic of "normal" aging. The data also suggest that studies of the aging process should be limited to subjects with normal blood pressure and glucose tolerance.

Adolescent↗

Protective effects of captopril against ischemic stress: role of cellular Mg.

Magnesium (Mg) deficiency enhances tissue sensitivity to ischemic damage, an effect reversed not only by Mg, but also by sulfhydryl (SH)-containing compounds. We therefore created an in vitro model of red blood cell ischemia to investigate whether the protective effects of these compounds might be related to effects on intracellular free Mg (Mg(i)) content. (31)P-nuclear magnetic resonance (NMR) spectroscopy was used to measure the high-energy metabolites ATP and 2,3-diphosphoglycerate (DPG) and Mg(i) and inorganic phosphate (P(i)) levels in erythrocytes before and for 6 hours after progressive oxygen depletion in the presence or absence of SH-compounds, including captopril, N-acetyl-L-cysteine (NAC), penicillamine, and N-(2-mercaptopropionyl)-glycine (MPG). Under basal aerobic conditions, captopril increased Mg(i) in a dose- and time-dependent fashion (174.5+/-5.3 to 217.1+/-5.1 micromol/L, P<0. 05 at 100 micromol/L, 60 minutes). The SH compounds NAC, penicillamine, and MPG but not the non-SH compound enalaprilat also significantly raised Mg(i) in erythrocytes (P<0.05). With oxygen deprivation, a consistent decrease occurred in both ATP and 2,3-DPG levels associated with a rise in P(i) and in the P(i)/2,3-DPG ratio used as an index of high-energy metabolite depletion. Captopril, compared with control, retarded the rise in P(i) and reduced the P(i)/2,3-DPG ratio (P<0.008 and P<0.025 at 4 and 6 hours, respectively). Furthermore, the higher the initial Mg(i) and the greater the captopril-induced rise in Mg(i), the greater the metabolite-protective effect (r=0.799 and r=0.823, respectively; P<0. 01 for both). Altogether, the data suggest that Mg influences the cellular response to ischemia and that the ability of SH compounds such as captopril to ameliorate ischemic injury may at least in part be attributable to the ability of such compounds to increase cytosolic free Mg levels.

Adult↗

Cardiovascular risk factors in South America and the Caribbean.

Facing the conclusion of the twentieth century, cardiovascular disease (CVD) remains a major cause of morbidity and a leading contributor to mortality worldwide. Developing countries, including those in South America and the Caribbean, contribute substantially to the global burden of CVD. Indeed, 8 to 9 million deaths attributable to CVD (63% of world total) occurred in developing countries in 1990, compared to 5.3 million deaths in developed nations. Over the next 25 years, it is projected that there will be a rise in CVD mortality rates in the developing countries, linked not only to demographic changes (expansion and aging of the population), but also to progressive urbanization and lifestyle modifications. As such, the ratio of deaths from CVD to deaths from infectious disease is likely to triple during the next 20 years in South America and the Caribbean. The identification of major risk factors and the implementation of control strategies (eg, community education and target of high risk individuals) have contributed to the fall in CVD mortality rates observed in industrialized nations. Most countries of South America and the Caribbean lack an efficient health care system, and the medical and socio-economic consequences of the projected rise in CVD will further strain financial resources. Therefore, appropriate strategies based on knowledge extrapolated from research among other populations should be initiated. The agenda of any lifestyle-related disease control program should include the promotion of healthy diet, exercise, and should encourage decreasing tobacco and alcohol usage.

Adult↗

Magnesium responsiveness to insulin and insulin-like growth factor I in erythrocytes from normotensive and hypertensive subjects.

Depletion of intracellular free magnesium (Mg(i)) is a characteristic feature of insulin resistance in essential hypertension, but it is not clear to what extent low Mg(i) levels contribute to insulin resistance, result from it, or both. As insulin-like growth factor I (IGF-I) may improve insulin resistance, we investigated whether this peptide could similarly improve Mg(i) responsiveness to insulin in hypertension, and whether this effect was related to any direct IGF-I effect on Mg(i). 31P-Nuclear magnetic resonance spectroscopy was used to measure Mg(i) in erythrocytes from 13 fasting normotensive and 10 essential hypertensive subjects before and 30, 60, and 120 min after incubation with a physiologically maximal dose of insulin (200 microU/mL) and with different doses of recombinant human IGF-I (0.1-100 nmol/L). In normotensive subjects, IGF-I elevated Mg(i) (P < 0.05) in a dose- and time-dependent fashion, as did insulin (P < 0.05). However, in hypertensive subjects, maximal Mg(i) responses to insulin, but not to IGF-I, were blunted [insulin, 163+/-11 to 177+/-10 micromol/L (P=NS); IGF-I, 164+/-6 to 190+/-11.7 micromol/L (P < 0.05)]. Furthermore, for insulin, but not for IGF-I, cellular Mg(i) responsiveness was closely and directly related to basal Mg(i) levels (insulin: r=0.72; P < 0.01; IGF-I: r=0.18; P=NS). Lastly, blunted Mg(i) responses to insulin could be reversed by preincubation of hypertensive cells with IGF-I. We conclude that 1) both IGF-I and insulin stimulate erythrocyte Mg(i) levels; 2) cellular Mg(i) responses to insulin, but not to IGF-I, depend on basal Mg(i) levels, i.e. the higher the Mg(i) the greater the sensitivity to insulin; and 3) IGF-I potentiates insulin-induced stimulation of Mg(i) at doses that themselves do not raise Mg(i). These effects of IGF-I may underlie at least in part its ability to improve insulin sensitivity clinically. Together, these data support a role for IGF-I in cellular magnesium metabolism and emphasize the importance of magnesium as a determinant of insulin action.

Adult↗

Bronchial reactivity and intracellular magnesium: a possible mechanism for the bronchodilating effects of magnesium in asthma.

1. Increased bronchial smooth muscle contractility with consequent bronchial hyperreactivity are characteristic physiopathological events of asthma. Since magnesium intervenes in calcium transport mechanisms and intracellular phosphorylation reactions, it constitutes an important determinant of the contraction/relaxation state of bronchial smooth muscle. In the present study we investigated the relationship between bronchial reactivity, assessed by methacholine-provocation test, and magnesium concentrations both at extracellular and intracellular levels measured by spectrophotometry. Twenty-two patients with mild-to-moderate asthma and 38 non-asthmatic subjects with allergic rhinitis (24 allergic to Parietaria pollen and 14 allergic to Grass pollen) were recruited to the study. Exclusion criteria included renal failure, hepatic diseases, heart failure and arterial hypertension. 2. The salient finding of our study is that there is a strong positive correlation between bronchial reactivity and the level of intracellular magnesium (r=0.72, P<0.0001), both when the groups are analysed separately or together. Intracellular magnesium concentrations in the group of patients with asthma were significantly lower (1.8+/-0. 01 mmol/l; n=22) when compared with levels in rhinitis subjects allergic to Parietaria (1.9+/-0.01 mmol/l; n=24, P<0.05), and with levels in rhinitis subjects allergic to Grass pollen (2.0+/-0.03 mmol/l; n=14, P<0.05). Serum levels of the ion were similar in all groups. 3. We conclude that the level of intracellular magnesium may be an important determinant of bronchial hyperreactivity, as supported by the significant positive correlation between these two parameters in allergic patients with known bronchial hyperresponsiveness. This finding, in addition to reports of the bronchodilating effects of magnesium administration in patients with asthma, confirms the proposed role of this ion in the pathogenesis and treatment of asthma.

Adult↗