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Biomedical subjects

C Pastori

Publications and source records attributed to C Pastori.

At least 19 recordsLinked to original sources
PubMed2005

Activation of cerebral endothelium is required for mononuclear cell recruitment in a novel in vitro model of brain inflammation.

Brain inflammation is a common event in the pathogenesis of several neurological diseases. It is unknown whether leukocyte/endothelium interactions are sufficient to promote homing of blood-borne cells into the brain compartment. The role of mononuclear cells and endothelium was analyzed in a new experimental model, the isolated guinea-pig brain maintained in vitro by arterial perfusion. This preparation allows one to investigate early steps of brain inflammation that are impracticable in vivo. We demonstrate by confocal microscopy analysis that in vitro co-perfusion of pro-inflammatory agents and pre-activated fluorescent mononuclear cells induced endothelial expression of selectins and intracellular adhesion molecule-1 in correspondence of arrested mononuclear cells, and correlates with a moderate increase in blood-brain barrier permeability. Separate perfusion of pro-inflammatory agents and mononuclear cells induced neither mononuclear cell adhesion nor adhesion molecule expression. We demonstrate that co-activation of mononuclear cells and cerebral endothelium is an essential requirement for cell arrest and adhesion in the early stages of experimental cerebral inflammation.

Animals↗
PubMed2005

Induction of murine mucosal CCR5-reactive antibodies as an anti-human immunodeficiency virus strategy.

The genital mucosa is the main site of initial human immunodeficiency virus type 1 (HIV-1) contact with its host. In spite of repeated sexual exposure, some individuals remain seronegative, and a small fraction of them produce immunoglobulin G (IgG) and IgA autoantibodies directed against CCR5, which is probably the cause of the CCR5-minus phenotype observed in the peripheral blood mononuclear cells of these subjects. These antibodies recognize the 89-to-102 extracellular loop of CCR5 in its native conformation. The aim of this study was to induce infection-preventing mucosal anti-CCR5 autoantibodies in individuals at high risk of HIV infection. Thus, we generated chimeric immunogens containing the relevant CCR5 peptide in the context of the capsid protein of Flock House virus, a presentation system in which it is possible to engineer conformationally constrained peptide in a highly immunogenic form. Administered in mice via the systemic or mucosal route, the immunogens elicited anti-CCR5 IgG and IgA (in sera and vaginal fluids). Analogous to exposed seronegative individuals, mice producing anti-CCR5 autoantibodies express significantly reduced levels of CCR5 on the surfaces of CD4+ cells from peripheral blood and vaginal washes. In vitro studies have shown that murine IgG and IgA (i) specifically bind human and mouse CD4+ lymphocytes and the CCR5-transfected U87 cell line, (ii) down-regulate CCR5 expression of CD4+ cells from both humans and untreated mice, (iii) inhibit Mip-1beta chemotaxis of CD4+ CCR5+ lymphocytes, and (iv) neutralize HIV R5 strains. These data suggest that immune strategies aimed at generating anti-CCR5 antibodies at the level of the genital mucosa might be feasible and represent a strategy to induce mucosal HIV-protective immunity.

Amino Acid Sequence↗
PubMed2004

Catecholamine-induced regulation in vitro and ex vivo of intralymphocyte ionized magnesium.

Despite the importance of the adrenergic activity and of the metabolism of magnesium in some important cardiovascular pathologies, very little is known about how intracellular ionized magnesium (Mgi2+) is regulated by catecholamines. We made an in-vitro study of the variations in the concentration of ionized magnesium in human lymphocytes using the fluorescent probe furaptra in response to different catecholamines. We also made an ex-vivo study of the changes in intracellular ionized magnesium in lymphocytes in 20 subjects with essential arterial hypertension, 10 treated with 120 mg/d of propranolol and 10 with placebo. Norepinephrine and isoproterenol significantly decrease Mgi2+ and this effect is blocked by beta-blockers but not by alpha-blockers. The EC50 of the effect of norepinephrine is within the range of concentrations physiologically present in plasma. The substitution of extracellular sodium with choline blocks the decrease in intracellular ionized magnesium induced by norepinephrine, which leads us to suppose that the magnesium-reducing effect of catecholamines is a result of the activation of a Na+-Mg2+ exchanger. We were not able to demonstrate any change in intracellular ionized magnesium after 1 and 17 days of active treatment in essential hypertensives. The impossibility of demonstrating ex vivo the mechanism of catecholamine-mediated regulation that is evident in vitro is perhaps due to our experimental conditions or to substances which in vivo inhibit the action of the catecholamines on magnesium, such as insulin and/or glucose.

Adrenergic alpha-Agonists↗
PubMed2004

A new prospective against HIV infection: induction of murin CCR5-downregulating antibodies.

Natural resistance to HIV is widely growing in humans. An example of an extremely efficacious resistance is represented by exposed seronegative (ESN) subjects, i.e. individuals who, despite repeated sexual and/or parenteral exposure to HIV, remain seronegative and apparently uninfected. A small group within ESN produces anti-CCR5 antibodies which cause antigen down-modulation and a CCR5 minus phenotype. It has been previously demonstrated that a single conformed extracellular domain (corresponding to first cystein loop) of CCR5 is recognized by ESN antibodies. In order to verify the possibility to induce and reproduce infection-protecting anti-CCR5 antibodies in individuals at high risk of HIV infection, we generated immunogens containing the relevant CCR5 peptide. Since the first cysteine loop of human CCR5 is identical in sequence to its mouse homologue, mice were immunized according to an intra-peritoneal procedure with CCR5 peptide loop, #90-103. Anti-CCR5-responses elicited in mice did share the same specificity and functions as human anti-CCR5 immunoglobulins previously identified in ESN cohorts. In particular, murine IgG and IgA: 1. Specifically recognize both mouse and human CCR5. 2. Down-modulate CCR5 expression on CD4+ cells of both untreated mice and human. 3. Downregulate "in vivo" peripheral CCR5 expression on mice CD4+CCR5+ cells. 4. Inhibit CD4+ CCR5+ lymphocytes chemotaxis. These findings show that CCR5-mediated effects on CD4+ cells can be achieved in mice both "in vitro" and "in vivo". Therefore, novel immune strategies aimed at generating partial or complete immune protection through anti-CCR5 downregulation at genital mucosa could be elicited successfully also in monkey and eventually in humans.

Animals↗
PubMed2000

Immune activation in africa is environmentally-driven and is associated with upregulation of CCR5. Italian-Ugandan AIDS Project.

BACKGROUND: HIV infection in Africa is associated with immune activation and a cytokine profile that stimulates CCR5 expression. We investigated whether this immune activation is environmentally driven; if a dominant expression of CCR5 could indeed be detected in African individuals; and if R5 HIV strains would be prevalent in this population. METHODS: Freshly drawn peripheral blood mononuclear cells from HIV-uninfected African and Italian individuals living in rural Africa, from HIV-uninfected Africans and Italians living in Italy, and from HIV-infected African and Italian patients were analysed. Determinations of HIV coreceptor-specific mRNAs and immunophenotype analyses were performed in all samples. Virological analyses included virus isolation and characterization of plasma neutralizing activity. FINDINGS: Results showed that: immune activation is detected both in Italian and African HIV-uninfected individuals living in Africa but not in African subjects living in Italy; CCR5-specific mRNA is augmented and the surface expression of CCR5 is increased in African compared with Italian residents (CXCR4-specific mRNA is comparable); R5-HIV strains are isolated prevalently from lymphocytes of African HIV-infected patients; and plasma neutralizing activity in HIV-infected African patients is mostly specific for R5 strains. CONCLUSIONS: Immune activation in African residents is environmentally driven and not genetically predetermined. This immune activation results in a skewing of the CCR5 : CXCR4 ratio which is associated with a prevalent isolation of R5 viruses. These data suggest that the selection of the predominant virus strain within the population could be influenced by an immunologically driven pattern of HIV co receptor expression.

Africa↗
PubMed2000

CCR5-reactive antibodies in seronegative partners of HIV-seropositive individuals down-modulate surface CCR5 in vivo and neutralize the infectivity of R5 strains of HIV-1 In vitro.

Exposure to HIV does not necessarily result in infection. Because primary HIV infection is associated with CCR5-tropic HIV variants (R5), CCR5-specific Abs in the sera of HIV-seronegative, HIV-exposed individuals (ESN) might be associated with protection against infection. We analyzed sera from ESN, their HIV-infected sexual partners (HIV+), and healthy controls (USN) searching for CCR5-specific Abs, studying whether incubation of PBMC with sera could prevent macrophage inflammatory protein 1 beta (Mip1 beta) (natural ligand of CCR5) binding to CCR5. Results showed that Mip1 beta binding to CCR5 was not modified by sera of either 40 HIV+ or 45 USN but was greatly reduced by sera of 6/48 ESN. Binding inhibition was due to Abs reactive with CCR5. The CCR5-specific Abs neutralized the infectivity of primary HIV isolates obtained from the corresponding HIV+ partners and of R5-primary HIV strains, but not that of CXCR4-tropic or amphitropic HIV strains. Immunoadsorption on CCR5-transfected, but not on CXCR4-transfected, cells removed CCR5-specific and virus-neutralizing Abs. Epitope mapping on purified CCR5-specific Abs showed that these Abs recognize a conformational epitope in the first cysteine loop of CCR5 (aa 89-102). Affinity-purified anti-CCR5-peptide neutralized the infectivity of R5 strains of HIV-1. Anti-CCR5 Abs inhibited Mip1beta-induced chemotaxis of PBMC from healthy donors. PBMC from two ESN (with anti-CCR5 Abs) were CCR5-negative and could not be stimulated by Mip1beta in chemotaxis assays. These results contribute to clarifying the phenomenon of immunologic resistance to HIV and may have implications for the development of a protective vaccine.

Binding Sites, Antibody↗
PubMed2000

Anti-cell antibodies in exposed seronegative individuals with HIV type 1-neutralizing activity.

Despite repeated exposures to HIV-1, some individuals remain seronegative. This study reports that sera from a fraction of exposed seronegative (ESN) subjects showed HIV-neutralizing activity; 5 of 17 ESN sera and none of 17 controls neutralized two different HIV-1 primary isolates (range of neutralizing titers: 1/20 to 1/60). The neutralizing activity was associated with the IgG fraction of 4 of 4 neutralizing ESN sera. Moreover, in 11 of 17 and 9 of 17 ESN sera (but none of the control sera) we found antibodies against HLA class I and CD4, respectively. One of the ESN sera (EU22) neutralized efficiently the primary virus derived from the seropositive partner and showed a good broadly cross-reactive neutralization. Immunoadsorption of two IgG fractions from EU19 and EU22 on peripheral blood mononuclear cells (PBMC) removed virus-neutralizing antibodies. The correlations between the ESN status and neutralizing activity (p<0.05), anti-HLA antibodies (p<0.0002), and anti-CD4 antibodies (p<0.001) were statistically significant. However, there was no statistically significant correlation between neutralizing activity and either anti-HLA or anti-CD4 antibodies. It can therefore be said that exposure to HIV-1 without seroconversion is, in some individuals, associated with HIV-neutralizing antibodies (not directed against viral antigens) and/or with anti-cell autoantibodies, which are possibly specific for cellular antigens involved in the infection/entry process.

Autoantibodies↗
PubMed2000

Intralymphocyte free magnesium in patients with primary aldosteronism: aldosterone and lymphocyte magnesium homeostasis.

It is known that hyperaldosteronism has been associated with magnesium deficiency, yet there are no data on the intracellular concentration of ionized magnesium ([Mg(2+)(i)]) in subjects with primary aldosteronism (PA). We measured intralymphocyte free magnesium ([Mg(2+)(i)]) and intralymphocyte free calcium ([Ca(2+)(i)]) in 16 patients with PA and 26 normotensive control subjects (NCs). [Mg(2+)(i)] and [Ca(2+)(i)] were also measured in blood lymphocytes incubated in vitro with aldosterone, according to a fluorimetric method. In subjects with PA, [Mg(2+)(i)] was significantly lower than that in NCs (mean+/-SD; PA 203+/-56 micromol/L, NCs 291+/-43 micromol/L, 95% confidence interval 57 to 119, P=0.001). In the patients, [Ca(2+)(i)] did not prove to be statistically different from that of NCs (mean+/-SD; PA 47.2+/-10.6 nmol/L, NCs 53.2+/-11 nmol/L). The lymphocytes exposed to the action of aldosterone showed a significant reduction in [Mg(2+)(i)] (n=15, NCs 271+/-28 micromol/L, aldosterone treatment 188+/-39 micromol/L, P=0.001, 95% confidence interval 57 to 108). The dose-effect curve of aldosterone on [Mg(2+)(i)] showed an EC(50) value of approximately 0.5 to 1 nmol/L aldosterone. The reduction in [Mg(2+)(i)] mediated by aldosterone is antagonized by the receptor inhibitor of aldosterone; it is inhibited by inhibitors of protein synthesis and is not measurable when the lymphocytes are incubated in an Na(+)-free medium. The data are consistent with the hypothesis that aldosterone affects the cellular homeostasis of magnesium, probably through modification of the activity of the Na(+)-Mg(2+) antiporter.

Adult↗
PubMed1999

Human immunodeficiency virus (HIV)-specific IgA and HIV neutralizing activity in the serum of exposed seronegative partners of HIV-seropositive persons.

The presence and activity of human immunodeficiency virus (HIV)-specific antibodies were analyzed in the sera of 15 sexually exposed seronegative persons who had systemic HIV-specific cell-mediated immunity and IgA-mediated mucosal immunity and in their HIV-infected partners. The HIV-positive subjects had HIV-specific serum IgG and IgA; the seronegative persons had HIV-specific serum IgA in the absence of IgG. Testing of the seronegative persons 1 year after the interruption of at-risk sex showed that no IgG seroconversion had occurred and that HIV-specific IgA serum concentrations had declined. Serum from the HIV-exposed seronegative persons was analyzed for the ability to neutralize primary HIV-1 isolates. Neutralizing activity was detected in 5 of 15 sera and in 2 cases was retained by serum-purified IgA. Thus, the immunologic picture for resistance to HIV infection should include HIV-specific cell-mediated immunity as well as HIV-specific IgA-mediated mucosal and systemic immunity.

Female↗
PubMed1999

Preliminary communication on intralymphocyte ionized magnesium in hypertensive patients under treatment with beta-blockers.

We measured free intralymphocyte magnesium (Mgi) in 10 hypertensive subjects (HS) before and after treatment with atenolol (A) and in 16 normotensive control subjects (NC). We also carried out in vitro studies on human lymphocytes to test the effect of catecholamines and beta-antagonists on Mgi. Mgi in HS was not statistically different before and after the treatment with A (M +/- SD, basal: 227 +/- 31 + mumol/l; A: 236 +/- 47 mumol/l; NS). Mgi in NC proved not statistically different as compared to HS without treatment (M +/- SD, NC: 232 +/- 35 mumol/l; HS before treatment: 227 +/- 31 mumol/l; NS). The Mgi of the lymphocytes treated in vitro with noradrenaline (NA) significantly decreased in comparison with the control (M +/- SD, basal: 244 +/- 26 mumol/l; NA: 198 +/- 25 mumol/l; p = 0.0001), whereas it did not change after incubation with NA and propranolol (P) (M +/- SD, basal: 238 +/- 32 mumol/l; NA + P: 239 +/- 30 mumol/l; NS). On the other hand Mgi decreased significantly after incubation with NA and A (M +/- SD, basal: 255 +/- 21 mumol/l; NA + A: 202 +/- 34 mumol/l). Our in vivo data show that the Mgi of HS remains unvaried after treatment with A, and that there is not statistical difference between Mgi of NC and of HS before treatment. The in vitro study demonstrated that catecholamines cause a significant reduction in Mgi. This effect is only inhibited by a non-selective beta-blocker such as P. These results seem to explain the ineffectiveness of treatment with atenolol on our patients' Mgi.

Adrenergic alpha-Agonists↗
PubMed1998

Intralymphocyte free magnesium and plasma triglycerides.

To evaluate the relative effect of hypertension and plasma triglycerides on intralymphocyte magnesium we measured ionized intralymphocyte magnesium (Mg(i)) concentration by means of a fluorimetric method based on the dye Furaptra in 4 groups of subjects: 18 normotensive normotriglyceridemic controls (NTNC), 9 hypertriglyceridemic normotensive patients (HTN), 8 hypertriglyceridemic essential hypertensive patients (HTEH), 17 normotriglyceridemic essential hypertensive patients (NTEH). Hypercholesterolemic, diabetic patients and alcoholics were excluded from the study. Mg(i) was found to be statistically reduced (ANOVA test F=10.41, P=0.0001) in both HTN and HTEH (M+/- SD, HTN: 0.235 +/- 0.01, HTEH: 0.236 +/- 0.01 mmol/l) as compared to both NTNC and NTEH (M +/- SD, NTNC: 0.294 +/- 0.008, NTEH: 0.297 +/- 0.009 mmol/l). A statistically significant negative correlation was found in the population as a whole between Mg(i) and plasma triglycerides (n=52, R= -541, P=0.00004). Our data suggest that hypertriglyceridemia per se and possibly the so-called plurimetabolic syndrome is characterized by low intralymphocyte free magnesium.

Adult↗
PubMed1998

Intralymphocyte free magnesium and calcium and insulin tolerance test in a group of essential hypertensive patients.

In order to assess the links which are claimed to exist between peripheral insulin resistance and intracellular magnesium and calcium concentrations, we measured free intralymphocyte magnesium (Mg(i)) and calcium (Ca(i)) concentrations as well as the rate constant of plasma glucose disappearance (K(itt)) after insulin injection (insulin tolerance test: ITT) in a group of 16 normotensive control subjects (NC) and 34 essential hypertensive subjects (EH). Mg(i) and Ca(i) were measured in triplicate by means of a fluorimetric technique based on the dyes furaptra and fura-2 respectively. K(itt) values proved significantly reduced in EH as compared to NC (M +/- SD, EH: 4.49 +/- 1.31 vs 5.28 +/- 1.19, P <0.05; 95% confidence limits: 0.23-1.5). Mg(i) and Ca(i) were not statistically different in EH as compared to NC subjects (Mg(i), NC: 266 +/- 20 micromol/l; EH: 245 +/- 50 micromol/l; Ca(i), NC: 47 +/- 9 nmol/l EH: 46 +/- 13 nmol/l). We found a statistically significant inverse correlation in the whole study group between K(itt) and body mass index (R= -0.363, P<0.01) and a statistically significant positive correlation between K(itt) and Mg(i) (R=0.347, P=0.013) was found. In a step-up multivariate regression analysis including blood pressure, plasma lipids, BMI, plasma magnesium, fasting insulin, fasting glucose, Mg(i) and Ca(i), the dependent variable K(itt) is statistically significantly correlated with body mass index and Mg(i). In a first attempt to study the relationships between insulin resistance, Mg(i) and Ca(i) in nucleated cells, the chosen index of peripheral resistance seems to be linked to intracellular free magnesium.

Adult↗
PubMed1997

[Peripheral insulin resistance and free intralymphocyte magnesium and calcium concentrations in patients with essential hypertension].

To ascertain the claimed links between peripheral insulin resistance and intracellular magnesium and calcium concentrations, we measured free intralymphocyte magnesium (Mg(i)) and calcium (Ca(i)) concentrations, as well as the rate constant of plasma glucose disappearance (K(itt)) after insulin injection (insulin tolerance test: ITT), in a group of 15 normotensive control subjects (NC) and 29 essential hypertensive subjects (EH). Mg(i) and Ca(i) were measured in triplicate by means of a fluorimetric technique based on the dyes furaptra and fura-2 respectively. K(itt) value were significantly reduced in hypertensive subjects as compared to control subjects (M +/- SD, EH: 4.54 +/- 1.31 vs 5.63 +/- 1.07; p < 0.02; 95% confidence limits: 0.22-1.96). Mg(i) and Ca(i) were not statistically different in hypertensive subjects as compared to control subjects (Mg(i), NC: 0.274 +/- 0.02 mmol/L; EH: 0.248 +/- 0.05 mmol/L; Ca(i), NC: 47.6 +/- 9 mmol/L, EH: 46.7 +/- 13.6 mmol/L). A statistically significant inverse correlation was found in the whole study group between K(itt) and body mass index (R = -0.394, p = 0.01) and a statistically significant positive correlation between K(itt) and Mg(i) (R = 0.386; p = 0.012). The latter correlation was no longer statistically significant if adjusted for body mass index. Our data are in favour of a link between index of peripheral insulin resistance and body mass index. A dependence from Mg(i) is possible but the study lack so far the statistical power to demonstrate it.

Blood Glucose↗
PubMed1996

Erythrocyte Na(+)-H+ exchanger kinetics and Na(+)-Li+ countertransport activity in essential hypertensive patients.

The authors measured Na(+)-H+ exchanger kinetics together with Na(+)-Li+ countertransport V(max) in the erythrocytes of 21 subjects with essential hypertension and 16 normotensive control subjects. Na(+)-H+ exchange V(max) appeared to be increased in patients with essential hypertension, while the Na(+)-H+ exchanger affinity for intracellular proton sites (K50%) proved to be unchanged and the index of cooperativity among intracellular proton binding sites as measured by Hill's coefficient (Hill's n) decreased as compared with normotensive control subjects. Na(+)-Li+ countertransport V(max) appeared to be higher in patients with essential hypertension than in control subjects. The authors were unable to find any correlations between Na(+)-H+ exchanger kinetic parameters and metabolic variables such as parameters of insulin resistance and plasma lipids. On the basis of the data obtained, erythrocyte Na(+)-H+ exchanger activity was found to be abnormal in two kinetic variables in essential hypertensive patients and showed no simple linear correlations with the main variables of glucose metabolism, plasma lipids, renin or aldosterone.

Adult↗
PubMed1996

Intralymphocyte free magnesium in a group of subjects with essential hypertension.

Despite the importance of magnesium in essential hypertension, few data are available on the ionized intracellular concentration of this ion. We therefore studied intralymphocyte free intracellular magnesium (Mgi) in 32 untreated essential hypertensive subjects and 27 normotensive control subjects by means of a fluorimetric technique based on the use of the new magnesium-sensitive dye furaptra. We also measured intralymphocyte ionized calcium (Cai) with fura 2. No statistically significant differences were found in Mgi in hypertensive compared with normotensive subjects (essential hypertensive, 0.291 +/- 0.053 mmol/L; normotensive, 0.293 +/- 0.043 [mean +/- SD]). A statistically significant inverse correlation was established between Mgi and plasma triglycerides in essential hypertensive subjects (r = -.521, P = .002). The hypertensive group was arbitrarily divided into two subgroups according to plasma triglyceride levels (> 2 [n = 10] or < 2 mmol/L [n = 22]), and Mgi proved to be significantly lower in the subgroup with high plasma triglyceride levels compared with either the subgroup with normal triglycerides (P = .009; 95% confidence interval, 0.013-0.088) or the normotensive control group as a whole (P = .03; 95% confidence interval, 0.003-0.069) (high-triglyceride hypertensive subgroup, Mgi = 0.256 +/- 0.045 mmol/L; normal-triglyceride hypertensive subgroup, Mgi = 0.307 +/- 0.049). No statistically significant differences were found in Cai in hypertensive compared with normotensive subjects (hypertensive, 53 +/- 12 nmol/L; normotensive, 54 +/- 14). We did not find statistically significant correlations between Cai and plasma triglycerides, nor did we find any differences in Cai between the subgroup of hypertensive subjects with high plasma triglyceride levels and either the subgroup of hypertensive subjects with normal triglycerides or the normotensive control group as a whole. The discrepancies between our results in lymphocytes and data relating to either erythrocytes or platelets emphasize the need for caution before the results are extrapolated from one tissue to the other. The decreased Mgi levels in the subgroup of high-triglyceride hypertensive subjects may suggest a role for magnesium in plurimetabolic syndrome.

Adult↗
PubMed1994

Erythrocyte Na(+)-H+ exchanger and Na(+)-Li+ countertransport activity in primary aldosteronism.

Several authors have described increased Na-H exchanger activity in essential hypertension but no data are available in secondary forms of hypertension such as primary aldosteronism. We measured Na-H exchanger kinetics together with Na-Li countertransport Vmax in the erythrocytes of eight patients with primary aldosteronism and in 15 normotensive control subjects. Plasma aldosterone, plasma renin and plasma potassium were also evaluated. Na-H exchanger Vmax appear to be increased in patients with primary aldosteronism and Hill's n, an index of co-operativity amongst intracellular proton binding sites, was significantly lower in patients than in controls. No statistically significant differences were found between affinity for intracellular protons (K50%) and for Na-Li countertransport Vmax between the two groups studied. We were unable to find any correlations between Na-H exchanger Vmax and Na-Li countertransport Vmax in the two groups considered as a whole. From the present data Na-H exchanger overactivity would not appear to be a specific feature of essential hypertension but seems to be characteristic in patients with primary aldosteronism.

Adult↗
PubMed1993

Erythrocyte Na(+)-H+ exchange activity in essential hypertensive and obese patients: role of excess body weight.

INTRODUCTION: Several authors have described increased Na(+)-H+ exchanger activity in essential hypertension, and an increase in activity of this transport system has also been postulated in situations of hyperinsulinism, such as obesity and essential hypertension. METHODS: We measured Na(+)-H+ exchanger activity in a group of 37 subjects with essential hypertension (18 obese, 19 non-obese), in a group of nine normotensive obese subjects and in a control group of 16 healthy volunteers. Plasma insulin and glucose values during an oral glucose tolerance test were evaluated, together with other variables such as plasma aldosterone, plasma renin activity and plasma potassium. RESULTS: Na(+)-H+ exchanger system activity did not appear to be abnormally raised in the hypertensive subjects, but was significantly increased in the normotensive obese group. Upon dividing the hypertensive subjects into two subgroups on the basis of body mass index, it was noted that, whereas the non-obese hypertensives showed Na(+)-H+ exchanger activity patterns similar to those in controls, the obese hypertensive subjects exhibited increased activity of the transport system. Na(+)-H+ activity correlates with body mass index and shows a significant inverse correlation with plasma potassium. No correlations were found between Na(+)-H+ exchanger activity and the sum of plasma insulin values during the oral glucose tolerance test. CONCLUSION: Na(+)-H+ exchanger overactivity appears to be characteristic in overweight subjects, but would not appear to be a specific feature of essential hypertension. The increased Na(+)-H+ exchanger activity observed in obese subjects may be postulated to be related to the hypermineralocorticoidism characteristic of this condition.

Adult↗