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Biomedical subjects

D Santoro

Publications and source records attributed to D Santoro.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Anticardiolipin antibodies in hemodialysis patients and in renal transplant recipients: prevalence and significance].

Increased anticardiolipin antibodies (aCL) serum levels have been recently described in haemodialysis patients and in renal transplant recipients, with a prevalence ranging from 4.8 to 46.4%. The causes and the clinical significance of aCL positivity in these patients are uncertain. We measured IgG- and IgM-aCL serum levels in 61 haemodialysis patients, in 14 renal transplant recipients and in 38 healthy controls. Increased levels of IgG-aCL were found in 4 haemodialysis patients (6.55%), in 2 transplant patients (14%) and in 2 of the healthy controls (5.26%). IgM-aCL serum levels were normal in all the patients. After one year of follow-up, no vascular events have been observed in aCL positive patients. It is probable that the presence of aCL in the serum of patients with end-stage renal disease is only an epiphenomenon and does not play a pathogenetic role.

Adult↗
PubMed1998

[AI-CARE: a multicentric study on unstable angina. Methodology and preliminary data of a project on the improvement of health care quality in Emilia-Romagna].

BACKGROUND: Recent Italian legislative directives have focused on lowering health-service costs and improving the quality of health care. The AI-CARE study on unstable angina represents the initial observational step in a survey on health-care quality in the Italian region Emilia-Romagna. AIM OF THE STUDY: This study was performed to identify the processes usually involved in the management of patients with unstable angina admitted to a regional cardiology department. The consumption of health service resources and the clinical events related to angina were evaluated. METHODS: AI-CARE is an observational, descriptive and prospective study. Between 15/3/95 and 15/6/95, the patients admitted consecutively to 25 cardiology units for unstable angina, as diagnosed on a clinical basis, were enrolled in the study. A six-week follow-up was provided. The data regarding demographics, history, entry electrocardiogram, symptoms, examinations, treatment and outcome were recorded on a detailed personal questionnaire. The participating centers have been divided according to complexity of organization: 18 with intensive care unit as level I, five with hemodynamic laboratory as level II and two with cardiosurgery as level III. Mortality, myocardial infarction, revascularization procedures and readmissions for angina were considered clinical events. RESULTS: We recruited 463 patients. At discharge, 411 patients were affected with unstable angina while other 40 developed non-Q wave infarctions. The final study population comprised 451 patients. The mean age was 68 years (range 61-76). There were 316 men (69%, mean age 68) and 135 women (mean age 72). All 451 patients were stratified according to the Braunwald classification: IIIB in 66.9%, IIIC in 9.9%, IB in 9.9%. Mean hospital stay was 10 +/- 6 days, while mean stay in intensive care units was 4.3 +/- 2.9 days. Medical treatment included antiplatelet agents (89%), nitrates i.v. (81%), nitrates per os (86%), heparin (55%) and beta-blockers (47%). The most common non-invasive test performed was echocardiogram (70% of patients), Holter ECG and exercise stress testing (19%). Selective coronary arteriography was performed in 50% of patients (23% during the first 10 days). Additionally, 32% of patients underwent revascularization. During follow-up, ten patients (2.21%) had a myocardial infarction, nine patients (1.99%) died and 49 patients (10.8%) were readmitted for angina. CONCLUSIONS: This study indicates that in spite of the poor use of diagnostic procedures (especially coronary arteriography) and myocardial revascularization, mortality and morbidity were relatively low. Our data are similar to the results of the recent Italian EARISA study but differ greatly from the results of foreign studies. Consequently, further observation of our study population is needed.

Aged↗
PubMed1997

Ethylene oxide allergy in dialysis patients.

DESIGN OF STUDY: Two groups of patients undergoing long-term dialysis were studied in order to evaluate the importance of ethylene oxide (EtO) in causing allergic reactions during dialysis. The first group of 50 subjects had never shown any hypersensitivity reactions related to dialysis, whereas the second group of 20 subjects had previously complained of reactions. All the patients underwent a prick test with a standard kit of aeroallergens in order to assess the presence of atopy (in doubtful cases a RAST test was carried out with the same aeroallergens). A blood sample for the investigation of EtO specific IgE antibodies was taken from all the patients; the immunoenzymatic method was used. RESULTS: Sensitivity to EtO is significantly higher in the group of patients with previous allergic reactions during dialysis (55 vs 6% in the control group).

Adult↗
PubMed1997

The renal hemodynamic response to an oral protein load is normal in IgA nephropathy.

The study was devised to explore the effects of an acute oral protein load on renal hemodynamic response in patients with IgA nephropathy (IgAN). The study was performed in 10 proteinuric IgAN patients (800 +/- 300 mg/day) and in 20 healthy controls (matched by sex, age, BMI, BSA, plasma creatinine, plasma urea, urinary urea and protein intake). Blood pressure and creatinine clearance were nearly identical in the two groups. GFR and RPF, measured as the clearance of inulin and of p-aminohippurate (PAH) were studied before and after a meat meal which provided 2 g of protein/kg BW. Following the protein load, renal reserve, percent renal reserve and postmeal cumulative changes of GFR were not significantly different in IgAN and controls. Filtration fraction (FF) at baseline was significantly higher (p < 0.01) in IgAN than in controls (25.5 +/- 1.41 vs. 19 +/- 2%). Postmeal hyperemia and hyperfiltration did not affect FF in either group. Filtration capacity in IgAN was lower (p<0.02) than in controls (117 +/- 5.6 vs. 137.9 +/- 7.0 ml/min x 1.73 m2), whereas the percent of filtration capacity utilized at rest was identical in controls and in IgAN. Creatinine clearance overestimated GFR in IgAN. The data indicate that renal hemodynamic response to proteins in IgAN is normal.

Adult↗
PubMed1997

Inhibition of colon carcinoma cell lung colony formation by a soluble form of E-selectin.

During metastasis, tumor cells adhere to vascular endothelia. E-selectin is an adhesive protein expressed by cytokine-activated endothelium that can support adhesion of colon cancer cells through the recognition of specific carbohydrate ligands. Using a series of colon carcinoma cell lines that displayed E-selectin adhesiveness and an increased metastatic capacity in cytokine-treated mice, we examined possible inhibition of cytokine-dependent experimental lung metastasis by a soluble form of E-selectin, the recombinant fusion protein E-selectin-immunoglobulin. We found that E-selectin-immunoglobulin bound to the surfaces of HT-29 colon carcinoma cells and blocked the formation of cytokine-inducible experimental lung metastases; control L-selectin-immunoglobulin also bound to HT-29 cells but had no effect on tumor cell lung colonization. E-selectin-immunoglobulin was found to interfere with E-selectin-dependent adhesion of HT-29 cells to activated vascular endothelium and to block the retention of these cells in the lung, a process that implies tumor cell adhesive interactions with the host vasculature. Our results demonstrate that E-selectin-immunoglobulin inhibits adhesion and formation of lung metastases by colon carcinoma cells and suggest that impairment of tumor cell-endothelium adhesion might represent a therapeutic approach to the metastatic diffusion of tumors.

Animals↗
PubMed1997

Renal reserve is normal in adults born with unilateral renal agenesis and is not related to hyperfiltration or renal failure.

This study was carried out to examine the renal hemodynamic response in adult patients with single kidneys born with unilateral renal agenesis. A group of 21 patients with unilateral renal agenesis were divided into three groups according to their glomerular filtration rate (GFR): 112 +/- 3 ml/min x 1.73 m2 in group A, 68 +/- 3.2 ml/min x 1.73 m2 in group B, and 40.7 +/- 3.3 ml/min x 1.73 m2 in group C. Mean arterial blood pressure was significantly higher in the patients of group C who were also proteinuric. The renal hemodynamic response to an oral protein load (2 g/kg of protein as beefsteak) was normal in all groups and unrelated to hyperfiltration or to renal failure and proteinuria. The study indicates that in patients with renal agenesis, the hemodynamic response to a protein challenge is similar to that of kidney donors, renal transplant recipients and uninephrectomized patients. The paper also demonstrates that the renal response to a protein challenge is inadequate to identify patients with renal agenesis who are at risk of developing renal disease. Finally, in renal agenesis with renal disease, creatinine clearance overestimated the GFR by an average of 32.7%.

Adaptation, Physiological↗
PubMed1995

Renal functional reserve in children.

Renal reserve in children is related to changes in renal plasma flow (RPF) in health and renal disease. Peak glomerular flow rate (GFR) correlates with peak RPF. The renal hemodynamic response to protein is associated with a decrease in renal vascular resistance. Studies in children are less numerous than in adults. The main findings of the studies on renal reserve in children have disclosed the following: (1) the lack of an age dependency, (2) the normalcy of renal reserve in renal disease, (3) the return of renal reserve in type 1 diabetes mellitus by a reduction in protein intake, and (4) the suppressibility of renal reserve by somatostatin infusion.

Adult↗
PubMed1995

Sequential analysis of variation in glomerular filtration rate to calculate the haemodynamic response to a meat meal.

BACKGROUND: The renal haemodynamic response to a meat meal is usually measured as either filtration capacity (maximal achieved GFR), or renal reserve (maximal GFR increase over baseline), or percent renal reserve (maximal GFR increase as a percentage of baseline). The time-course of GFR response to a meat meal varies in different individuals as the peak GFR tends to occur late in renal disease. This study proposes a new method to measure the GFR response independently of differences in peaking time. METHODS: The study is based on measurement of GFR (inulin clearance, ml/min x 1.73 m2 BSA) in three 30-min pre-meal clearance periods (baseline) followed by analysis of the GFR changes for up to 180 min (four 30-min and one 60-min clearance periods) after a meat meal (2 g of protein/kg of BW as red cooked meat). Data were analysed from 85 healthy people (GFR > or = 100) and 273 individuals with renal disease (RD) who were divided into three groups based on their baseline GFR (RD1, n = 115, GFR 99-66; RD2, n = 85, GFR 65-33; RD3, n = 73, GFR < 33). RESULTS: In healthy people after the meat meal GFR peaked between 30 and 60 min and returned to baseline by 120 min. In the three RD groups GFR peaked later than in healthy people (P < 0.001) and remained higher than baseline for up to 180 min (P < 0.001). Cumulative post-meal GFR changes, calculated as cumulative GFR increase over baseline up to 120 min after meal (ml/120 min x 1.73 m2 BSA), were significantly different (P < 0.01) in the four groups (healthy people, 937 +/- 141; RD1, 1222 +/- 141; RD2, 587 +/- 104; RD3, 361 +/- 89). Interindividual variability in cumulative GFR increase was only partially explained by the value of filtration capacity (r2 = 0.285), renal reserve (r2 = 0.640), and percent renal reserve (r2 = 0.175). CONCLUSION: The data indicate that commonly used parameters are poor indices of the actual total time-course of the renal response to a protein load.

Adult↗
PubMed1994

Role of the mevalonate pathway of isoprenoid synthesis in IL-8 generation by activated monocytic cells.

The highly regulated enzyme HMG-CoA reductase generates mevalonate, the precursor of a complex series of isoprenoids that posttranslationally modify (isoprenylate) certain proteins (e.g., the low-molecular-weight GTP-binding proteins) or that are incorporated into cholesterol and other end products. We recently reported that isoprenoids are required for NADPH oxidase activity in granulocytes via LMW GTP-binding protein isoprenylation. In this study, we evaluated the effects of isoprenoid depletion on the expression of proinflammatory genes in human monocytic THP-1 cells. We selected conditions under which pretreatment for 24 h with isoprenoid synthesis inhibitors (HMG-CoA reductase inhibitor lovastatin or compactin at 10 microM) did not compromise cell viability but markedly suppressed H2O2 generation. Under these conditions interleukin-8 (IL-8) production was attenuated (by 50-90%) in response to lipopolysaccharide, granulocyte-macrophage colony-stimulating factor, and phorbol myristate acetate. Coincubation of reductase inhibitor-treated cells with mevalonate prevented the attenuation of IL-8 production by reductase inhibitors. The effects of isoprenoid depletion on cytokine production were selective: IL-1 beta generation was not inhibited but the production of IL-6 and IL-8 was concomitantly suppressed. IL-8 induction was suppressed at least in part through attenuation of the increase in mRNA in stimulated cells. We conclude that isoprenoid generation through the mevalonate pathway is a requirement for IL-8 induction by activated monocytic cells in vitro. Isoprenylation inhibitors have the potential to alter monocyte proinflammatory function.

Cell Division↗
PubMed1994

Oxidized LDL induces monocytic cell expression of interleukin-8, a chemokine with T-lymphocyte chemotactic activity.

T lymphocytes, macrophages, and oxidized low-density lipoprotein (Ox-LDL) are collocalized in early atherosclerotic lesions. Using a low-endotoxin in vitro system, we observed that Ox-LDL but not native LDL induced the production, by both freshly adherent human peripheral blood monocytes and human monocytic THP-1 cells, of the alpha chemokine interleukin (IL)-8, a potent chemoattractant for T lymphocytes. Marked IL-8 induction by Ox-LDL did not require IL-1 beta generation in THP-1 cells. Ox-LDL-induced chemokine production was selective, as Ox-LDL did not stimulate the production by THP-1 cells of the T-lymphocyte chemotactic beta chemokine macrophage inflammatory protein (MIP)-1 alpha. IL-8 induction increased in proportion to the extent of oxidation of LDL as measured by the content of lipid oxidation end products. To identify potentially active components of Ox-LDL, we tested malondialdehyde, an arachidonate-derived lipid oxidation product, and 9-hydroxyoctadecadienoic acid, an oxidation product of linoleate, the major polyunsaturated fatty acid in LDL, and observed that they induced IL-8 generation in the absence of Ox-LDL. Furthermore, when most free lipid oxidation products were removed from Ox-LDL by dialysis, some IL-8-inducing activity was released into the dialysate. However, the major IL-8-inducing activity was not dialyzable. To address the nature of the LDL particle modification required to induce IL-8, acetylated or malondialdehyde-treated native LDL particles were monitored for activity. Neither procedure rendered LDL capable of inducing IL-8. However, phospholipase A2-treated LDL induced THP-1 cell expression of IL-8.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗
PubMed1994

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

Insulin-mediated vasodilation has been proposed as a determinant of in vivo insulin sensitivity. We tested whether sustained vasodilation with adenosine could overcome the muscle insulin resistance present in mildly overweight patients with essential hypertension. Using the forearm technique, we measured the response to a 40-min local intraarterial infusion of adenosine given under fasting conditions (n = 6) or superimposed on a euglycemic insulin clamp (n = 8). In the fasting state, adenosine-induced vasodilation (forearm blood flow from 2.6 +/- 0.6 to 6.0 +/- 1.2 ml min-1dl-1, P < 0.001) was associated with a 45% rise in muscle oxygen consumption (5.9 +/- 1.0 vs 8.6 +/- 1.7 mumol min-1dl-1, P < 0.05), and a doubling of forearm glucose uptake (0.47 +/- 0.15 to 1.01 +/- 0.28 mumol min-1dl-1, P < 0.05). The latter effect remained significant also when expressed as a ratio to concomitant oxygen balance (0.08 +/- 0.03 vs 0.13 +/- 0.04 mumol mumol-1, P < 0.05), whereas for all other metabolites (lactate, pyruvate, FFA, glycerol, citrate, and beta-hydroxybutyrate) this ratio remained unchanged. During euglycemic hyperinsulinemia, whole-body glucose disposal was stimulated (to 19 +/- 3 mumol min-1kg-1), but forearm blood flow did not increase significantly above baseline (2.9 +/- 0.2 vs 3.1 +/- 0.2 ml min-1dl-1, P = NS). Forearm oxygen balance increased (by 30%, P < 0.05) and forearm glucose uptake rose fourfold (from 0.5 to 2.3 mumol min-1dl-1, P < 0.05). Superimposing an adenosine infusion into one forearm resulted in a 100% increase in blood flow (from 2.9 +/- 0.2 to 6.1 +/- 0.9 ml min-1dl-1, P < 0.001); there was, however, no further stimulation of oxygen or glucose uptake compared with the control forearm. During the clamp, the ratio of glucose to oxygen uptake was similar in the control and in the infused forearms (0.27 +/- 0.11 and 0.23 +/- 0.09, respectively), and was not altered by adenosine (0.31 +/- 0.9 and 0.29 +/- 0.10). We conclude that in insulin-re15-76sistant patients with hypertension, adenosine-induced vasodilation recruits oxidative muscle tissues and exerts a modest, direct metabolic effect to promote muscle glucose uptake in the fasting state. Despite these effects, however, adenosine does not overcome muscle insulin resistance.

Adenosine↗
PubMed1993

Some metabolic aspects of essential hypertension and its treatment.

We tested whether patients with essential hypertension (EH) have metabolic evidence of increased adrenergic activity, and if a relationship exists between carbohydrate metabolism and the blood pressure (BP) response to angiotensin-converting enzyme (ACE) inhibition. Study 1 included 59 subjects who underwent resting ambulatory BP, heart rate, and resting energy expenditure (REE) measurement (by indirect calorimetry). REE was directly related to lean body mass (LBM) (r = 0.56, p < 0.0001) and to fasting plasma insulin levels (p < 0.03), after adjusting for LBM and age) but not to BP. The 38 subjects with EH had significantly higher fasting plasma insulin levels (54 +/- 4 vs 42 +/- 4 pM; p < 0.05) than the 21 normotensive subjects. When normalized by the LBM, the hypertensive patients had significantly higher REE values than the normotensive subjects (89 +/- 2 vs 78 +/- 3 J min-1.kg-1; p < 0.005). No differences in the other measured variables were found between the two groups. Thus, in this group of lean patients with stable EH, relative hyperinsulinemia is associated with a small increase in REE, the significance of which remains to be determined. In study 2, 20 patients with EH received an oral glucose tolerance test and a euglycemic insulin clamp before and after 3 months of treatment with cilazapril. Glucose-induced insulin response, but not insulin sensitivity, was improved by treatment in the whole group. Before therapy, the 12 responders (diastolic BP < 95 mm Hg) had similar glucose tolerance and insulin sensitivity to the eight nonresponders. Responders, however, had lower fractional potassium excretion than nonresponders both during fasting (9.6 +/- 1 vs 16.0 +/- 2.4%; p < 0.02) and during the glucose load (9.1 +/- 1.4 vs 13.1 +/- 1.1%; p < 0.04). In the responders, fasting potassium levels at baseline were directly related to the decrease in BP (p < 0.01) and to the improvement of glucose-induced insulin response (p < 0.04) achieved after treatment. Thus, the therapeutic effect of ACE inhibition is in part related to fractional potassium excretion, which, in turn, affects glucose tolerance through the influence of potassium levels on glucose-induced insulin release.

Adult↗
PubMed1993

High-mobility-group (HMG) proteins and histone H1 subtypes expression in normal and tumor tissues of mouse.

Exhaustive extraction of mouse tissues with perchloric acid has been used together with reverse-phase HPLC and electrophoresis to quantify the amounts of chromosomal proteins HMG17, HMG14 and HMGI, relative to histone H1. Normal lung and thymus contain approximately 3% HMG17/HMG14 but only approximately 2% HMGI. In tumor tissues (Lewis lung carcinoma and lymphoma NQ35), the amount of HMG17/HMG14 is not greatly altered but HMGI levels rise considerably, reaching 10% in Lewis lung carcinoma. HMGI synthesis does not replace HMG17/HMG14 proteins, suggesting that HMGI proteins contribute to the structure of chromatin regions in a manner distinct from those of HMG17/HMG14. Ion-spray mass spectrometry has been used to determine the molecular masses of H1 subtypes from the same four mouse tissues. In addition to the six known species H1 zero, H1a, H1b, H1c, H1d and H1e, a newly defined subtype of mass 21,756 Da from Lewis lung carcinoma, named H1L was identified. Several phosphorylated H1 subtypes have also been defined by mass spectrometry. The combined use of reverse-phase HPLC and electrophoresis permitted quantification of these seven histone H1 subtypes in the four mouse tissues. Increased phosphorylation of H1 subtypes in tumors parallels the phosphorylation of HMGI proteins which are present in great amounts, showing that both are involved as post-translational-modified forms in the structure of the chromatin of neoplastic systems.

Animals↗
PubMed1993

Insulin sensitivity in familial hypercholesterolemia.

Insulin resistance is found in association with obesity, non-insulin-dependent diabetes mellitus, and essential hypertension, which are all risk factors for atherosclerotic cardiovascular disease. Furthermore, hyperinsulinemia has been reported in familial combined hyperlipoproteinemia and endogenous hypertriglyceridemia. Finally, relatively high serum triglyceride and low high-density lipoprotein (HDL) cholesterol concentrations invariably accompany hyperinsulinemia. Whether insulin sensitivity is affected by the isolated presence of high levels of serum low-density lipoprotein (LDL) cholesterol has not been clearly established. We studied 13 subjects with heterozygous familial hypercholesterolemia (FHC) and 15 normocholesterolemic subjects selected to be free of any other known cause of insulin resistance. Thus FHC patients and controls had normal body weight and fat distribution, glucose tolerance, blood pressure, and serum triglyceride and HDL cholesterol concentrations, but were completely separated on plasma LDL cholesterol concentrations (6.05 +/- 0.38 v 3.27 +/- 0.15 mmol/L, P < .0001). Fasting plasma levels of glucose, insulin, free fatty acids (FFA), and potassium and fasting rates of net carbohydrate and lipid oxidation were superimposable in the two study groups. During a 2-hour euglycemic (approximately 5 mmol/L) hyperinsulinemic (approximately 340 pmol/L) clamp, whole-body glucose disposal rates averaged 30.4 +/- 2.3 and 31.1 +/- 3.0 mumol.kg-1 x min-1 in FHC and control subjects, respectively (P = 0.88). The ability of exogenous hyperinsulinemia to stimulate carbohydrate oxidation and energy expenditure and suppress lipid oxidation and plasma FFA and potassium levels was equivalent in FHC and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of acute hypercarnitinemia during increased fatty substrate oxidation in man.

To test whether carnitine availability is rate-limiting for fat oxidation under conditions of augmented oxidative use of fatty substrates, two series of studies were performed. In study no. 1, L-carnitine (1 g + 0.5 g/h intravenously [i.v.]) or saline was given to eight volunteers during a 4-hour infusion of a 10% triglyceride emulsion, thereby increasing plasma free-carnitine levels from 38 +/- 4 to 415 +/- 55 mumol/L. Fat infusion increased plasma triglyceride levels (80%) and lipid oxidation (30%), and decreased (28%) carbohydrate oxidation (as measured by indirect calorimetry); hypercarnitinemia had no influence on these responses. In study no. 2 in 12 healthy subjects a bolus of L-carnitine (3 g) or saline was administered 40 minutes before aerobic exercise (bicycling for 40 minutes at 60 W), followed by 2 minutes of anaerobic exercise (250 W) and 50 minutes of recovery. Oxygen consumption (VO2), increased to 18.3 +/- 0.7 mL.min-1 x kg-1 during aerobic exercise, reached a maximum of 46.0 +/- 0.8 mL.min-1 x kg-1 during the anaerobic bout, and returned to baseline within a few minutes, with no difference between control and carnitine. At virtually identical mean energy expenditure rates (196 +/- 7 v 197 +/- 7 J.min-1 x kg-1, saline v carnitine), after carnitine administration the entire exercise protocol was sustained by a lower mean carbohydrate oxidation rate (42.1 +/- 3.6 v 36.5 +/- 2.3 mumol.min-1 x kg-1, P < .03) and a higher mean lipid oxidation rate (6.7 +/- 1.0 v 8.3 +/- 0.7 mumol.min-1 x kg-1, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Relationship between insulin release, antinatriuresis and hypokalaemia after glucose ingestion in normal and hypertensive man.

1. Insulin simultaneously causes hypokalaemia and antinatriuresis, and it has been suggested that the two effects are tightly coupled. Whether these actions are preserved in patients with essential hypertension is not known. 2. Eight hypertensive patients and eight normotensive control subjects were studied before and after the ingestion of 75 g of glucose. Despite similar glycaemic profiles, the patients showed a hyperinsulinaemic response incremental area 49 +/- 8 versus 27 +/- 6 nmol l-1 3 h, P < 0.04) but a blunted hypokalaemic response (-7 +/- 1 versus -16 +/- 1%, P < 0.001). Both absolute and fractional urinary excretion of sodium and potassium were significantly decreased during glucose-induced hyperinsulinaemia in hypertensive patients as well as in normotensive subjects (P < 0.05 for all changes). 3. To test whether hypokalaemia is required for insulin-induced antinatriuresis, each hypertensive patient received another oral glucose load during which enough potassium chloride was given to clamp the plasma potassium concentration at baseline. Under these conditions, significant insulin-induced antinatriuresis still occurred. In addition, whereas the glycaemic profile was superimposable, the response of the plasma insulin concentration was significantly greater with than without maintenance of the plasma potassium concentration (total area 79 +/- 14 versus 63 +/- 8 nmol l-1 3 h, P < 0.04). 4. We conclude that (a) insulin causes antinatriuresis, antikaliuresis and hypokalaemia under physiological conditions; (b) in hyperinsulinaemic (insulin-resistant) patients with essential hypertension, the antinatriuretic action of insulin is quantitatively preserved; and (c) clamping plasma potassium levels prevents insulin-induced antikaliuresis but not antinatriuresis, and potentiates the insulin secretory response to glucose.

Adult↗