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Biomedical subjects

L A Sechi

Publications and source records attributed to L A Sechi.

At least 127 records · Page 7Linked to original sources
PubMed1991

Evaluation of insulin-induced changes in the renal response to furosemide in normal subjects.

Over the last years, a large mass of information has accumulated indicating that changes in the serum insulin concentration can affect renal electrolyte excretion. We analyzed the response of the kidney to furosemide in 5 healthy men, in the presence of both normal physiological serum insulin levels and levels at the upper limit of the physiological range, obtained by the hyperinsulinemic-euglycemic clamp technique. After furosemide administration, glomerular filtration rate, urine flow, urine sodium excretion, free water clearance, urine pH, plasma renin activity and plasma aldosterone exhibited the same behavior in the presence of both serum insulin concentrations. The rise in urinary potassium excretion following furosemide administration was significantly lower in the presence of high insulin concentrations. Although we observed a slight decrease in plasma potassium levels during the equilibration phase of the clamp required before the administration of furosemide, a significantly lower increase in potassium fractional excretion indicated a direct tubular effect of insulin. Thus, in conditions in which natriuresis is mildly stimulated, as in the case of the administration of low doses of furosemide, insulin does not affect the rate of renal sodium reabsorption. Conversely, the hormone has an appreciable influence on the modulation of tubular potassium exchanges.

Adult↗
PubMed1990

Evidence for a direct and non-receptor-mediated action of 5HT2 antagonists on transmembrane cation transport systems.

Changes in transmembrane sodium fluxes have been reported in normotensive and in hypertensive subjects after ketanserin administration. In this study, the effects of the serotonergic system on transmembrane sodium transport mechanisms have been investigated in vitro. In erythrocytes drawn from ten healthy subjects, we studied the effects of serotonin (5HT) on the Na/K pump, Na/K cotransport, Na/Li countertransport, and passive permeability of Na. No significant changes were found. A direct, non-receptor-mediated action of ketanserin was then suspected, and the effects of two concentrations of ketanserin (5 x 10(-8) and 5 x 10(-7) M) were evaluated in erythrocytes from 12 normal volunteers. Both concentrations of ketanserin significantly decreased the activity of the Na/K pump and increased the activity of Na/Li countertransport. Na/K cotransport and passive permeability were not affected. Indirect evidence of the action of ketanserin on sodium transmembrane fluxes came from other experiments. In the red blood cells taken from five normal subjects and incubated for 2 hours in a plasma pool, we evaluated the changes in intracellular sodium concentration induced by the presence of 5HT or ketanserin. A significant decrease in intracellular sodium concentration occurred only with ketanserin. This study indicates that ketanserin has a direct influence on transmembrane sodium fluxes. If this action were also present in other cells, it might contribute to the actions of the drug at vascular, nervous, and renal tubular levels.

Adult↗
PubMed1990

Insulinemia and blood pressure. Relationships in patients with primary and secondary hypertension, and with or without glucose metabolism impairment.

In order to investigate the relationships between insulinemia and hypertension, fasting insulinemia has been assessed in 117 subjects: 69 normotensive subjects, 36 with essential hypertension, and 12 with renovascular hypertension, all untreated and newly diagnosed, classified in subgroups (euglycemic nonobese, euglycemic obese, with impaired glucose tolerance and with non-insulin-dependent diabetes mellitus). In the patients with essential hypertension fasting insulinemia was significantly higher than in normotensive subjects (P less than .0005). The patients with secondary hypertension and the normotensive subjects had similar fasting insulinemia values. In each subgroup fasting insulinemia was higher in hypertensive patients than among normotensive subjects (P less than .05). A significant correlation between fasting insulinemia and mean blood pressure has been found in patients with essential hypertension (r = 0.408, P less than .05), but not in patients with renovascular hypertension. Our data suggest a possible direct relationship between fasting insulinemia and blood pressure, especially in obese patients or patients with impaired glucose metabolism, and that increased blood pressure per se is not an insulin resistant state.

Adult↗
PubMed1990

Effects of ketanserin on transmembrane sodium transport in erythrocytes.

Ketanserin, an antagonist of 5-HT2-serotonergic and alpha 1-adrenergic receptors, has come into use for the therapy of mild to moderate arterial hypertension. Quite recent observations have shown changes in transmembrane sodium (Na) transport after the acute administration of high doses of this drug to normal subjects. It is well known that some of these transport systems have an altered activity in essential hypertension. We evaluated the effects of long-term (3 months) administration of ketanserin (40-80 mg/day) on Na and potassium (K) intracellular concentrations and transmembrane fluxes in red blood cells (RBCs) from 12 essential hypertensive patients. In addition the present study describes the in vitro effects of two different concentrations of the drug (5 x 10(-8) and 5 x 10(-7) M) on erythrocytes in normal subjects. In the first study, both systolic and diastolic blood pressure were significantly lowered by the treatment with ketanserin (from 165/103 to 143/89; p less than 0.001). Na and K intraerythrocyte concentrations fell markedly during ketanserin administration (both p less than 0.001). A marked decrease in Na,K-pump activity (p less than 0.001) and an increase in Na,lithium(Li)-countertransport function (p less than 0.001) were observed. Na outward cotransport, Na leak, and K leak were not modified by the therapy. Direct correlation was found between the fall in mean blood pressure and in Na and K intraerythrocyte concentration (respectively, p less than 0.01 and p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Trans-membrane cationic flow and hemodialysis].

Abnormalities of intracellular ion concentrations and transmembrane fluxes were reported in uremia. In RBC from 12 chronically hemodialyzed patients (age 41 + 12, 7 men, 5 women; mean dialysis duration 31 + 24 months), we evaluated the acute effects of hemodialysis on intracellular Na and K concentrations, ouabain sensitive Na/K pump, furosemide sensitive Na/K cotransport, Na/Li countertransport, and passive permeability to Na. Six patients were normotensive and 6 were taking antihypertensive drugs which were withdrawn before the study. When compared to our normal reference group, uremic patients showed a significant increase in intracellular K concentration and a significant decrease in ouabain-sensitive Na/K pump. Intracellular sodium was not increased. No correlation was found between the activity of sodium-potassium pump and the duration of hemodialysis. The other transport systems were comparable to normal. No significant change was observed between the values measured before and after dialysis. Ouabain sensitive Na/K pump was lower in hypertensive as compared to normotensive patients, but this difference was not significant. Our data support the existence of ion transport derangements in uremia, which are not acutely affected by hemodialysis.

Adult↗
PubMed1990

Renal response to furosemide in normal subjects during hyperinsulinaemic clamp.

The study has been performed in an attempt to provide further data on the supposed direct action of insulin on the kidney, based on the assumption that any effect of insulin on sodium reabsorption via co-transport should shift the dose-response curve to the furosemide administration. In five normal male volunteers plasma insulin concentration was changed by means of a hyperinsulinaemic euglycaemic clamp. The diuresis and natriuresis following intravenous injections of furosemide (in increasing doses) were measured in basal conditions and during clamp. No significant difference was found between the experiments performed in the two conditions. Our study has not identified a direct sodium-retaining effect of insulin on the furosemide-sensitive mechanisms of the renal tubule.

Adult↗
PubMed1990

Effects of furosemide on blood pressure in anephric rats.

This study has been performed in order to evaluate whether furosemide can induce changes in blood pressure independently of its diuretic effects,and whether its pressor effects are connected with the ability to synthetize renal prostaglandins. The experiments were performed in four groups of volume-expanded rats: the first (n.5) had bilateral ligation of the renal vessels; the second (n.8) had bilateral ligation of the ureters; the third group (n.6) had ureters ligation after pre-treatment with indomethacin; the fourth group (n.2) received a pre-treatment with captopril. After blood pressure stabilization, furosemide was administered i.v. (0.125 mg/100 g. of body weight). Indirect readings of the blood pressure were obtained at 1, 2, 3, 4, 5, 7.5, 10, 15, 20 min. After furosemide administration, blood pressure fell down quickly in the rats with ureteral ligation and in those with captopril pretreatment, while the tensive response to furosemide was blunted by the indomethacin treatment. In conclusion, furosemide can reduce blood pressure by a mechanism non related with its diuretic properties, which, however, requires the integrity of the renal connections with the circulatory system.

Animals↗
PubMed1990

[Insulin resistance in the uremic patient: effects of hemodialysis].

The carbohydrate metabolism abnormalities present in uremia have been attributed to a combination of peripheral resistance to insulin and inhibition of insulin release secondary to beta cells insensitivity. Previous studies evaluated the chronic effects of hemodialysis on glucose metabolism, while acute effects were not examined. In 12 uremic subjects undergoing hemodialysis (3 times a week) the fasting serum levels of glucose, insulin and C-peptide were measured, and the glucose/insulin ratio was calculated as an index of peripheral sensitivity to insulin before and after dialysis. While glucose did not change, insulin and C-Peptide rose significantly after dialysis. The rise in insulin and C-Peptide was directly correlated with the fall in body weight due to the fluid loss. This might indicate that the increase in insulin and C-peptide was due to a concentration phenomenon. However, it could reflect a reaction to hypoglycemia. The glucose/insulin ratio exhibited trend towards a fall after hemodialysis. Although not significant, this might indicate an acute worsening of the peripheral sensitivity to insulin, induced by the procedure.

Adult↗
PubMed1990

Insulin resistance and beta-cell hypersecretion in essential hypertension.

To determine whether a decreased sensitivity to insulin is involved in the pathogenesis of essential hypertension, fasting blood glucose, serum insulin, serum C peptide, the glucose:insulin ratio and the insulin:C-peptide ratio were measured in 14 lean normotensives, 17 overweight normotensives, 17 lean hypertensives and 20 overweight hypertensives. Compared with the lean normotensives, the patients who were overweight, those with hypertension and those who were both overweight and hypertensive showed increased fasting serum insulin and C-peptide levels, and a lower glucose:insulin ratio. No significant difference between the normotensive and the hypertensive subjects was found in the insulin:C-peptide ratio. Diastolic blood pressure was directly correlated with serum insulin (P less than 0.01) and with C-peptide levels (P less than 0.01), and inversely correlated with the glucose:insulin ratio (P less than 0.02). We conclude that insulin resistance is present in both essential hypertensive and overweight subjects. Since the present study showed that hepatic insulin clearance was normal in hypertensives, the hyperinsulinaemia in essential hypertension appears to be due to beta-cell hypersecretion in response to a defective peripheral action of the hormone.

Adult↗
PubMed1989

Antihypertensive effect of insulin reduction in diabetic-hypertensive patients.

Body weight, urinary volume, sodium and potassium excretion, and blood pressure were evaluated for six days in twelve type II diabetic women, taking insulin doses over their need, after insulin daily dosage reduction. Six of them were suffering from essential hypertension. A significant decrease in body weight with an increase in urinary volume and in urinary sodium excretion was found in all patients. However, no significant variation in plasma renin activity and urinary aldosterone output was observed. Urinary potassium excretion remained unchanged. In normotensive subjects no variation of blood pressure levels occurred. On the contrary, hypertensive patients exhibited, after insulin reduction, a fall in systolic and diastolic blood pressure, which correlated directly with body weight decrease and inversely with urinary volume and urinary sodium excretion increases. Hypotheses relating insulin action to hypertension are discussed.

Aged↗
PubMed1989

[Disseminated intravascular coagulation and acute hepatic necrosis at the end of pregnancy. A case report].

A 30-year-old woman in the 36th week of her second pregnancy, suddenly developed jaundice with remarkable liver necrosis, accompanied by generalized bleeding due to disseminated intravascular coagulation (DIC). She underwent a caesarean and a dead foetus was extracted from the uterus. Heparin and frozen plasma infusion resulted in a prompt recovery from the haemostatic disorder. The course of the disease involved the successive appearance of haemorrhagic shock, intestinal ileus and pulmonary embolism all of which she recovered from. The liver biopsy showed severe cholestasis without derangement of the lobular structure. Hypotheses of acute veno-occlusive disease caused by the DIC, and acute fatty liver of pregnancy are discussed.

Acute Disease↗
PubMed1989

[Paroxysmal nocturnal hemoglobinuria with multiple venous thrombosis and acute renal insufficiency. Description of a case].

Oral anticoagulants were administered to a young woman suffering from P.N.H. after the development of portal vein thrombosis. She interrupted the treatment and developed multiple splanchnic thromboses followed by acute renal failure, from which she recovered four weeks later. Although the pathogenetic mechanism could include renal vascular microthrombosis, the possibility of renal ischemic damage due to massive blood pooling within the splanchnic district is discussed.

Acute Kidney Injury↗
PubMed1988

In vitro action of insulin on erythrocyte sodium transport mechanisms: its possible role in the pathogenesis of arterial hypertension.

The effects of insulin on sodium and potassium metabolism have been well known for many years; clinical observation and laboratory experience showed different results about the insulin effect on the sodium-potassium pump. Moreover, studies about the insulin effect on the sodium-potassium cotransport are not available. Therefore, the effects of insulin on Na+,K+ pump and Na+,K+ cotransport were evaluated. Results show that insulin inhibits Na+,K+ pump, while Na+,K+ cotransport is markedly activated. The possible link between pathogenesis of arterial hypertension in hyperinsulinemic subjects and present data is examined.

Adult↗
PubMedDate not supplied

Heterogeneous derangement of cellular sodium metabolism in Bartter's syndrome. Description of two cases and review of the literature.

The basic tubular alteration present in Bartter's syndrome is still a subject of controversy. The possibility that a generalized defect in transmembrane ion transport underlies the disease has been extensively investigated. Previous evaluations of cellular sodium metabolism in Bartter's patients showed extremely variable findings. In the present study we have examined in red blood cells of two patients with Bartter's syndrome the intracellular Na+ and K+ concentrations, the activity of ouabain-sensitive Na+/K+ pump, furosemide sensitive Na+/K+ cotransport, Na+/Li+ countertransport, and the rate constant of Na+ and K+ passive permeability. We have compared these values with those of a control group. Ouabain-sensitive Na+/K+ pump activity was decreased in both patients, whereas Na+/Li+ countertransport was activated. One of the patients also exhibited markedly decreased intraerythrocyte K+ concentration and decreased furosemide-sensitive Na+/K+ cotransport. The other had increased Na+/K+ cotransport activity and Na+ passive permeability. Intracellular Na+ and passive permeability to K+ were normal in both subjects. Our results are partially consistent with previously reported observations, and indicate the existence of heterogeneous alterations of erythrocyte sodium transport systems in patients with Bartter's syndrome. Although some of these alterations could be secondary to the electrolyte metabolism derangements of this disease, others might be genetically transmitted and could cause the different renal tubular defects shown in Bartter's disease so far.

Adult↗