[Insulin resistance in the uremic patient: effects of hemodialysis]. / Insulino-resistenza nell 'uremico: effetti dell 'emodialisi.

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.

[Increase of circulating levels of insulin and C-peptide: common factors in essential hypertension and overweight]. / Aumento dei livelli circolanti di insulina e C-peptide: fattore commune nell'ipertensione essenziale e nel sovrappeso.

The aim of our study was to investigate the hypothesis that insulin resistance is involved in the pathogenesis of essential hypertension, and to explain whether hyperinsulinemia in this condition is the result of either pancreas overproduction or defective hepatic insulin clearance. In 14 lean normotensive, 17 overweight normotensive, 17 lean essential hypertensive, and 20 overweight essential hypertensive subjects, we measured, after overnight fasting, blood glucose, serum insulin, and serum C-peptide, and calculated the glucose/insulin and the insulin/C-peptide ratios, which can be commonly taken as indexes of peripheral sensitivity to insulin and hepatic insulin clearance, respectively. When compared to lean normotensives, overweight and/or hypertensive patients exhibited higher serum insulin and C-peptide concentrations, and a lower glucose/insulin ratio. No difference was found in the insulin/C-peptide ratio between normotensive and hypertensive subjects. Diastolic blood pressure was directly correlated with serum insulin (p less than 0.01) and C-peptide (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. Considering the normality of the insulin/C-peptide ratio when taken as the hepatic insulin clearance index, we believe that hyperinsulinemia is caused by a beta-cell hypersecretory response to the defective peripheral action of the hormone.

[Trans-membrane cationic flow and hemodialysis]. / Flussi cationici trans-membrana ed emodialisi.

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.

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.

Sublingual and intravenous ketanserin versus sublingual nifedipine in the treatment of severe hypertension: a randomized study.

Thirty-seven patients with severe hypertension were randomly assigned to receive 20 mg of ketanserin sublingually, 10 mg of ketanserin intravenously, or 20 mg of nifedipine sublingually. Systolic and diastolic blood pressures fell significantly after the three treatments. The maximum effects were reached 25 minutes after sublingual ketanserin (with decreases of 7.7% in systolic and 7.1% in diastolic blood pressure), six minutes after intravenous ketanserin (decreases of 9.4% and 9.6%, respectively), and 25 minutes after sublingual nifedipine (decreases of 16.9% and 15.9%, respectively). Blood pressure returned to pretreatment levels 20 minutes after intravenous ketanserin. Heart rate increased significantly in the group receiving nifedipine. No changes in plasma aldosterone, sodium, or potassium levels or in erythrocyte sodium and potassium levels were found after ketanserin. It is concluded that even intravenous ketanserin is inferior to sublingual nifedipine in the control of blood pressure.