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L A Sechi

Publications and source records attributed to L A Sechi.

129 records · Page 8Linked to original sources

[Increase of circulating levels of insulin and C-peptide: common factors in essential hypertension and overweight].

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.

Adult↗

[Evaluation of acute and chronic effects of ketanserin in the treatment of hypertension and hypothesis on a new mechanism of action].

Ketanserin is a specific antagonist of the 5-HT2 serotoninergic receptors; it is located on the smooth muscle cells of the vessel wall, and its stimulation causes vasoconstriction. The aim of this study is to evaluate the antihypertensive effect of ketanserin in patients with essential and secondary hypertension. Both systolic and diastolic blood pressure significantly decreased, in 18 patients, after chronic treatment with oral therapy (40-80 mg/day), and in 37 patients, after acute administration of sublingual (20 mg) and intravenous (10 mg) ketanserin. Acute administration of ketanserin was less effective than nifedipine (10 mg) in severe hypertension. Ketanserin, compared to placebo, permitted the normalization of blood pressure in 6/10 patients. Cardiovascular effects of ketanserin were studied with the ECOCG method in 8 patients with hypertension: peripheral resistances decreased, but left ventricular function and structure did not change. The effect of ketanserin on Na transmembrane transport systems in erythrocytes was studied both in vivo and in vitro, in order to evaluate the ketanserin action mechanism. The Na/K pump decreased and Na/Li countertransport increased, while different concentrations of serotonin did not change the transmembrane transport systems. In conclusion, ketanserin has a direct effect on transmembrane transport systems, not mediated by the serotonin receptors. This effect, with an antagonist of 5-HT2 serotoninergic and alpha 1 adrenergic receptor action, can cause a hypotensive effect.

Adult↗

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.

Administration, Sublingual↗