title: Effect of nifedipine, captopril and prazosin on secretory function of pancreatic beta-cells in hypertensive patients with type-2 (non-insulin-dependent) diabetes and in hypertensive non-diabetics.
abstract: The aim of our study was to compare the effect of captopril--the angiotensin-converting enzyme inhibitor, nifedipine--the calcium antagonist, and prazosin--the alpha blocker, on the secretory function of pancreatic beta-cells in hypertensive patients with NIDDM and with normal glucose tolerance. The effect of a 2-week treatment with nifedipine, captopril and prazosin upon glycaemia, serum insulin (IRI) and C-peptide (CP) following oral and intravenous glucose load were investigated in three groups, each including 10 non-diabetic patients with essential hypertension (h) and 10 hypertensive type 2 (non-insulin-dependent) diabetics (h + d), aged 32-63 years. Nifedipine produced increase in glycaemia in the oral test in both groups. In the (h) group, but not in the (h + d) group, the drug caused reduction of the glucose-dependent increases in serum IRI and CP, more marked with respect to CP, as expressed by the decrease in the molar serum CP/IRI ratio. These results indicate that in non-diabetic patients, nifedipine reduces the early response of beta-cells to glucose, but this effect is partly compensated by a decreased insulin uptake by the liver. In patients with type 2 diabetes, this phenomenon does not become manifest because of absence or reduction in the early glucose-dependent insulin release. After captopril, lower values of glycaemia and serum IRI and CP were observed in both groups suggesting an improvement of insulin sensitivity. In conclusion, nifedipine has a small influence, and captopril and prazosin are devoided of any influence on the secretory function of pancreatic beta-cells. These drugs may be recommended for the treatment of hypertension in patients with type 2 (non-insulin-dependent) diabetes.
authors.affiliation: Department of Gastroenterology and Metabolic Diseases, University School of Medicine in Warsaw, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Jasik
authors.forename: A
authors.initials: A
authors.lastname: Kasperska-Dworak
authors.forename: A
authors.initials: A
authors.lastname: Czyzyk
mesh_terms: D000328:Adult; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects; D002096:C-Peptide / Q000097:blood; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000494:pharmacology / Q000627:therapeutic use*; D011224:Prazosin / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000959:Antihypertensive Agents; D001786:Blood Glucose; D002096:C-Peptide; D002121:Calcium Channel Blockers; D007328:Insulin; D002216:Captopril; D009543:Nifedipine; D011224:Prazosin