Do KCa channels and carbonic anhydrase play a role in thiazide-induced hyperglycaemia?

P Pickkers; M Schachter; P S Sever; A D Hughes

Do KCa channels and carbonic anhydrase play a role in thiazide-induced hyperglycaemia?

J Hum Hypertens. 1995 Aug;9(8):691-3.

Authors

P Pickkers¹, M Schachter, P S Sever, A D Hughes

Affiliation

¹ Department of Clinical Pharmacology, Queen Elizabeth the Queen Mother Wing, St. Mary's Hospital Medical School, Imperial College of Science Technology and Medicine, London, UK.

PMID: 8523393

Abstract

Thiazide diuretics are widely used to treat hypertension, but their use is associated with impaired glucose tolerance. We propose that the diabetogenic action of thiazides may be due to their ability to open calcium-activated potassium (KCa) channels in pancreatic beta-cells.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Benzothiadiazines*
Calcium Channels / drug effects*
Calcium Channels / metabolism
Carbonic Anhydrase Inhibitors / pharmacology
Carbonic Anhydrases / drug effects*
Carbonic Anhydrases / metabolism
Diuretics
Humans
Hyperglycemia / chemically induced*
Hyperglycemia / etiology
Hypertension / drug therapy
Islets of Langerhans / drug effects*
Islets of Langerhans / metabolism
Potassium Channels / drug effects*
Potassium Channels / metabolism
Sodium Chloride Symporter Inhibitors / adverse effects*
Sodium Chloride Symporter Inhibitors / therapeutic use

Substances

Benzothiadiazines
Calcium Channels
Carbonic Anhydrase Inhibitors
Diuretics
Potassium Channels
Sodium Chloride Symporter Inhibitors
Carbonic Anhydrases