Do KCa channels and carbonic anhydrase play a role in thiazide-induced hyperglycaemia?
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.
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.
P
P
Pickkers
M
M
Schachter
P S
PS
Sever
A D
AD
Hughes
D001581:Benzothiadiazines; D015220:Calcium Channels / Q000187:drug effects* / Q000378:metabolism; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D002256:Carbonic Anhydrases / Q000187:drug effects* / Q000378:metabolism; D004232:Diuretics; D006801:Humans; D006943:Hyperglycemia / Q000139:chemically induced* / Q000209:etiology; D006973:Hypertension / Q000188:drug therapy; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects* / Q000378:metabolism; D049993:Sodium Chloride Symporter Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use
D001581:Benzothiadiazines; D015220:Calcium Channels; D002257:Carbonic Anhydrase Inhibitors; D004232:Diuretics; D015221:Potassium Channels; D049993:Sodium Chloride Symporter Inhibitors; D002256:Carbonic Anhydrases