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Role of hyperglycaemia in the pathogenesis of hypotension observed in type‐1 diabetic rats
Author(s) -
Liu IMin,
Chang Cheng Kuei,
Juang ShiowWen,
Kou DaiHuang,
Tong YatChing,
Cheng KaiChun,
Cheng JueiTang
Publication year - 2008
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2008.00595.x
Subject(s) - medicine , endocrinology , pathogenesis , phenylephrine , blood pressure , muscarinic acetylcholine receptor , diabetes mellitus , streptozotocin , agonist , type 2 diabetes , heart rate , baroreflex , receptor
Summary The role of hyperglycaemia in the pathogenesis of hypotension in diabetic disorders was investigated using the changes in cardiac M 2 ‐muscarinic receptor (M 2 ‐mAChR) gene expression in type‐1‐like diabetic rats and cultured cardiomyocytes. Blood pressure was markedly decreased in diabetic rats following the intravenous injection of streptozotocin (STZ) for 8 weeks. Also, the baroreflex sensitivity (ΔHR/ΔBP), as measured by the changes in heart rate (ΔHR) and mean blood pressure (ΔBP) 1 min after the intravenous injection of phenylephrine (10 μg/kg), was significantly increased. Arecaidine propargyl ester (APE), a M 2 ‐mAChR agonist produced a marked reduction in heart rate in these diabetic rats. Normalization of plasma glucose in diabetic rats using insulin (0.5 IU) or phlorizin (1 mg/kg) injection attenuated the blood pressure reduction and reversed the mRNA and protein levels of cardiac M 2 ‐mAChR. A high concentration of glucose (20 mmol/l) directly influenced the increase in gene expression of M 2 ‐mAChR in the H9c2 cardiac cell line. Hyperglycaemia induced an increase in cardiac M 2 ‐mAChR gene expression, suggesting a role in the pathogenesis of hypotension in diabetic disorders.