Impaired KATP channel function in the fetoplacental circulation of patients with type 1 diabetes mellitus

Autor: Jeroen van der Laak, Tanya M. Bisseling, Jenny J.H. Copius Peereboom-Stegeman, Paul Smits, Frans G. M. Russel, Joop M.P.M. Borggreven, Marieke G. Versteegen, Eric A.P. Steegers, Selina van der Wal
Přispěvatelé: Obstetrics & Gynecology
Rok vydání: 2005
Předmět:
medicine.medical_specialty
Potassium Channels
Endothelium
Charybdotoxin
Pregnancy in Diabetics
Membrane transport and intracellular motility [NCMLS 5]
Vascular medicine and diabetes [UMCN 2.2]
In Vitro Techniques
Apamin
Glibenclamide
chemistry.chemical_compound
SDG 3 - Good Health and Well-being
Pregnancy
Internal medicine
Glyburide
Medicine
Humans
Channel blocker
Placental Circulation
4-Aminopyridine
Renal disorder [IGMD 9]
Molecular diagnosis
prognosis and monitoring [UMCN 1.2]

Cardiovascular diseases [NCEBP 14]
business.industry
Endocrinology and reproduction [UMCN 5.2]
Effective Hospital Care [EBP 2]
Obstetrics and Gynecology
Endothelial Cells
Potassium channel
Renal disorders [UMCN 5.4]
Blood pressure
Endocrinology
medicine.anatomical_structure
Diabetes Mellitus
Type 1

chemistry
Fetoplacental Circulation
Female
business
Perfusion
medicine.drug
Zdroj: American Journal of Obstetrics and Gynecology, 192, 3, pp. 973-9
American Journal of Obstetrics and Gynecology, 192, 973-9
American Journal of Obstetrics and Gynecology, 192(3), 973-979. Mosby Inc.
ISSN: 0002-9378
Popis: Contains fulltext : 47618.pdf (Publisher’s version ) (Open Access) OBJECTIVE: The increased perinatal morbidity in diabetes may be partly related to vascular dysfunction. Because potassium channels play an important role in the regulation of vascular tone, this study explores the impact of diabetes on potassium channel function in the fetoplacental vascular bed. STUDY DESIGN: Vascular potassium channel function was investigated by ex vivo dual perfusion of isolated placental cotyledons (n = 47). Appropriate control experiments were carried out to exclude nonspecific effects. RESULTS: Glibenclamide (KATP channel blocker) increased perfusion pressure to a maximum fetoplacental arterial pressure of 37 +/- 6 mm Hg in controls versus 15 +/- 6 mm Hg in diabetes (P < .05). 4-Aminopyridine (KV channel blocker) equally increased fetoplacental arterial pressure in controls, and in diabetes (21 +/- 4 mm Hg vs 22 +/- 2 mm Hg). Apamin and charybdotoxin (KCa channel blockers) caused a negligible rise in fetoplacental arterial pressure. CONCLUSION: In the fetoplacental circulation, KATP channels and KV channels significantly contribute to baseline vascular tone. In diabetes, vascular KATP channel function is impaired.
Databáze: OpenAIRE