Long-term diet-induced hypertension in rats is associated with reduced expression and function of small artery SKCa, IKCa, and Kir2.1 channels

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Anna Katrina Jógvansdóttir Gradel, Max Salomonsson, Charlotte Mehlin Sørensen, Niels-Henrik von Holstein-Rathlou, Lars Jørn Jensen

Rationale: Abdominal obesity and/or a high intake of fructose may cause hypertension. K+ channels, Na/K-ATPase, and voltage-gated Ca2+ channels are crucial determinants of resistance artery tone and thus the control of blood pressure. Limited information is available on the role of K+ transporters in long-term diet-induced hypertension in rats.
Hypothesis: A 28-week diet rich in fat, fructose, or both, will lead to changes in K+ transporter expression and function, which is associated with increased blood pressure and decreased arterial function.
Methods and Results: Male Sprague Dawley rats received a diet containing normal chow (Control), high-fat chow (High Fat), high-fructose in drinking water (High Fructose), or a combination of high-fat and high-fructose diet (High Fat/Fruc) for 28 weeks from age 4-weeks. Measurements included body weight (BW), systolic blood pressure (SBP), mRNA expression of vascular K+ transporters, and vessel myography in small mesenteric arteries. BW was increased in the High Fat and High Fat/Fruc groups, and SBP was increased in the High Fat/Fruc group. mRNA expression of SKCa, IKCa, and Kir2.1 K+ channels were reduced in the High Fat/Fruc group. Reduced EDH-type relaxation to acetylcholine was seen in the High Fat and High Fat/Fruc groups. Ba2+-sensitive dilatation to extracellular K+ was impaired in all experimental diet groups.
Conclusions: Reduced expression and function of SKCa, IKCa and Kir2.1 channels is associated with elevated blood pressure in rats fed a long-term high fat/high fructose diet. Rats fed a 28-week high fat/high fructose diet provide a relevant model of diet-induced hypertension.
OriginalsprogEngelsk
TidsskriftClinical Science
Vol/bind132
Udgave nummer4
Sider (fra-til)461–474
Antal sider14
ISSN0143-5221
DOI
StatusUdgivet - 28 feb. 2018

ID: 190211614