Preservation of the arterial pressure response to leptin in diet-induced obese mice: A potential mechanism for obesity hypertension
Author(s) -
Kamal Rahmouni,
Gareth Morgan,
Donald A. Morgan,
A MARK,
William G. Haynes
Publication year - 2005
Publication title -
american journal of hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.009
H-Index - 136
eISSN - 1941-7225
pISSN - 0895-7061
DOI - 10.1016/j.amjhyper.2005.03.556
Subject(s) - leptin , medicine , endocrinology , mean arterial pressure , blood pressure , obesity , diet induced obese , heart rate , insulin resistance
by 34.62% (P 0.05) vs the control. IRI and C-peptid initial levels in group III increased by about 4 times compared to group I and the control (P 0.05). These factors decreased 25.81% (P 0.05) and 52.68% (P 0.05) compared to the initial values and the control. The concentration of VEGF in group I was twice as high as in the control at 29.80 4.73 ng/ml vs 19.33 2.09 ng/ml in the control (P 0.05). E-1 levels for group I did not change at 2.63 0.95 pg/ml vs 1.50 0.15 pg/ml in the control (P 0.05). VEGF level decreased to that of the control (P 0.05) and E-1 level remained at that value. VEGF levels in groups II and III appeared to be 1.5-2 times higher than the control. VEGF after treatment decreased but was still higher than the control by 22.65% (P 0.05). The E-1 blood levels in groups II and III were higher by a factor of 5 and 7 times (P 0.05) vs the control. E-1 levels decreased by a factor of 2-3, but did not reach the control. In conclusion, moxonidine decreased the level of hyperinsulinemia, normalized the insulin secretion and endothelial vasoregulation in patients with AH and IR.
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