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Impaired Arterial Pressure Stability Is Improved by Sodium‐glucose Co‐transporter 2 Inhibitor in Streptozotocin‐induced Diabetic Rat
Author(s) -
Yoshikawa Tomoko,
Kishi Takuya,
Hirooka Yoshitaka
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.753.3
Subject(s) - streptozotocin , diabetes mellitus , medicine , endocrinology , blood pressure , lability , chemistry , biochemistry
Background Although all anti‐diabetic agents could not certainly prevent cardiovascular events, arterial pressure (AP) reduction has been determined to have beneficial prevention for cardiovascular mortality in patients with diabetes mellitus (DM). Moreover, patients with DM have impaired AP variability. In these aspects, a new anti‐diabetic agent sodium‐glucose co‐transporter 2 (SGLT2) inhibitor has been focused on its unique AP lowering effect. We examined whether DM model rats would destabilize AP or not, and if so, whether SGLT2 inhibitor could ameliorate the disruptive AP lability. Methods We used streptozotocin‐induced diabetic (STZ) rats with telemetric AP monitoring. At 10 days after the injection of streptozotocin, SGLT2 inhibitor (ipragliflozin 1mg/kg/day) was orally administered to established hyperglycemic STZ rats for 15 days. We calculated the average and standard deviation (SD) of AP as the index of lability from AP histograms. Results After streptozotocin injection, mean AP did not change both in day (rest)‐time and night (active)‐time. SD of AP increased in rest‐time (3.2 mmHg to 3.7 mmHg, n=2) but not changed in active‐time. SGLT2 inhibitor for 15 days reduced mean AP both in rest‐ (−5.6 mmHg, n=2) and active‐time (−5.9 mmHg, n=2), and ameliorated SD of AP both in rest‐ (3.7 mmHg to 3.0 mmHg, n=2) and active‐time (3.5 mmHg to 2.5 mmHg, n=2). Conclusions SGLT2 inhibitor ameliorates the disruptive AP lability in rest‐ and active‐time with depressor response in diabetic model rats. Support or Funding Information This study was supported by a Grant‐in‐Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (24390198 to Dr. Hirooka and 22790709 to Dr. Kishi).