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Different susceptibility to vascular damage induced by chronic hyperglycemia in aortic and pulmonary arteries from Sprague Dawley and Wistar Kyoto rats
Author(s) -
De Jesus Luis,
Zurita Enedina,
Gomez Ma. de Jesus,
Suarez Jorge
Publication year - 2015
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.29.1_supplement.964.7
Subject(s) - phenylephrine , medicine , aorta , pulmonary artery , thoracic aorta , pulmonary hypertension , endocrinology , cardiology , blood pressure , vascular resistance , vascular smooth muscle , smooth muscle
In this study was evaluated the effect of chronic hyperglycemia in the vascular response of thoracic aorta and pulmonary trunk in two strain rats. Chronic hyperglycemia was induced in male Wistar Kyoto (WK) and Sprague Dawley (SD) rats for single injection of streptozotocin (60 mg/kg, ip.). After 8 weeks, body weight, glucose, systemic arterial blood pressure (SABP) and right ventricular systolic pressure (RVSP) were measured. Thoracic aorta and pulmonary trunks were removed for vascular reactivity studies. Cumulative concentration‐response curves with phenylephrine (Phe) and Acetylcholine (ACh) were made in aorta and pulmonary rings. Glucose blood levels (mg/dl) were similar in both groups, 525±2 vs. 502±3. SABP in mmHg was increased in hyperglycemic SD compared to WK rats 160±2 vs. 140±2, while RVSP was higher in WK than SD rats 41±2.6 vs. 22±1.5 (P<0.001). Maximal tension contraction (g) response with Phe was higher in hyperglycemic SD against hyperglycemic WK aortic rings (2.1±0.1 vs. 1.2±0.1, P<0.001), with similar response in the pulmonary rings in both groups. ACh‐induced relaxation (%) response was reduced in SD aorta and pulmonary rings, 58±3 vs 66±4, and this response was attenuated inaorta 78±3, and pronounced in pulmonary rings, 49±3, from WK rats (P<0.001). The results shown that chronic hyperglycemia induce vascular damage predominantly in pulmonary artery in WK rats as consequence pulmonary hypertension, whereas in SD rats, systemic hypertension consecutive to aorta damage is mainly developed suggesting that a genetic factor determine the vascular damage induced by chronic hyperglycemia.