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Evaluation of the Cardiovascular Responses in Nicotinamide+Streptozotocin Diabetic Pithed Rats
Author(s) -
Centurion David,
TorresGutierrez Miriam,
GutierrezLara Erika,
SanchezLopez Araceli
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.627.6
Subject(s) - methoxamine , streptozotocin , sodium nitroprusside , endocrinology , medicine , nicotinamide , diabetes mellitus , saline , nad+ kinase , chemistry , nitric oxide , biochemistry , agonist , enzyme , receptor
In vitro studies have demonstrated that during diabetes a vascular dysfunction is observed. However, very few studies in vivo have confirmed these findings in the systemic vasculature. Thus, this study evaluated the vasopressor responses induced by sympathetic stimulation or by i.v. bolus injections of the agonists noradrenaline (α 1/2 ), methoxamine (α 1 ), UK 14,304 (α 2 ), and the vasodepressor responses induced by acetylcholine and sodium nitroprusside in rats pretreated with: (i) nicotinamide + streptozotocin (NAD+STZ), (ii) saline + buffer, (iii) saline + streptozotocin (SAL+STZ); and (iv) nicotinamide + buffer. For this purpose, rats were treated with a single dose of nicotinamide (230 mg/kg, i.p.) or its vehicle (saline, 1 ml/kg) and 15 min after streptozotocin (65 mg/kg, i.p.) or its vehicle (citrate buffer, 1 ml/kg) was administered. 12 weeks latter, a tolerance glucose curve was determined after administration of glucose (1 g/kg, p.o.). Then, under anesthesia, the animals were pithed and prepared to measure blood pressure and heart rate. In animals treated with NAD+STZ intolerance to glucose was observed. Moreover, the vasopressor responses to sympathetic stimulation or noradrenaline, methoxamine and UK 14,304 remained unchanged. In contrast, in animals treated with SAL+STZ, the vasopressor responses induced by sympathetic stimulation or by methoxamine and UK 14,304 were blunted. Furthermore, the vasodepressor responses induced by acetylcholine, but not those induced by sodium nitroprusside, were significantly decreased in rats treated with NAD+STZ or SAL+STZ. These results suggest that in NAD‐STZ diabetic rats an impairment on the vasodepressor responses induced by acetylcholine was observed probably by an endothelial mechanism.