Sodium Selenate Partially Corrects Impaired Functional Responses in Detrusor Muscle in Streptozotocin-Induced Diabetic Rats

Abstract

Selenium selenate was administered to streptozotocin-induced diabetic rats to assess its effects on the detrusor muscle. Thirty-two rats were divided into four groups of eight subjects each. The study animals were made diabetic by means of a single intravenous injection of streptozotocin (STZ). The responsiveness of the detrusor was improved in the group injected with sodium selenate. Diabetes caused significant increases in carbachol and beta,gamma-MeATP-evoked contractions and significant decrease of contractions induced by electrical stimulation. Isoprenaline-induced relaxation of the detrusor muscle was diminished by diabetes, whereas ATP relaxation appeared to be increased. Although adenosine-induced relaxations in controls and in diabetic rats were accompanied by unchanged responses in normoxic conditions, a significant enhancement in the detrusor muscle was observed during hypoxia. This enhancement of adenosine responsiveness in hypoxic conditions is inhibited in diabetes. Treatment with sodium selenate prevented alterations of both carbachol-induced contractility and isoprenaline-evoked relaxation, whereas nerve-mediated contractions and purinergic responses were not improved in diabetic rats after treatment. Our data suggest that changes in cholinergic and adrenergic responses were the result of selenium deficiency in diabetic rats.

Adenosine Actions are Preserved in Corpus Cavernosum from Obese and Type II Diabetic db/db Mouse

“…Adenosine‐induced increases in coronary flow rate are lower in hearts from diabetic db/db mice when compared with hearts from nondiabetic animals [42]. In addition, adenosine‐induced relaxations in the detrusor muscle from streptozotocin‐induced diabetic rats are preserved in normoxic conditions, but the enhancement of adenosine responsiveness in hypoxic conditions observed in tissues from control animals is impaired in the detrusor muscle from diabetic rats [43]. Adenosine‐induced relaxation is also decreased in aortic rings of diabetic (streptozotocin‐induced) Wistar‐Kyoto (WKY) and spontaneously hypertensive (SHR) rats compared with nondiabetic WKY and SHR.…”