Abstract
Contractures induced by 10(-9)-10(-4) M phenylephrine (PE) or 10-70 mM KCl were observed in aortas isolated from untreated and insulin-treated streptozotocin-diabetic rats. The experiments were conducted at 2-wk intervals for a 12-wk period after the induction of diabetes. Diabetes caused an average decrease of 58 and 60% in the K and PE contractures, respectively. Although the PE contractures in aortas from the insulin-treated diabetic animals (81%) were significantly greater than those in aortas from the untreated diabetic animals (60%), they were significantly less than those in control tissues (100%). Insulin treatment completely reversed the diabetes-induced decrease in the K contracture (102%). It appears that the diabetes-induced decreases in tension may result from an altered sensitivity of the tissues to KCl but not PE. Histological examination of the tissues revealed that the diminished contractions were not due to any detectable change in mural structure. The data indicate that diabetes-induced inhibition of the mechanisms involved in mediating the K contracture are completely reversible by insulin treatment, whereas those mediating the PE contracture are only partially reversible.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
