Chronic diabetes and hypertension impair the in vivo functional response to phenylephrine independent of α-adrenoceptor expression.

Eur J Pharmacol

Laboratorio de Señalización Intracelular, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Ciudad de México, México. Electronic address:

Published: September 2020

Diabetes and hypertension can coexist and exacerbate each other. In the early stages of diabetes, there is a decreased vascular response of the sympathetic nervous system (SNS), probably due to lower expression of α-adrenoceptors; however, it is unclear how diabetes in advanced stages changes the functionality of the SNS, especially the expression of α-adrenoceptors. Thus, the aim of this work was to analyse the functional response to phenylephrine, a selective α-adrenoceptor agonist, and the expression of α-adrenoceptors in chronic diabetes and hypertension. Male SHR and WKY rats aged 10-12 weeks were administered either streptozotocin (60 mg/kg i.p.) or a vehicle (control group). Eight weeks after administration, dose-response curves to phenylephrine were generated and the gene and protein expression of α-adrenoceptor subtypes (α-, α- and α-adrenoceptors) in the heart and aorta were measured. The response to phenylephrine was diminished in hypertensive rats and in normotensive diabetic rats. The coexistence of both diabetes and hypertension produced an even smaller response to phenylephrine than that observed for each condition separately. In the heart and aorta of diabetic rats, no changes in α-, α- or α-adrenoceptor mRNA expression were observed; however, protein expression was increased, mainly for the α-adrenoceptor. Hypertension increased mRNA and protein expression of α-adrenoceptors in a tissue-dependent manner. The coexistence of both diabetes and hypertension produced differences in the regulation of mRNA and protein expression (increase or decrease) in both the heart and aorta. In conclusion, diabetes, hypertension and the coexistence of both pathologies impairs the in vivo response to phenylephrine. However, the differences in α-, α- and α-adrenoceptor expression cannot explain the reduced response to the agonist. This should be further explored in future experiments.

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http://dx.doi.org/10.1016/j.ejphar.2020.173283DOI Listing

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