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      Enhanced A1 adenosine receptor-induced vascular contractions in mesenteric artery and aorta of in L-NAME mouse model of hypertension

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      European Journal of Pharmacology
      Elsevier BV

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          Abstract

          L-NAME-induced hypertension is commonly used to study endothelial dysfunction and related vascular effects. It has been reported that genetic deletion of A 1 adenosine receptor (AR) reduces blood pressure (BP) increases in mice and thus, suggesting the involvement of A 1 AR. Thus, we sought to determine whether A 1 AR-induced vascular responses were altered in this mouse model of hypertension. L-NAME (1 mg/ml) was given in the drinking water for 28 days to mice. The BP was monitored using non-invasive tail-cuff system. Muscle tension studies were performed using DMT for mesenteric arteries (MAs) and organ bath for aorta. Protein expression was analyzed by western blot. Significantly, higher systolic and mean arterial blood pressure was noted in L-NAME mice. In MAs, higher 2-Chloro-N 6 -cyclopentyladenosine (CCPA, selective A 1 AR agonist) induced contractions in hypertensive mice were observed. This enhanced contraction was inhibited by HET0016 (Cytochrome 450 4A inhibitor, 10 µM, 15 min). Contrary, 5′-(N-Ethylcarboxamido) adenosine (NECA, non-selective AR agonist) induced vascular responses were comparable in both groups. Pinacidil (K ATP channel opener) induced relaxation was significantly increased in hypertensive mice. In aorta, CCPA-induced contractions were enhanced and inhibited by HET0016 in hypertensive mice. Notably, NECA-induced contractions in aorta were enhanced in hypertensive mice. Higher expressions of A 1 AR and Cyp4A were noted in MAs of hypertensive mice. In addition, in aorta, higher A 1 AR and comparable Cyp4A levels were observed in hypertensive mice. A 1 AR-induced vascular contractions were enhanced in hypertensive mice aorta and MAs. Cyp4A plays a role in altered vascular responses in MAs.

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          Author and article information

          Journal
          European Journal of Pharmacology
          European Journal of Pharmacology
          Elsevier BV
          00142999
          October 2018
          October 2018
          Article
          10.1016/j.ejphar.2018.10.024
          6296900
          30347181
          fddc86e7-588c-4d8b-abfe-2afc312cf83c
          © 2018

          https://www.elsevier.com/tdm/userlicense/1.0/

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