Defining the roles of arrestin2 and arrestin3 in vasoconstrictor receptor desensitization in hypertension.
Bottom Line: Desensitization of UTP-stimulated vessel contractions was increased in 12-wk-old (but not 6-wk-old) SHR animals.In conclusion, arrestin2 and 3 expression is elevated in resistance arteries during the emergence of the early hypertensive phenotype, which underlies an enhanced ability to desensitize vasoconstrictor signaling and vessel contraction.Such regulatory changes may act to compensate for increased vasoconstrictor-induced vessel contraction.
Affiliation: Department of Cell Physiology and Pharmacology, University of Leicester, Leicester, United Kingdom; and email@example.com.Show MeSH
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Mentions: Since expression of arrestin2 and arrestin3 was elevated in small mesenteric arteries of 12-wk-old SHR and considering their key roles in suppressing the signaling of several contractile GPCRs within the vasculature (4, 14, 21, 22), we next compared the abilities of vasoactive agents to induce vasoconstriction in both SHR and WKY arteries. When normalized to vessel tension, contractions induced by K+ (60 mM) were similar in WKY to our previous findings in arterial preparations of adult male Wistar rats (21). However, K+-induced contractions were greater in SHR- compared with WKY-derived mesenteric vessels irrespective of age (Fig. 3, A and C). In both WKY- and SHR-derived vessels, contractions induced by K+ were completely ablated by preaddition of the L-type voltage-operated Ca2+-channel antagonist, nifedipine (data not shown).
Affiliation: Department of Cell Physiology and Pharmacology, University of Leicester, Leicester, United Kingdom; and firstname.lastname@example.org.