We investigated the relationship between tension development and the cytosolic free Ca
2+ level ([Ca
2+]
1) in responses to norepinephrine (NE) and selective
α2-adrenoceptor agonist, UK14, 304 of the endothelium-denuded rat aorta loaded with fura PE-3. NE (3×10
-8 M) evoked a rapid increase in [Ca
2+]
1 followed by slight decreasing to a steady state level and produced a contraction. After the NE-induced increase in [Ca
2+]
1 had reached a maximum, the [Ca
2+]
1 showed persistent oscillations. The Ca
2+ oscillations were super-imposed on the sustained increase in [Ca
2+]
1 . UK14, 304 (3×10
-6 M) also evoked an increase in [Ca
2+]
1 and produced a contraction. However, the UK14, 304-induced effect on [Ca
2+]
1 was characterized by pronounced oscillations, and the amplitude of the sustained increase in [Ca
2+]
1 was less than that seen with NE. Protein kinase C inhibitor, Ro31-8220 (3×10
-6 M) and verapamil (10
-5 M) abolished both NE- and UK14, 304-evoked Ca
2+ oscillations. UK14, 304-induced contractions were also strongly inhibited by Ro31-8220 and verapamil. However, NE-induced contractions were partly inhibited by these inhibitors. The sustained increases in [Ca
2+]
1 evoked NE and UK14, 304 were not significantly inhibited by Ro31-8220 and verapamil. These results suggest that NE and UK14, 304 produce Ca
2+ oscillations during sustained contractions in rat aorta. The
α2-adrenoceptor agonist, UK14, 304-induced sustained contraction and Ca
2+ oscillations may be due to PKC activation and opening of voltage-dependent L-type Ca
2+ channels.
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