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1 Laboratoire de Pharmacologie et Physico-Chimie des Intéractions Cellulaires et Moléculaires, Unité Mixte de Recherche, Centre National pour les Recherches Scientifiques 7034, Université Louis Pasteur de Strasbourg, Faculté de Pharmacie, 67401 Illkirch-Cedex; and 2 Centre Hospitalier Universitaire, Hôpital de Hautepierre, Service de Réanimation Médicale, 67098 Strasbourg, France
The mechanisms of Ca2+ handling and sensitization were investigated in human small omental arteries exposed to norepinephrine (NE) and to the thromboxane A2 analog U-46619. Contractions elicited by NE and U-46619 were associated with an increase in intracellular Ca2+ concentration ([Ca2+]i), an increase in Ca2+-independent signaling pathways, or an enhancement of the sensitivity of the myofilaments to Ca2+. The two latter pathways were abolished by protein kinase C (PKC), tyrosine kinase (TK), and Rho-associated protein kinase (ROK) inhibitors. In Ca2+-free medium, both NE and U-46619 elicited an increase in tension that was greatly reduced by PKC inhibitors and abolished by caffeine or ryanodine. After depletion of Ca2+ stores with NE and U-46619 in Ca2+-free medium, addition of CaCl2 in the continuous presence of the agonists produced increases in [Ca2+]i and contractions that were inhibited by nitrendipine and TK inhibitors but not affected by PKC inhibitors. NE and U-46619 induced tyrosine phosphorylation of a 42- or a 58-kDa protein, respectively. These results indicate that the mechanisms leading to contraction elicited by NE and U-46619 in human small omental arteries are composed of Ca2+ release from ryanodine-sensitive stores, Ca2+ influx through nitrendipine-sensitive channels, and Ca2+ sensitization and/or Ca2+-independent pathways. They also show that the TK pathway is involved in the tonic contraction associated with Ca2+ entry, whereas TK, PKC, and ROK mechanisms regulate Ca2+-independent signaling pathways or Ca2+ sensitization.
Rho-associated protein kinases; calcium ion
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