Abstract
In central nervous system (CNS), pericytes have been proposed to play a role in broad functional activities including blood–brain barrier, microcirculation, and macrophage activity. However, contractile responses and Ca 2+ signaling in CNS pericytes have not been elucidated. The aim of the present study is to investigate contractility and Ca 2+ influx pathway in CNS pericytes. CNS pericytes were cultured from rat brain. Contraction of the pericytes in response to various stimuli was evaluated by the change in surface area measured by a light microscope with a digital camera. Reverse transcription and polymerase chain reaction (RT–PCR) was performed to examine the expression of mRNA of α-smooth muscle actin. Intracellular Ca 2+ was measured using fura-2 fluorescence spectroscopy. A23187 (Ca 2+ ionophore), high external K + (4×10 −2 mol/l), endothelin-1, and serotonin induced contraction of CNS pericytes. RT–PCR analysis revealed the expression of α-smooth muscle actin in CNS pericytes. Cytosolic Ca 2+ ([Ca 2+]i) increased after application of high concentration of external K +, tetraethylammonium, and charybdotoxin, which was inhibited by nicardipine and removal of external Ca 2+. Angiotensin-II, serotonin, acetylcholine, ATP, and endothelin-1 caused biphasic response in [Ca 2+]i. In response to these agents, [Ca 2+]i rapidly increased and then decayed to a relatively constant Ca 2+ plateau. The Ca 2+ plateau was partially inhibited by nicardipine and completely abolished by omission of external Ca 2+. After intracellular Ca 2+ store was depleted by the removal of external Ca 2+ and addition of thapsigargin, reapplication of external Ca 2+ evoked increases in [Ca 2+]i. These results indicate that CNS pericytes express mRNA of α-smooth muscle actin and possess contractile ability. In CNS pericytes, resting membrane potential is regulated by large conductance Ca 2+-activated K + channels and Ca 2+ enters into the cells via L-type voltage-dependent Ca 2+ channels, agonist-activated Ca 2+ permeable channels, and capacitative Ca 2+ entry pathways.
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