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Intracellular Ca2+ release in cerebral arteries
1Department of Pharmacology, United Medical School, Guy's Hospital, London, U.K.
Pharmacology & Therapeutics
|January 1, 1994
Summary
Vasoconstricting agonists increase intracellular Ca2+ in smooth muscle cells. Cerebral arteries show varied Ca2+ release dependence, with thromboxane A2 significantly impacting intracellular Ca2+ release.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Cellular Biology
Background:
- Vasoconstricting agonists elevate intracellular Ca2+ and induce vascular smooth muscle cell tension.
- Ca2+ influx and release from intracellular stores contribute to this process.
- The significance of Ca2+ release varies across vascular beds.
Purpose of the Study:
- To review the role of intracellular Ca2+ release in cerebral artery activation by vasoconstrictors.
- To compare the dependence on Ca2+ release for different vasoconstricting stimuli in cerebral arteries.
- To explore the implications of Ca2+ release in pathological cerebrovascular conditions.
Main Methods:
- Literature review of studies on cerebral artery vasoconstriction.
- Analysis of agonist-induced Ca2+ signaling pathways.
- Examination of the role of Ca2+ release versus Ca2+ influx.
Main Results:
- Cerebral artery activation by 5-hydroxytryptamine and noradrenaline shows minimal dependence on Ca2+ release.
- Thromboxane A2 induces significant intracellular Ca2+ release in cerebral arteries.
- Other agonists can trigger endothelial release of thromboxane A2.
Conclusions:
- Intracellular Ca2+ release is a key mechanism in cerebral artery vasoconstriction induced by certain stimuli like thromboxane A2.
- Pathological conditions such as delayed cerebrovascular constriction post-subarachnoid hemorrhage may rely on intracellular mechanisms, including Ca2+ release and protein kinase C activation.
- Ca2+ influx blockers may have limited efficacy in treating such conditions.