Accumulation of H+ and ADP in cytoplasm plays an important role in modifying the cellular functions under pathological conditions such as hypoxia. Cerebral vasospasm is a major cause of death and disability after subarachnoid hemorrhage (SAH), of which pathogenesis, nevertheless, is poorly understood. Using β-escin-permeabilized basilar artery that enabled us to control the intracellular solute composition under near-physiological conditions, we studied the possible involvement of increased intracellular H+ ([H+]i) and ADP ([ADP]i) in the pathogenesis of cerebral vasospasm. It was found that combined increase in [H+] and [ADP] led to an increase in the resting tension and a subsequent irreversible increase in the Ca2+ sensitivity of contraction accompanying a high level of phosphorylation in smooth muscle 20-kDa myosin light-chain (MLC20). The results suggest that intracellular metabolic inhibitions accompanying an increase in [H+]i and [ADP]i may play a role in the development of cerebral vasospasm after SAH through impairing the regulation of MLC20 phosphorylation in arterial smooth muscle cells.
|Number of pages||4|
|Publication status||Published - 2001|
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)