Abstract 472: Calcium Current by Somatostatin Leads to Vasoconstriction in Rabbit Cerebral Artery
Somatostatin-containing neurons have a widespread distribution in the central nervous system. Moreover, the level of somatostatin in bloody cerebrospinal fluid and plasma is elevated patients with stroke.
However, there is little evidence to support that somatostatin is a possible factor of vasopasm after stroke. This experiment was to undertaken to evaluate the effects of somatostatin on Ca2+ currents using the whole-cell voltage-clamp techniques and on Ca2+ transients using whole-cell fluorescence in cerebral arteries of the rabbit.
During rectangular pulses, both peak and steady-state Ca2+ currents
were significantly increased by the application of somatostatin. Somatostatin had little effect on the steady-state activation kinetics, however, significant effect on the time constants for current decay. τ increased monotonically with voltage and was slightly slower in somatostatin-treated cells between 0 and +30 mV. The half maximal concentration of somatostatin was 8.5±1.3 pM in dose-response relation. Moreover, Ca2+ transients by somatostatin were significantly increased in cells.
From these results, the activation of Ca2+ currents by somatostatin could be involved in pathogenesis of vasospasm after stroke.
- © 2012 by American Heart Association, Inc.