Role of Ca²⁺ in the vascular contraction caused by a thrombin receptor activating peptide

Abstract

Thrombin receptor activating peptide (TRAP) caused a slowly developing, sustained contraction of endothelium denuded rat aortic rings. Both nifedipine (10 μM) and removal of Ca²⁺ from the physiological salt solution (PSS) caused significant (60–75%) reductions in the contractile response to TRAP. In Ca²⁺-free PSS the response to both phenylephrine and TRAP were markedly reduced. Readministration of Ca²⁺ quickly restored the full response to phenylephrine. In contrast, readministration of Ca²⁺ only partially restored the TRAP response. Depletion of TRAP-sensitive intracellular Ca²⁺ stores had no effect on the phenylephrine response in Ca²⁺-free PSS. A threshold contracting concentration of TRAP (10 μM) enhanced contractions to the activator of voltage regulated Ca²⁺ channels bay K 8644. Similarly, Bay K 8644 enhanced responses to TRAP. It is concluded that the contractile response of rat aortic rings to TRAP is largely mediated by influx of extracellular Ca²⁺. Furthermore, the intracellular Ca²⁺ pool(s) activated appears to be different from the phenylephrine-sensitive pools, which cannot be depleted by TRAP.