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Stress proteins have been implicated in pathological cardiovascular conditions. We hypothesized that a heat-shock response modulates contractility of vascular smooth muscles. Rat aortic ring preparations were mounted in organ baths, exposed to 42 degrees C for 45 min, and subjected to contractions. Expression of HSP70 and phosphorylation of myosin light chain were examined with immunoblots. Heat shock enhanced contractile response to KCl in parallel with HSP70 expression in rat aortic rings from 8 h but not 1 h after the end of heat shock. Heat shock also augmented vascular contractility to phenylephrine whether endothelium was intact or denuded. Treatment of heat shock-preconditioned aortic rings with Bay K8644, a calcium channel activator, but not treatment with phorbol dibutyrate (1 micromol/l), a protein kinase C activator, enhanced contractions of the rings as compared with those of the control. The levels of phosphorylation of myosin light chains after administration of phenylephrine in heat shock-preconditioned tissues were statistically significantly higher than those in control tissues. Pretreatment with wortmannin (300 nmol/l), an inhibitor of myosin light chain kinase, decreased both contractility and phosphorylation of myosin light chains in parallel. However, heat-shock response did not affect relaxation responses to either acetylcholine in endothelium-intact aortic rings or sodium nitroprusside in endothelium-denuded rings. These results suggest that the heat-shock response is associated with enhanced vascular smooth muscle contractility through a modulation of thick-filament regulation.

Paralytic shellfish poisoning toxin profiles of dinoflagellate cultures of Gymnodinium catenatum Graham from the Yellow and South Seas in Korea were investigated by high performance liquid chromatography fluorometric detection. Strains from the Yellow Sea had predominantly carbamate toxins, while strains from Sujeongri and Chindong in the South Sea contained the N-sulfocarbamoyl toxins, C1,2, as major components including the presence of GTX5 and dcSTX in some strains. Toxin profiles from St. Deukryang Bay strains (South Sea) showed both characteristics of those in the South Sea and those in the Yellow Sea. Thirty strains could be divided into three groups based on cluster analysis of toxin compositions. Group I (Yellow Sea strains) was distinguished from Group II (Sujeongri and Chindong strains) by the absence of GTX5 and dcSTX. Group III comprised Deukryang Bay strains. In conclusion, the Yellow Sea and the South Sea were found to have different dinoflagellate populations with different toxin compositions.

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