OBJECTIVE: To observe the impact of Shijueming (Concha Haliotidis) on spontaneously hypertensive rats via blood pressure, serum calcium, vascular smooth muscle membrane L-type calcium channel α1 C subunit (CaL-α1C), plasma membrane calcium-ATPase (PMCA) mRNA expression, and the L-type calcium channel in vascular smooth muscle cells. METHODS:Twelve-week-old male rats with spontaneous hypertension were divided into three groups: a Shijueming (Concha Haliotidis) group (group 1), a nifedipine group (group 2), and a distilled water group (group 3). All were given a four-week treatment. Blood pressure and dissociative serum calcium were examined before treatment. Blood pressure was taken every week during treatment. Atomic absorption spectrometry was used to examine dissociative serum calcium. Re-verse transcription-polymerase chain reaction was used to examine the expression of CaL-α1C and PM-CA1 mRNA. The patch clamp technique was used to examine the electrophysiological characteristics of the vascular smooth muscle cell calcium channels. RESULTS: After treatment, blood pressure of the Shijueming (Concha Haliotidis) group lowered but not significantly (P>0.05). Blood pressure of the nifedipine group lowered significantly (P<0.05). Blood pressure of the distilled water group remained high. The concentration of serum calcium in the Shijueming (Concha Haliotidis) and the distilled water groups lowered (P<0.05). Expression of CaL-α1C mRNA in the nifedipine group decreased compared with the distilled water group (P<0.01). There was the decreasing trend in the Shijueming (Concha Haliotidis) group, but it was not statistically significant. Shijueming (Concha Haliotidis) also had effects on the expression of PMCA1 mRNA but with- out statistical significance. However, there was a significant decreasing effect on vascular smooth muscle cell I Ca-L flow. CONCLUSION: This study indicated that Shijueming (Concha Haliotidis) could increase serum calcium and decrease blood pressure. It may work by influencing calcium channels, expression of PMCA1 mRNA, and regulating ion calcium channels and calcium-ATPase.
