Role of R-voltage-dependent calcium channels in myogenic tone of cerebral arteries and its molecular in rats after subarachnoid hemorrhage

Abstract

Objective To explore whether R-voltage-dependent calcium channels (VDCCs) affect myogenic tone (MT) maintenance of cerebral arteries in rats after subarachnoid hemorrhage (SAH). Methods Nineteen SD rats were randomly divided into sham-operated group (n=10) andSAH group (n=9), and SAH animal models were established via autologous arterial blood injection into the suprasellar cistern. Five d after modeling, cerebral arteries of Willis ring were performed sharp dissection, and myocytes were performed acute isolation with enzymatic digestion method. Accordingly, pressurized angiography was performed to detect the artery diameters and MT, and patch clamp was applied to observe the VDCCs electric currents, and subsequently diameter and MT of cerebral arteries and VDCCs currents were measured when they were varied with different VDCCs blockers in extracellular fluids (without blockers, 1 μmol/L nifedipine, and 1 μmol/L nifedipine plus 200 nmol/L SNX-482) to determine their responses to these blockers. Results (1) In rats of the sham-operated group, cerebral arteries were dilated and MT was compromised completely in rats treated with 1 μmol/L nifedipine as compared with those without blockers, with significant differences (P 0.05). Differently, in rats of the SAH group, cerebral arteries were dilated and MT was compromised partly but not completely in rats treated with 1 μmol/L nifedipine as compared with those in rats without blockers, with significant differences (P<0.05), and cerebral arteries were dilated and MT was compromised completely in rats treated with 1 μmol/L nifedipine combined with 200 nmol/L SNX-482 as compared with those in rats treated with 1 μmol/L nifedipine, with significant differences (P<0.05). (2) The maximum currents density of sham-operated group was -4.88±0.41, which was completely sensitive to 1 μmol/L nifedipine; the maximum currents density of SAH group was -4.97±0.41, which was partly sensitive to 1 μmol/L nifedipine with remnant maximum currents density of -1.96±0.37; all the remnant currents of SAH group were completely sensitive to the addition of 200 nmol/L SNX-482. Conclusion The emergency of R-VDCCs currents is correlated with MT maintenance of cerebral arteries following SAH, and this has been considered as a key in dysfunction of cerebral blood flow autoregulation. Key words: Subarachnoid hemorrhage; Voltage-dependent calcium channel; Myogenic tone