Voltage-activated Ca(2+) channels in rat renal afferent and efferent myocytes: no evidence for the T-type Ca(2+) current.

AIMS: Based on indirect methods, it has been suggested that both L- and T-type Ca(2+) channels mediate signalling in the renal afferent arteriole and that T-type Ca(2+) channels are involved in signalling in the efferent arteriole. However, Ca(2+) currents have never been studied in these two vessels. Our study was initiated to directly determine the type of Ca(2+) channels in these vessels for the first time, using patch clamp.

METHODS AND

RESULTS

Native myocytes were obtained from individually isolated rat renal afferent and efferent arterioles and from rat tail arteries (TA). TA myocytes, which possess both L- and T-type Ca(2+) currents, served as a positive control. Inward Ca(2+) and Ba(2+) currents (I(Ca) and I(Ba)) were measured in 1.5 mmol/L Ca(2+) and 10 mmol/L Ba(2+), respectively, using the whole-cell configuration. By exploiting known differences in activation and inactivation characteristics and differing sensitivities to nifedipine and kurtoxin, the presence of both L- and T-type Ca(2+) channels in TA myocytes was readily demonstrated. Afferent arteriolar myocytes exhibited relatively large I(Ca) densities (-2.0 ± 0.2 pA/pF) in physiological Ca(2+) and the I(Ba) was 3.6-fold greater. These currents were blocked by nifedipine, but not by kurtoxin, and did not exhibit the activation and inactivation characteristics of T-type Ca(2+) channels. Efferent arteriolar myocytes did not exhibit a discernible voltage-activated I(Ca) in physiological Ca(2+).

CONCLUSION

Our findings support the physiological role of L-type Ca(2+) channels in the afferent, but not efferent, arteriole, but do not support the premise that functional T-type Ca(2+) channels are present in either vessel.