Abstract
We used combined patch-clamp-microfluorimetric recordings to examine the effects of bradykinin on [Ca2+]i transients and the Ca2+ current (ICa) in rat dorsal root ganglion neurons in vitro. Bradykinin increased [Ca2+]i in approximately 20% of dorsal root ganglion cells examined and inhibited the ICa in approximately 65% of dorsal root ganglion cells. Bradykinin also inhibited the ICa when [Ca2+]i was buffered with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid or when Ba2+ was the charge carrier. When ICa's of increasing duration were elicited in these neurons, [Ca2+]i transients were produced that increased in amplitude but eventually approached an asymptote at longer voltage steps. Similarly, the amplitude of the [Ca2+]i transient also approached an asymptote in current-clamp recordings when cells were induced to fire a large number of action potentials. The bradykinin-induced inhibition of the amplitude of the [Ca2+]i transient was more pronounced at shorter voltage steps. At pulse durations that produced asymptotic [Ca2+]i signals, bradykinin no longer decreased the amplitude of the rise in [Ca2+]i, although it still reduced the ICa. In current-clamp recordings, bradykinin also reduced the [Ca2+]i signal that accompanied the generation of action potentials, but again bradykinin was more effective for shorter spike trains. Bradykinin also depolarized the majority of neurons (65%). The reduction in [Ca2+]i produced by bradykinin in sensory neurons may be an important factor contributing to bradykinin-induced excitation of primary sensory afferents.
MolPharm articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|