N‐type calcium channels are not involved in increased nervous system activity in DOCA‐salt hypertensive rats

Hypertension is associated with an increase in sympathetic nervous system activity and ATP and norepinephrine release at the neuroeffector junction is disrupted in animal models of hypertension. For example, α 2 ‐adrenergic receptor (α 2 ‐AR) is dysfunctional in the DOCA‐salt hypertension, but the mechanism is unclear. We tested the hypothesis that α 2 ‐AR inhibition of the N‐type calcium channel (NTCC) is impaired in perivascular nerves supplying mesenteric arteries (MA). Immunohistochemical and physiological studies were conducted in vitro using mesenteric tissues from sham and DOCA‐salt rats to elucidate the role of NTCCs in mediating NT release at the neuroeffector junction. Electrical stimulation of periarterial nerves caused frequency‐dependent neurogenic constrictions which were inhibited by ω‐conotoxin GVIA (ω‐CTX), a NTCC blocker. There were no differences in sensitivity of sham and DOCA‐salt MA to the inhibitory effects of ω‐CTX on neurogenic constrictions. ATP induced constrictions of MA were unaffected by ω‐CTX confirming that there were no post‐junctional effects of ω‐CTX. Intensity of immunohistochemical staining of NTCCs was similar in sympathetic nerve fibers from DOCA‐salt and sham rats. We conclude that altered neurotransmitter release, from periarterial nerves, in DOCA‐salt hypertension, is not due to a change in number or function of NTCCs.