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Abstract
Capsaicin, an activator of the transient potential vanilloid receptor type 1 (TRPV1),
is a commonly used pharmacological tool for desensitising sensory nerves. Capsaicin
can induce vasorelaxation of isolated blood vessels by activating perivascular TRPV1
receptors, causing the release of vasoactive neuropeptides. This study attempted to
characterise the vascular effects of capsaicin in the rat isolated aorta and porcine
coronary arteries. Capsaicin elicited concentration-dependent vasorelaxation of both
rat aortae and porcine coronary arteries. Capsaicin-induced vasorelaxation of rat
aorta was unaffected by a chronic pre-treatment of vessels with capsaicin. Moreover,
relaxation was insensitive to the presence of capsazepine, a competitive TRPV1 antagonist,
in both the rat aorta and porcine coronary artery. It was hypothesised that capsaicin
may be inhibiting calcium influx into smooth muscle cells. Indeed, in vessels incubated
in a Ca²⁺-free high-k⁺ buffer, the presence of 30 μM capsaicin significantly inhibited
the contractile response to the re-introduction of Ca²⁺. In porcine coronary arteries
100 μM capsaicin completely abolished the contractile response to the re-introduction
of Ca²⁺. In addition, capsaicin also abolished the concentration-dependent contraction
of porcine coronary arteries induced by the L-type calcium activator Bay-K 8644. Therefore,
we suggest that capsaicin causes vascular responses in arteries through the inhibition
of L-type Ca²⁺ channels. In summary,we have identified a potential mechanism underlying
TRPV1-independent capsaicin-induced vasorelaxation. Our results also question the
use of chronic capsaicin pre-treatment in experimental pharmacology in order to elucidate
the role of sensory nerves in vascular responses.