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Cerebrovascular responses to capsaicin in vitro and in situ
Author(s) -
Edvinsson Lars,
Jansen Inger,
Kingman Tom A.,
McCulloch James
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb15801.x
Subject(s) - capsaicin , vasoconstriction , vasodilation , phentolamine , contraction (grammar) , nimodipine , chemistry , cerebral arteries , atropine , anesthesia , prostaglandin , propranolol , medicine , endocrinology , calcium , receptor
1 The cerebrovascular effects of capsaicin have been examined in vitro , in feline isolated cerebral arteries (circular segments, 2–3 mm long, 300–400 μm extended diameter) and, in situ , in pial arterioles (diameter 40–200 μ m ) on the cortical surface of chloralose‐anaesthetized cats. 2 In isolated middle cerebral arteries, low concentrations of capsaicin (10 −14 ‐10 −10 m ) effected a concentration‐dependent relaxation of vessels precontracted with prostaglandin F 2α . This relaxant response was markedly attenuated by repeated administration of capsaicin but was minimally affected by the presence of atropine, propranolol, cimetidine or spantide in the tissue bath. 3 In isolated middle cerebral arteries, higher concentrations of capsaicin effected a marked concentration‐dependent contraction. This contraction was not modified by 10 −6 μ phentolamine or 10 −6 m ketanserin. A markedly reduced contraction by capsaicin was found upon the removal of calcium ions from the buffer solution. Also the calcium entry blocker nimodipine reversed the capsaicin‐induced contraction. 4 Subarachnoid perivascular microapplication of capsaicin around individual pial arterioles in situ elicited a biphasic response (an immediate vasoconstriction followed by a sustained vasodilatation). The maximum vasoconstriction was a 60 ± 6% reduction in diameter from base line and the maximum vasodilatation a 38 ± 7% increase in diameter. Vasodilatation occurred at lower concentrations of capsaicin (EC 50 , approximately 5 × 10 −8 μ) than those required for vasoconstriction (EC 50 3 × 10 −7 μ). 5 Trigeminal ganglionectomy 10–16 days before the microapplication abolished the in situ vasodilator effects of capsaicin (10 −6 m ) applied perivascularly, but was without effect on the vasoconstrictor actions of this agent. 6 Repeated administration of capsaicin (10 −6 m ) around the same arteriole resulted in a progressive attenuation of the vasodilator phase of the response, with no modification of the vasoconstrictor phase. 7 The present study suggests that capsaicin‐induced cerebral vasodilatation is due to the release of vasoactive agents from cerebrovascular trigeminal nerve fibres, whereas the vasoconstrictor effect of capsaicin is due to a direct effect on the cerebral vasculature which is mediated via the transmembrane passage of extracellular calcium.