Capsaicin, a nociceptive agent produces triphasic pressure response in rats. The mechanisms underlying
capsaicin-induced pressure responses are not clear. Therefore, the present study was undertaken to determine the mechanisms involved in
capsaicin - induced pressure responses. The trachea, jugular vein and femoral artery were cannulated in anaesthetized rats.
Capsaicin (10 µg/kg; i.v) - induced reflex changes in the blood pressure, respiratory excursions and ECG were recorded before/after
vagotomy in the absence/presence of antagonists.
Capsaicin produced the triphasic pressure response characterized by immediate fall, recovery (intermediate phase) and delayed progressive fall. After
vagotomy, the immediate
hypotension was abolished and the intermediate pressure response was potentiated as a hypertensive response while the delayed hypotensive response persisted. The time-matched heart rate changes (
bradycardia) and respiratory changes (
tachypnea in delayed phase) were abolished after
vagotomy. Pretreatment with
endothelin receptor antagonist (
bosentan; 10 mg/kg) blocked the capsiaicn-induced intermediate hypertensive response in vagotomised animals but not the delayed
hypotension. Pretreatment with
nitric oxide synthase (NOS) inhibitor (
L-NAME; 30 pg/kg),
prostaglandin synthase inhibitor (
indomethacin; 10 mg/kg) and
kinin synthase inhibitor (
aprotinin; 6000 KIU) did not block the delayed hypotensive response. These results demonstrate that
capsaicin-induced intermediate hypertensive response involves
endothelin-dependent mechanisms and the delayed hypotensive response is independent of nitrergic, prostaglandinergic or kininergic mechanisms.