Reflex hypertensive response induced by capsaicin involves endothelin-dependent mechanisms.
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Date
2015-01
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Abstract
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 μg/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 capsaicininduced
intermediate hypertensive response involves endothelin-dependent mechanisms and the delayed
hypotensive response is independent of nitrergic, prostaglandinergic or kininergic mechanisms.
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Akella Aparna, Deshpande Shripad B. Reflex hypertensive response induced by capsaicin involves endothelin-dependent mechanisms. Indian Journal of Physiology and Pharmacology. 2015 Jan-Mar ; 59 (1) : 23-29.