Mechanisms underlying the hypertensive response induced by capsaicin

Abstract

Acute ingestion of large quantity of chili peppers (rich source of capsaicin) produced hypertensive crisis in a patient. The hypertensive response was explained on the basis of decreased vasodilator substance calcitonin gene-related peptide (CGRP) from sensory nerve terminals by capsaicin. Here we present our experimental observations in anaesthetized rats regarding the mechanisms underlying hypertensive response induced by capsaicin. Our results demonstrate non-involvement of adrenergic and angiotensinergic mechanisms and also the cardiac changes in producing the response. Thus, the direct action of capsaicin on vascular smooth muscle or the activation of endothelin is proposed.

Introduction

In a recent case report, patient consuming pepper in a large quantity manifested with hypertensive crisis [2]. Pepper contains an active ingredient, capsaicin and the hypertensive crisis in this report has been attributed to it. They explained the phenomenon on the basis of the depletion of vasodilator calcitonin gene-related peptide (CGRP) from C fibres by capsaicin. The patient exhibited very high systolic pressure which can also be mediated by adrenergic, angiotensinergic or cardiogenic mechanisms. Therefore, we present here our experimental observations in anaesthetized rats which provide the basis for possible explanations of capsaicin-induced hypertensive response.