Letter to the Editor
Mechanisms underlying the hypertensive response induced by capsaicin

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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.

Section snippets

Methods and Results

The experiments were performed on adult rats of Charles Foster strain (∼ body weight: 200 g). After urethane anaesthesia trachea, jugular vein and femoral artery were cannulated. Blood pressure was recorded by connecting Stathum transducer to the femoral artery. ECG potentials were recorded by needle electrodes in standard limb lead II configuration. Capsaicin (10 μg/kg) was injected via jugular vein and the ECG and blood pressure were recorded on a chart recorder.

Our observations (Fig. 1) reveal

Discussion

Capsaicin-induced hypertensive response can be mediated by decreased vasodilatation (CGRP, kinin or prostaglandin) or increased vasoconstriction (catecholamines, angiotensin or endothelin) or by enhanced cardiac activity (rate and force). The present study excludes the involvement of adrenergic and angiotensinergic vasoconstrictive mechanisms. Further, it reveals that the hypertension is not related to heart rate as hypertensive response persisted with bradycardia. This is further supported by

Acknowledgements

The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [5]. This work is supported by the grants from University Grants Commission, New Delhi.

References (5)

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