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The Blood Pressure Lowering Effect of the Aqueous Calyx Extract of Hibiscus sabdariffa May Occur via a Sympathetic Nervous System Dependent Mechanism
Author(s) -
Mojiminiyi Frank,
Aliyu Buhari,
Oyeniran Oluwatosin,
Alex Isu
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.675.17
Subject(s) - blood pressure , hibiscus sabdariffa , sympathetic nervous system , calyx , mean arterial pressure , medicine , basal (medicine) , heart rate , endocrinology , pharmacology , traditional medicine , anatomy , insulin
The aqueous calyx extract of Hibiscus sabdariffa (HS) has been reported to lower blood pressure (BP) in animals and man. This study tested the hypothesis that the hypotensive effect of HS may occur through a sympathetic nervous system (SNS) dependent mechanism. Following ethical approval and informed consent, the Harvard step test (HST) was performed in healthy subjects (n=14) to activate the sympathetic nervous system (SNS) before and after the oral administration of HS (15mg/Kg). The BP and pulse rate (PR) responses were measured. Mean arterial pressure (MAP; taken as representative BP) was calculated. Experiments were performed in accordance with the Principles of the Declaration of Helsinki. Results are expressed as mean ±SEM. Paired t test was used for statistical analyses and P<0.05 was considered significant. HST without HS resulted in a significant rise in MAP and PR (112.6 ± 2.7mmHg and 97.7 ± 2.5/min) from the basal values (98.5±2.3mmHg and 76.6±2.0/min; P<0.001 and 0.01 respectively). In the presence of HS, HST‐induced changes (ΔMAP=14.2±2.6 ΔPR= 11.4±3.5) were significantly dampened compared to its absence (ΔMAP= 24.1±2.5 ΔPR= 20.1±3.1; P<0.001 and 0.01 respectively). The HST‐induced increases in BP and PR suggest SNS activation. These were dampened by HS suggesting that its hypotensive effect may occur through the inhibition of systemic vascular resistance mediated by the SNS.