CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 1, February 2012
AFRICA
17
Removal of the agonist (SBE) therefore resulted in the termina-
tion of Ca
2+
release from the intracellular stores.
SBE has been reported to contain a number of chemical
compounds, including tannins, polyphenols, coumarins, triter-
penoids and phytosterols.
7,10,17
The flavonoids present in
S birrea
leaves include quercetin and kaempferol, as well as their esters,
gallic acid, myricetin and catechin gallates, such as (-)-epigallo-
catechin 3-
O
-galloyl ester and (-)-epicatechin 3-
O
-galloyl ester.
18
Although the exact chemical constituents of SBE responsible for
the observed contractile effects of the plant extract on mamma-
lian isolated vascular tissue remain speculative at present, the
synergistic effects of (-)-epigallocatechin 3-
O
-galloyl, (-)-epicat-
echin 3-
O
-galloyl, gallic acid and myricetin have previously been
reported.
7,17,19
The results obtained in this study suggest that SBE-induced
contraction of smooth muscles may have been mediated via acti-
vation of the cyclo-oxygenase pathways. In a study by Gil-Longo
and Gonzalez-Vazquez,
19
pre-incubating smooth muscle with
indomethacin practically abolished the contractile effects of
gallic acid. This was attributed to the generation of free radicals,
which inactivate endothelial resting vasodilator NO.
The flavonoids commonly found in SBE, myricetin and
quercetin, have previously been reported to elicit smooth muscle
contraction. Myricetin has been observed to elicit smooth muscle
contraction via activation of the phospholipase-A
2
pathway,
resulting in the release of thromboxane A
2
by increasing Ca
2+
concentrations.
20
Quercetin has been identified as a novel, specific activator of
L-type calcium channels
21
and it increases the influx of Ca
2+
,
21
which contradicts its well-known vasodilatory effects.
22
The
myorelaxant effect of quercetin in tissue preparations has been
suggested to originate from its reaction with a second target
beyond the Ca
2+
channel.
21
In the present study, however, it may
be argued that the SBE-induced contractile effects were likely
to have been a result of the sudden influx of calcium into the
cells, due to the quercetin activation of L-type calcium channels.
It can therefore be speculated that the pharmacological effects
observed with SBE in our experiments may in part have been due
to a synergistic effect of the flavonoids present in SBE.
Conclusion
The findings of this study show that SBE exerted contrac-
tile effects on isolated vascular smooth muscles
in vitro
. The
SBE-induced vasoconstriction may have been mediated, at least
in part, by the actions of endothelium-derived vasoconstrictors
such as prostaglandins and endothelin-1, as well as by the influx
of extracellular Ca
2+
and release of intracellular Ca
2+
. These
observations suggest that SBE may increase blood pressure;
hence it may exacerbate hypertension in vulnerable patients.
Further
in vivo
investigations are suggested.
The authors thank Ms Kogi Moodley and Mr Witness Chiwororo for
their technical assistance, and the staff of the Boimedical Resource Unit,
University of KwaZulu-Natal, Durban, for their assistance with the animals.
This work was supported financially by the research office of the University
of KwaZulu-Natal.
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