CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 1, February 2012
16
AFRICA
tissue were unlikely to have been mediated via
α
1
-adrenoceptor
stimulation (Fig. 2E).
Pre-treating the animals with reserpine, a drug that depletes
catecholamines from tissue stores, had no effect on the
SBE-induced contractions of the venous tissue (Fig. 2F). This
may imply that the SBE-induced contractile responses of the
venous tissue were unlikely to have been mediated via catecho-
lamine release from tissue stores.
Pre-incubation of the portal vein preparations in calcium-free
Krebs-Henseleit solution resulted in contractile responses after
SBE addition. The contractions were completely reversed by
washing out the SBE solutions (Fig. 2D). However, SBE was
unable to reverse the verapamil-induced suppression of the rat
portal vein contractility. This could imply that SBE acted as an
agonist for intracellular Ca
2+
release, but this required an influx
of extracellular calcium, which was blocked by verapamil.
Fig. 2. Effects of SBE on rat isolated portal vein preparations. A: SBE (100 mg/ml) was sequentially added to the bath
fluid and then washed out four to five times. B: Contractile response to graded concentrations of SBE. *
p
<
0.05; **
p
<
0.01; ***
p
<
0.001 versus control (zero). C: Contractile responses to SBE (200 mg/ml) in Ca
2+
-free Krebs-Henseleit
physiological solution. D: Effect of verapamil (2 μg/ml) on SBE-induced (100 mg/ml) contractions. E: Pre-incubation
of isolated tissue with prazosin (1–3
μ
g/ml) followed by SBE administration. F: Contractile responses to SBE (100 mg/
ml) in reserpine pre-treated tissues.
A
C
E
B
D
F
