Angiotensin II-induced inotropism requires an endocardial endothelium-nitric oxide mechanism in the in-vitro heart of Anguilla anguilla
Sandra Imbrogno1,
Maria Carmela Cerra1,2 and
Bruno Tota1,3,*
1 Department of Cellular Biology, University of Calabria, 87030, Arcavacata di
Rende, CS, Italy
2 Department of Pharmaco-Biology, University of Calabria, 87030, Arcavacata di
Rende, CS, Italy
3 Zoological Station `A. Dohrn', Villa Comunale, 80121 Naples, Italy
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Fig. 1. Cumulative dose–response curve showing the effect of angiotensin II
(ANG II; from 10-10 to 10-7 mol l-1) on heart
rate in isolated and perfused unpaced eel hearts. Percentage changes were
evaluated as means ± S.E.M. of five
experiments. *Significantly different from the control value
(P<0.05).
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Fig. 2. Cumulative dose–response curve showing the effect of for angiotensin
II (ANG II; from 10-11 to 10-7 mol l-1) on
(A) stroke volume (VS) and (B) stroke work
(WS) in isolated and perfused paced eel hearts. Percentage
changes were evaluated as means ±
S.E.M. of five experiments.
*Significantly different from the control value
(P<0.05).
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Fig. 3. Effects of angiotensin II (ANG II; 10-8 mol l-1)
before and after treatment with CGP42112 (10-6 mol l-1),
losartan (10-6 mol l-1) and CV11974 (10-7 mol
l-1) on stroke volume (VS) and stroke work
(WS) in isolated and perfused paced eel hearts. For
details, see Materials and methods. Percentage changes are shown as means
± S.E.M. of 4-5 experiments for each
drug. *Significantly different from the control value
(P<0.05).
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Fig. 4. Effects of angiotensin II (ANG II; 10-8 mol l-1)
before and after treatment with atropine (10-6 mol l-1)
and pertussis toxin (PTx; 10-11 mol l-1) on stroke
volume (VS) and stroke work (WS) in
isolated and perfused paced eel hearts. For details, see Materials and
methods. Percentage changes are shown as means ±
S.E.M. of four experiments for each drug.
*Significantly different from the control value
(P<0.05).
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Fig. 5. Effects of angiotensin II (ANG II; 10-8 mol l-1)
before and after treatment with propanolol (10-8 mol
l-1) and phentolamine (10-8 mol l-1), sotalol
(10-7 mol l-1), isoproterenol (ISO; 10-9 mol
l-1) and phenylephrine (Phenyl; 10-9 mol l-1)
on stroke volume (VS) and stroke work
(WS) in isolated and perfused paced eel hearts. For
details, see Materials and methods. Percentage changes are shown as means
± S.E.M. of 4-5 experiments for each
drug. *Significantly different from the control value
(P<0.05).
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Fig. 6. Effects of angiotensin II (ANG II; 10-8 mol l-1)
before and after injection with Triton X-100 (0.05%), or perfusion with
L-arginine (L-Arg; 10-6 mol l-1),
haemoglobin (Hb; 10-6 mol l-1),
L-N5(1-iminoethyl)ornithine (L-NIO;
10-5 mol l-1),
NG-monomethyl-L-arginine (L-NMMA;
10-5 mol l-1) and
1H-(1,2,4)oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ; 10-5 mol
l-1) on stroke volume (VS) and stroke work
(WS) in isolated and perfused paced eel hearts. For
details of treatment and perfusions, see Materials and methods. Percentage
changes are shown as means ± S.E.M. of
4-5 experiments for each drug. *Significantly different from the
control value (P<0.05).
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Fig. 7. Effects of angiotensin II (ANG II; 10-8 mol l-1)
before and after treatment with KT5328 (10-7 mol l-1) on
stroke volume (VS) and stroke work
(WS) in isolated and perfused paced eel hearts. Percentage
changes are shown as means ± S.E.M. of
four experiments. *Significantly different from the control value
(P<0.05).
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Fig. 8. Effects of preload elevation on (A,C) stroke volume
(VS) and (B,D) stroke work (WS) (A,B)
in control conditions and (C,D) after treatment with angiotensin II (ANG II;
10-8 mol l-1) in isolated and perfused paced eel hearts.
Percentage changes are shown as means ±
S.E.M. of five experiments for each group. A
paired Student's t-test was used for comparison within groups; a
two-way ANOVA analysis was used for comparison between groups. (A,B) The
baseline control (0 min) and the untreated time-control (30 min) values (see
Materials and methods). (C,D) Values without ANG II (0 min) and with ANG II
(30 min).
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Fig. 9. Cross talk between the endocardial endothelium (EE) and the myocardium in
A. anguilla. Endoluminal ANG II activates AT1-like
receptors in the EE that stimulate NO release, eliciting in the subjacent
myocardium the negative inotropism through a cGMP-PKG mechanism. NO, nitric
oxide; Gi/o, Gi/o proteins; MR, muscarinic receptor;
PKG, cGMP-activated protein kinase; GC, guanylate cyclase; eNOS, endothelial
nitric oxide synthase.
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© The Company of Biologists Ltd 2003
