TY - JOUR
T1 - Cardiac effects of angiotensin I and angiotensin II
T2 - Dose-response studies in the isolated perfused rat heart
AU - Traquandi, Cristina
AU - Riva, Emma
PY - 1998/1
Y1 - 1998/1
N2 - We investigated the effects of angiotensin I (4 x 10-9, 4 x 10-8 and 4 x 10-7 M) on myocardial contractility, heart rate and coronary perfusion in the isolated rat heart before and after inhibition of angiotensin-converting enzyme (ACE) by captopril (4 x 10-4 M). We also studied the post-ischaemic recovery of cardiac function in isolated hearts subjected to global myocardial ischaemia and reperfused with various doses of angiotensin II (1 x 10-9, 1 x 10-8 and 1 x 10-7 M). Angiotensin I significantly reduced coronary flow, the vasoconstrictor effect of a second identical dose was attenuated after inhibition of ACE with captopril. Angiotensin II reduced coronary flow to the same extent as angiotensin I at a concentration four times lower. Left ventricular developed pressure was reduced by angiotensin I and angiotensin II in a dose-dependent manner. Heart rate was not affected by angiotensin I and was significantly lowered by the highest doses (1 x 10-8 and 1 x 10-7 M) of angiotensin II. Post-ischaemic recoveries of vascular and contractile function were similar in control hearts and in hearts given angiotensin II during reperfusion. However, left ventricular end-diastolic pressure was increased by the highest dose (1 x 10-7 M) of angiotensin II throughout reperfusion compared with control, or hearts receiving lower doses (NS). In conclusion the attenuated vasoconstrictor response to angiotensin I after captopril pre-treatment confirms the existence of an intracardiac renin-angiotensin system operative in vitro. Our results also suggest that angiotensin II, at a high concentration, may play a negative role in relaxation in the ischaemic-reperfused injured heart.
AB - We investigated the effects of angiotensin I (4 x 10-9, 4 x 10-8 and 4 x 10-7 M) on myocardial contractility, heart rate and coronary perfusion in the isolated rat heart before and after inhibition of angiotensin-converting enzyme (ACE) by captopril (4 x 10-4 M). We also studied the post-ischaemic recovery of cardiac function in isolated hearts subjected to global myocardial ischaemia and reperfused with various doses of angiotensin II (1 x 10-9, 1 x 10-8 and 1 x 10-7 M). Angiotensin I significantly reduced coronary flow, the vasoconstrictor effect of a second identical dose was attenuated after inhibition of ACE with captopril. Angiotensin II reduced coronary flow to the same extent as angiotensin I at a concentration four times lower. Left ventricular developed pressure was reduced by angiotensin I and angiotensin II in a dose-dependent manner. Heart rate was not affected by angiotensin I and was significantly lowered by the highest doses (1 x 10-8 and 1 x 10-7 M) of angiotensin II. Post-ischaemic recoveries of vascular and contractile function were similar in control hearts and in hearts given angiotensin II during reperfusion. However, left ventricular end-diastolic pressure was increased by the highest dose (1 x 10-7 M) of angiotensin II throughout reperfusion compared with control, or hearts receiving lower doses (NS). In conclusion the attenuated vasoconstrictor response to angiotensin I after captopril pre-treatment confirms the existence of an intracardiac renin-angiotensin system operative in vitro. Our results also suggest that angiotensin II, at a high concentration, may play a negative role in relaxation in the ischaemic-reperfused injured heart.
KW - Angiotensins
KW - Captopril
KW - Diastolic dysfunction
KW - Heart
KW - Ischaemia
KW - Rat
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U2 - 10.1006/phrs.1997.0265
DO - 10.1006/phrs.1997.0265
M3 - Article
C2 - 9503481
AN - SCOPUS:0031940536
VL - 37
SP - 57
EP - 65
JO - Pharmacological Research
JF - Pharmacological Research
SN - 1043-6618
IS - 1
ER -