TY - JOUR
T1 - Enhanced α-adrenoceptor responsiveness and receptor number during global ischaemia in the Langendorff perfused rat heart
AU - Butterfield, M. C.
AU - Chess-Williams, R.
PY - 1990/7
Y1 - 1990/7
N2 - 1. Idioventricular rate responses and adrenoceptor number have been examined in normal Langendorff hearts perfused at 70 cmH2O and in 'ischaemic' hearts perfused at 10 cmH2O. 2. In hearts perfused at normal pressure, ventricular rate responses to phenylephrine in the presence of propranolol were biphasic with low concentrations of phenylephrine reducing, and high concentrations increasing, ventricular rate. Both responses were abolished in the presence of prazosin (100 nM). In hearts perfused at low pressure, the negative chronotropic responses to phenylephrine were no longer present and positive chronotropic responses were enhanced compared with those of control tissues. The number of ventricular [3H]-prazosin binding sites was also significantly increased during ischaemia. 3. Idioventricular rate responses to isoprenaline were depressed in ischaemic tissues compared with controls, but [3H]-dihydroalprenolol binding was not altered in these hearts. 4. The incidence and duration of arrhythmias which occurred during 30 min of global ischaemia and reperfusion were not significantly altered in the presence of 100 nM prazosin. 5. These results demonstrate that reducing the perfusion pressure of rat isolated hearts enhances α-adrenoceptor-mediated responses and increases α-adrenoceptor density. Whether the increase in α-adrenoceptor responsiveness during ischaemia is involved in arrhythmogenesis requires further investigation.
AB - 1. Idioventricular rate responses and adrenoceptor number have been examined in normal Langendorff hearts perfused at 70 cmH2O and in 'ischaemic' hearts perfused at 10 cmH2O. 2. In hearts perfused at normal pressure, ventricular rate responses to phenylephrine in the presence of propranolol were biphasic with low concentrations of phenylephrine reducing, and high concentrations increasing, ventricular rate. Both responses were abolished in the presence of prazosin (100 nM). In hearts perfused at low pressure, the negative chronotropic responses to phenylephrine were no longer present and positive chronotropic responses were enhanced compared with those of control tissues. The number of ventricular [3H]-prazosin binding sites was also significantly increased during ischaemia. 3. Idioventricular rate responses to isoprenaline were depressed in ischaemic tissues compared with controls, but [3H]-dihydroalprenolol binding was not altered in these hearts. 4. The incidence and duration of arrhythmias which occurred during 30 min of global ischaemia and reperfusion were not significantly altered in the presence of 100 nM prazosin. 5. These results demonstrate that reducing the perfusion pressure of rat isolated hearts enhances α-adrenoceptor-mediated responses and increases α-adrenoceptor density. Whether the increase in α-adrenoceptor responsiveness during ischaemia is involved in arrhythmogenesis requires further investigation.
UR - http://www.scopus.com/inward/record.url?scp=0025292087&partnerID=8YFLogxK
U2 - 10.1111/j.1476-5381.1990.tb15860.x
DO - 10.1111/j.1476-5381.1990.tb15860.x
M3 - Article
C2 - 2167740
AN - SCOPUS:0025292087
SN - 0007-1188
VL - 100
SP - 641
EP - 645
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
IS - 3
ER -