Enhanced α-adrenoceptor responsiveness and receptor number during global ischaemia in the Langendorff perfused rat heart

M. C. Butterfield, R. Chess-Williams

Research output: Contribution to journalArticleResearchpeer-review

12 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)641-645
Number of pages5
JournalBritish Journal of Pharmacology
Volume100
Issue number3
DOIs
Publication statusPublished - Jul 1990
Externally publishedYes

Fingerprint

Adrenergic Receptors
Ischemia
Prazosin
Phenylephrine
Dihydroalprenolol
Pressure
Ventricular Pressure
Isoproterenol
Propranolol
Reperfusion
Cardiac Arrhythmias
Perfusion
Binding Sites
Isolated Heart Preparation
Incidence

Cite this

@article{eebed1a02bce4f838e181ea094072de9,
title = "Enhanced α-adrenoceptor responsiveness and receptor number during global ischaemia in the Langendorff perfused rat heart",
abstract = "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.",
author = "Butterfield, {M. C.} and R. Chess-Williams",
year = "1990",
month = "7",
doi = "10.1111/j.1476-5381.1990.tb15860.x",
language = "English",
volume = "100",
pages = "641--645",
journal = "British journal of pharmacology and chemotherapy",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "3",

}

Enhanced α-adrenoceptor responsiveness and receptor number during global ischaemia in the Langendorff perfused rat heart. / Butterfield, M. C.; Chess-Williams, R.

In: British Journal of Pharmacology, Vol. 100, No. 3, 07.1990, p. 641-645.

Research output: Contribution to journalArticleResearchpeer-review

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

VL - 100

SP - 641

EP - 645

JO - British journal of pharmacology and chemotherapy

JF - British journal of pharmacology and chemotherapy

SN - 0007-1188

IS - 3

ER -