Effects of β1and β2-adrenoceptor stimulation on hemodynamics in the anesthetized rat

A. Abdelrahman, R. Tabrizchi, C. C Y Pang

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The role of β1-adrenoceptors in mediation of vasodilatation is not clear. The microsphere technique was used to compare the effects of mixed β-, β1-, and β2-stimulation on blood flow and conductance changes in five groups of pentobarbital-anesthetized rats: I, vehicle; II, mixed β-stimulation; III, β1-stimulation; IV, β2-stimulation; and V, mixed β-blockade. Isoproterenol (32 ng/kg/min) was infused into rats either without (group II) or with ICI 118,551 β2-blocker, 30 μg/kg, group III), atenolol (β1-blocker, 100 μg/kg, group IV), or both blockers (group V), respectively. At the doses selected, ICI 118,551 shifted the dose-vasodepressor response curve of salbutamol β2-agonist) to the right but had no effect on the dose-chronotropic response curve of dobutamine (β1-agonist), whereas atenolol shifted the dosechronotropic response curve of dobutamine to the right and had no effect on the dose-vasodepressor response curve of salbutamol. The results show that isoproterenol increased heart rate (HR) and arterial conductances in the coronary and skeletal muscle beds but had no effects in other beds. Combined with ICI 118,551, isoproterenol caused similar increases in HR and coronary arterial conductance but markedly less increase in skeletal muscle conductance. Atenolol abolished the increase in HR by isoproterenol but did not affect the increases in coronary and muscular arterial conductances. With both blockers, isoproterenol produced no increase in coronary and skeletal muscle conductance. Therefore, both β1- and β2-adrenoceptors play a role in coronary and skeletal muscle vasodilatation. Whether coronary vasodilatation subsequent to β1-stimulation is entirely due to metabolic factors or is additionally contributed to by direct effects is not clear.

Original languageEnglish
Pages (from-to)720-728
Number of pages9
JournalJournal of Cardiovascular Pharmacology
Volume15
Issue number5
Publication statusPublished - 1990

Fingerprint

Isoproterenol
Adrenergic Receptors
Hemodynamics
Atenolol
Skeletal Muscle
Vasodilation
Dobutamine
Albuterol
Heart Rate
Pentobarbital
Microspheres
ICI 118551

Keywords

  • Atenolol
  • ICI 118,551
  • Isoproterenol
  • Rats
  • Salbutamol
  • Vasodilatation
  • β<inf>1</inf>- and β<inf>2</inf>-adrenoceptors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Effects of β1and β2-adrenoceptor stimulation on hemodynamics in the anesthetized rat. / Abdelrahman, A.; Tabrizchi, R.; Pang, C. C Y.

In: Journal of Cardiovascular Pharmacology, Vol. 15, No. 5, 1990, p. 720-728.

Research output: Contribution to journalArticle

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AB - The role of β1-adrenoceptors in mediation of vasodilatation is not clear. The microsphere technique was used to compare the effects of mixed β-, β1-, and β2-stimulation on blood flow and conductance changes in five groups of pentobarbital-anesthetized rats: I, vehicle; II, mixed β-stimulation; III, β1-stimulation; IV, β2-stimulation; and V, mixed β-blockade. Isoproterenol (32 ng/kg/min) was infused into rats either without (group II) or with ICI 118,551 β2-blocker, 30 μg/kg, group III), atenolol (β1-blocker, 100 μg/kg, group IV), or both blockers (group V), respectively. At the doses selected, ICI 118,551 shifted the dose-vasodepressor response curve of salbutamol β2-agonist) to the right but had no effect on the dose-chronotropic response curve of dobutamine (β1-agonist), whereas atenolol shifted the dosechronotropic response curve of dobutamine to the right and had no effect on the dose-vasodepressor response curve of salbutamol. The results show that isoproterenol increased heart rate (HR) and arterial conductances in the coronary and skeletal muscle beds but had no effects in other beds. Combined with ICI 118,551, isoproterenol caused similar increases in HR and coronary arterial conductance but markedly less increase in skeletal muscle conductance. Atenolol abolished the increase in HR by isoproterenol but did not affect the increases in coronary and muscular arterial conductances. With both blockers, isoproterenol produced no increase in coronary and skeletal muscle conductance. Therefore, both β1- and β2-adrenoceptors play a role in coronary and skeletal muscle vasodilatation. Whether coronary vasodilatation subsequent to β1-stimulation is entirely due to metabolic factors or is additionally contributed to by direct effects is not clear.

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