Article date: August 1993
By: A. Ferro, A.J. Kaumann, M.J. Brown, in Volume 109, Issue 4, pages 1053-1058
We have recently reported that patients taking β1‐adrenoceptor‐selective antagonists exhibit marked sensitization of β2‐adrenoceptor responses but unaltered β1‐adrenoceptor responses in the heart, both in vitro and in vivo. We therefore investigated β1‐ and β2‐adrenoceptor‐mediated relaxant responses in rings of human internal mammary artery and saphenous vein without endothelium, taken from β1‐blocked and non‐β‐blocked patients undergoing coronary artery bypass graft surgery, for comparison. We also examined α1‐adrenoceptor‐mediated contraction in these vessels, to determine whether β1‐blockade had any cross‐regulatory effect.
Following α‐blockade with 10 μm phenoxybenzamine, both noradrenaline and adrenaline produced concentration‐dependent relaxations in both blood vessels, their effects being mediated predominantly through β2‐adrenoceptors; a lesser β1‐adrenoceptor component to relaxation was also found in internal mammary artery and a minor β1‐adrenoceptor component was present in saphenous vein. No differences were found in β1‐ or in β2‐adrenoceptor‐mediated vasorelaxation between β1‐blocked and non‐β‐blocked patients.
Methoxamine produced concentration‐dependent contractions in both blood vessels, and the potency and efficacy were not significantly different between vessels from β1‐blocked and from non‐β‐blocked patients.
These findings indicate that, in these tissues, which possess a relatively minor β1‐adrenoceptor component in contrast to myocardial tissue, chronic β1‐blocker treatment does not alter either β1‐ or β2‐adrenoceptor responses. Likewise, in such tissues, α1‐adrenoceptor responses are unaffected by prior β1‐blockade.
We have recently reported that patients taking β1‐adrenoceptor‐selective antagonists exhibit marked sensitization of β2‐adrenoceptor responses but unaltered β1‐adrenoceptor responses in the heart, both in vitro and in vivo. We therefore investigated β1‐ and β2‐adrenoceptor‐mediated relaxant responses in rings of human internal mammary artery and saphenous vein without endothelium, taken from β1‐blocked and non‐β‐blocked patients undergoing coronary artery bypass graft surgery, for comparison. We also examined α1‐adrenoceptor‐mediated contraction in these vessels, to determine whether β1‐blockade had any cross‐regulatory effect.
Following α‐blockade with 10 μm phenoxybenzamine, both noradrenaline and adrenaline produced concentration‐dependent relaxations in both blood vessels, their effects being mediated predominantly through β2‐adrenoceptors; a lesser β1‐adrenoceptor component to relaxation was also found in internal mammary artery and a minor β1‐adrenoceptor component was present in saphenous vein. No differences were found in β1‐ or in β2‐adrenoceptor‐mediated vasorelaxation between β1‐blocked and non‐β‐blocked patients.
Methoxamine produced concentration‐dependent contractions in both blood vessels, and the potency and efficacy were not significantly different between vessels from β1‐blocked and from non‐β‐blocked patients.
These findings indicate that, in these tissues, which possess a relatively minor β1‐adrenoceptor component in contrast to myocardial tissue, chronic β1‐blocker treatment does not alter either β1‐ or β2‐adrenoceptor responses. Likewise, in such tissues, α1‐adrenoceptor responses are unaffected by prior β1‐blockade.
DOI: 10.1111/j.1476-5381.1993.tb13728.x
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