Article date: November 1987
By: Serafini Guimarães, Maria Q. Paiva in Volume 92, Issue 3, pages 505-512
The effect of different concentrations of phenoxybenzamine (0.1, 0.3, 1, 3, 10 and 30 nmol l−1) on the concentration‐response curves to phenylephrine (a selective α1‐adrenoceptor agonist) and noradrenaline (a mixed α1‐ and α2‐adrenoceptor agonist) was compared in two kinds of vascular tissue: dog saphenous vein (has both postsynaptic α1‐ and α2‐adrenoceptors) and dog mesenteric and renal arteries—where only postsynaptic α1‐adrenoceptors have been shown to exist.
In the saphenous vein, where both α1‐ and α2‐adrenoceptors coexist, at only one concentration of phenoxybenzamine, 3 nmol l−1, the concentration‐response curve of noradrenaline was shifted to the right without a reduction of the maximum; and this shift was small (by 0.4 log units).
In tissues where only α1‐adrenoceptors exist postsynaptically (mesenteric and renal arteries) phenoxybenzamine never caused any shift of the noradrenaline concentration‐response curves to the right without depressing the maximum effect.
In none of the tissues did phenoxybenzamine at any concentration shift the concentration‐response curve of phenylephrine to the right without depressing its maximum.
All these results indicate that in the dog saphenous vein there is a ‘false’ α‐adrenoceptor reserve for noradrenaline, since two kinds of receptors participate in the response to this amine.
The calculation of the occupancy‐response relationship for the renal artery showed that 24% of the maximal response occurs when only 2% of α1‐adrenoceptors are activated and 50% of maximum at 9% occupation. However, for 95% of the maximal response an 83% occupancy is required. Similar values were calculated for the mesenteric artery.
Thus, the surplus α1‐adrenoceptors which is very large for a half‐maximal response becomes smaller and smaller as the magnitude of the response increases and probably disappears at the 100% response level.
If we retain the original definition of ‘spare receptors’–receptors in ‘excess’ of those required to produce a maximal response, we conclude, that there is no receptor reserve in the dog mesenteric and renal arteries.
The effect of different concentrations of phenoxybenzamine (0.1, 0.3, 1, 3, 10 and 30 nmol l−1) on the concentration‐response curves to phenylephrine (a selective α1‐adrenoceptor agonist) and noradrenaline (a mixed α1‐ and α2‐adrenoceptor agonist) was compared in two kinds of vascular tissue: dog saphenous vein (has both postsynaptic α1‐ and α2‐adrenoceptors) and dog mesenteric and renal arteries—where only postsynaptic α1‐adrenoceptors have been shown to exist.
In the saphenous vein, where both α1‐ and α2‐adrenoceptors coexist, at only one concentration of phenoxybenzamine, 3 nmol l−1, the concentration‐response curve of noradrenaline was shifted to the right without a reduction of the maximum; and this shift was small (by 0.4 log units).
In tissues where only α1‐adrenoceptors exist postsynaptically (mesenteric and renal arteries) phenoxybenzamine never caused any shift of the noradrenaline concentration‐response curves to the right without depressing the maximum effect.
In none of the tissues did phenoxybenzamine at any concentration shift the concentration‐response curve of phenylephrine to the right without depressing its maximum.
All these results indicate that in the dog saphenous vein there is a ‘false’ α‐adrenoceptor reserve for noradrenaline, since two kinds of receptors participate in the response to this amine.
The calculation of the occupancy‐response relationship for the renal artery showed that 24% of the maximal response occurs when only 2% of α1‐adrenoceptors are activated and 50% of maximum at 9% occupation. However, for 95% of the maximal response an 83% occupancy is required. Similar values were calculated for the mesenteric artery.
Thus, the surplus α1‐adrenoceptors which is very large for a half‐maximal response becomes smaller and smaller as the magnitude of the response increases and probably disappears at the 100% response level.
If we retain the original definition of ‘spare receptors’–receptors in ‘excess’ of those required to produce a maximal response, we conclude, that there is no receptor reserve in the dog mesenteric and renal arteries.
DOI: 10.1111/j.1476-5381.1987.tb11350.x
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