Pharmacological characterization of adrenergic receptors of a rabbit cerebral artery in vitro.
In the light of controversy over the functional significance of the abundant sympathetic innervation of large cerebral blood vessels, an in vitro analysis of the adrenergic receptors mediating contractile effects in the rabbit basilar artery was undertaken. Beta adrenergic stimulation had no effect, and agents that block norepinephrine (NE) uptake did not alter contractile responses to l-NE. The l-NE dose-response curve could be resolved into two components S-shaped curves: the first had an ED50 OF 10(-5) M and reached a plateau at 10(-4) M; the second component continued above 10(-3) M without reaching a plateau. Phenylephrine and epinephrine dose-response curves were also biphasic; d-NE responses corresponded to the second phase of the l-NE curve. Relative potencies for the two components were different. For the first component, these were 1:0.23:0.18:0.03 for l-NE, epinephrine, phenylephrine and d-NE, respectively; relative potencies for the second component of the curve were 1:1:0.11:0.23. Phentolamine dissociation constants were analyzed separately for each component. The value for low l-NE concentrations was 5 X 10 (-8) M and, for higher concentrations, it was 3 X 10(-6) . The insensitivity of the alpha adrenergic receptor and the poor responsiveness of the muscle to its activation with agonist concentrations below 10(-4) M can probably account for the small contractile responses to nerve stimulation of large pial arteries in spite of their abundant innervation.
Pharmacological characterization of adrenergic receptors of a rabbit cerebral artery in vitro. In the light of controversy over the functional significance of the abundant sympathetic innervation of large cerebral blood vessels, an in vitro analysis of the adrenergic receptors mediating contractile effects in the rabbit basilar artery was undertaken. Beta adrenergic stimulation had no effect, and agents that block norepinephrine (NE) uptake did not alter contractile responses to l-NE. The l-NE dose-response curve could be resolved into two components S-shaped curves: the first had an ED50 OF 10(-5) M and reached a plateau at 10(-4) M; the second component continued above 10(-3) M without reaching a plateau. Phenylephrine and epinephrine dose-response curves were also biphasic; d-NE responses corresponded to the second phase of the l-NE curve. Relative potencies for the two components were different. For the first component, these were 1:0.23:0.18:0.03 for l-NE, epinephrine, phenylephrine and d-NE, respectively; relative potencies for the second component of the curve were 1:1:0.11:0.23. Phentolamine dissociation constants were analyzed separately for each component. The value for low l-NE concentrations was 5 X 10 (-8) M and, for higher concentrations, it was 3 X 10(-6) . The insensitivity of the alpha adrenergic receptor and the poor responsiveness of the muscle to its activation with agonist concentrations below 10(-4) M can probably account for the small contractile responses to nerve stimulation of large pial arteries in spite of their abundant innervation.