Key result
Acetylcholine has significant cyclooxygenase-dependent pressor activity in the rabbit pulmonary vascular bed mediated by a muscarinic M1-type receptor, while high tone unmasks a vasodilator response.
Why the study?
Does acetylcholine alter lobar arterial pressure differently under resting versus high tone conditions in the rabbit pulmonary vascular bed?
Does acetylcholine alter lobar arterial pressure differently under resting versus high tone conditions in the rabbit pulmonary vascular bed?
Acetylcholine induces a cyclooxygenase-dependent pressor response via M1 receptors under resting conditions, but unmasks a cyclooxygenase-independent vasodilator response via non-M1/non-M2 receptors under high pulmonary vascular tone in rabbits.
Answers are grounded in this paper and cite their sources.
Tone-dependent cholinergic pulmonary responses in rabbits; leaves open translation to human pulmonary vascular disease.
Pulmonary vascular responses to acetylcholine were compared under resting and high tone conditions of the intact-chest rabbit. Under resting tone conditions, intralobar injections of acetylcholine increased lobar arterial pressure in a dose-related manner. The pressor responses to acetylcholine under resting conditions were blocked by meclofenamate, indomethacin, atropine, and pirenzepine. When lobar vascular resistance was raised to a high steady level, low doses of acetylcholine decreased lobar arterial pressure, whereas higher doses elicited a biphasic response with the pressor component predominating at the highest dose studied. Under high tone conditions, only the pressor component of the response was blocked by meclofenamate or indomethacin, whereas pressor and depressor responses were blocked by atropine or the 600-micrograms/kg iv dose of pirenzepine. Pressor responses to acetylcholine under resting and high tone conditions were blocked by pirenzepine (50 micrograms/kg iv), whereas gallamine had no effect on responses to acetylcholine. The 50-micrograms/kg iv dose of pirenzepine had no effect on depressor responses or the depressor component of the response to acetylcholine. The present data support the concept that acetylcholine has significant cyclooxygenase-dependent pressor activity in the rabbit pulmonary vascular bed and suggest that this response is mediated by a muscarinic M1-type receptor. These data also show that, under high tone conditions, a vasodilator response or a vasodilator component of a biphasic response is unmasked. This response is not dependent on the release of cyclooxygenase products and is mediated by a muscarinic receptor that is neither of the M1- nor the M2-type.
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Hyman et al. (1989) studied Pulmonary vascular responses. Acetylcholine vs. Resting vs high tone conditions was evaluated on Lobar arterial pressure. Acetylcholine has significant cyclooxygenase-dependent pressor activity in the rabbit pulmonary vascular bed mediated by a muscarinic M1-type receptor, while high tone unmasks a vasodilator response.
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