The cholinergic pathway to cerebral blood vessels

Abstract

The effect of stimulating the greater superficial petrosal nerve (g.s.p.n.) upon retroglenoid venous blood flow has been tested in anaesthetized, paralysed and artificially ventilated rats. In 11 out of 15 tests, blood flow increased by an average of 25% with a time to peak response of 28 s. This response was abolished with the injection of atropine 0.1 mg kg-1 injected intra-arterially. With both petrosal nerves intact, the administration of 6-7% CO2 in air or 15% O2 in N2 caused average increases in blood flow of 105% and 45% respectively. These responses were not affected by bilateral section of the g.s.p.n. Similar experiments were carried out in 5 anaesthetized, spontaneously breathing rabbits in which, in addition to PaCO2 and PaO2, PO2, PCO2 and blood flow in the caudate nucleus were measured continuously using chronically implanted mass spectrometer catheters and heated thermistors. Caudate nucleus blood flow increased in response to hypoxia and hypercapnia and this response was not significantly affected by section of one or both g.s.p.n., sinus or vagus nerves. With section of sinus and vagus nerves, blood flow changed passively with arterial pressure.

Cholinergic mechanism in the large cat cerebral artery.

“…Results of the present study are in conflict with some in vivo findings that atropine blocks both pial vessel dilation and increased cerebral blood flow following electrical stimulation of the superficial petrosal nerve (Cobb and Finesinger, 1932;Vasquez and Purves, 1977;D'Alecy, 1977;Pinard et al, 1979). As we have suggested (Lee, 1980), one possible explanation for the discrepancy between in vitro and in vivo findings is that ACh may be involved in the dilator pathway at sites other than the terminal synapse.…”

Inhibition of Acetylcholinesterase Modulates the Autoregulation of Cerebral Blood Flow and Attenuates Ischemic Brain Metabolism in Hypertensive Rats

“…The cerebral vessels are richly supplied by cholinergic as well as sympathetic and peptidergic nerves and express much greater ACh contents than most extracranial vessels (Bevan et al, 1982;Duckles, 1981;Suzuki and Hardebo, 1993), al though the role of innervation in the regulation of CBF is still controversial. In the resting condition, even an electric stimulation of the Vth or VIIth cra nial nerves had a small or minimal effect on regional CBF (Busija and Heistad, 1981;Pinard et al, 1979). We recently reported that the intravenous ad ministration of phenoxybenzamine, an a-blocker (Shiokawa et al, 1989), or captopril, an angioten sin-converting enzyme inhibitor (Sadoshima et al, 1994) that decreases cerebrovascular sympathetic tone, shifts the lower limits of autoregulation to the lower levels of blood pressure with the reduction of vascular resistance in SHR.…”

Origins and Pathways of Choline Acetyltransferase—Positive Parasympathetic Nerve Fibers to Cerebral Vessels in Rat

“…Chorobski and Penfield (1932) in monkey and Za charias (1945) in rat. The projections of this gan glion have not been fully elucidated, but the gan glion cells display AChE reactivity (Vasquez and Purves, 1979), some cells are VIP positive (Suzuki et aI. , 1988), and in the caudal part of the ganglion substance P-and calcitonin gene-related peptide positive cells are found (Hardebo et aI., 1989;Su zuki et aI., 1989).…”

“…Key Words: Cerebral blood vessels-Choline acetyltransferase-Cerebro vascular innervation-Parasympathetic nerves Retrograde axonal tracing-Vasoactive intestinal poly peptide 1982), rat (Edvinsson et al, 1972;Licata et aI. , 1975;Vasquez and Purves, 1979;Kobayashi et aI., 1983;Hara et al, 1985;Hara and Weir, 1986), mouse, hamster, guinea pig, and cat (Edvinsson et al , 1972). All these histochemical studies were ex clusively based on nerve staining for AChE, origi nally developed by Koelle and Friedenwald (1949).…”