Neuroeffector transmission in arterioles of the guinea-pig choroid.
1. Using conventional microelectrode techniques, membrane potentials were recorded from smooth muscle cells of guinea-pig choroidal arterioles. 2. Transmural stimulation initiated excitatory junction potentials (EJPs) which were abolished by either guanethidine or alpha,beta-methylene-ATP but not by phentolamine, indicating that they resulted from activation of purinoceptors. 3. Trains of stimuli evoked EJPs which were followed by a slow depolarization, an inhibitory junction potential (IJP) or a biphasic membrane potential change which consisted of an IJP and a subsequent slow depolarization. 4. Slow depolarizations were abolished by either phentolamine or guanethidine, indicating that they resulted from activation of alpha-adrenoceptors. 5. IJPs were abolished by atropine but not by guanethidine, and were reduced by 50 % by apamin with the residual response being abolished by charybdotoxin, indicating that they resulted from the activation of muscarinic receptors which open two sets of Ca2+-activated K+ channels. 6. Most responses were followed by slow hyperpolarizations. These were almost abolished by L-nitroarginine, an effect which was partly overcome by L-arginine, and were abolished by glibenclamide, indicating that they resulted from the release of NO and activation of ATP-sensitive K+ channels. 7. Immunohistochemical analysis showed that arterioles were densely innervated by adrenergic nerve fibres. A population of fibres, likely to be cholinergic, was also identified. Furthermore, populations of nerve fibres immunoreactive to antibodies against either nitric oxide synthase (NOS) or substance P (SP) were also identified. 8. These findings indicate that choroidal arterioles of the guinea-pig are innervated by at least three different populations of nerves, adrenergic nerves which evoke excitatory responses, cholinergic nerves which evoke inhibitory responses and a population of nerves which cause the release of NO.
Hashitani
H
H
Department of Physiology, Nagoya City University Medical School, Nagoya 467-8601, Japan.
Windle
A
A
Suzuki
H
H
D000818:Animals; D001158:Arteries / Q000294:innervation; D001160:Arterioles / Q000294:innervation; D002829:Choroid / Q000098:blood supply*; D004558:Electric Stimulation; D017629:Gap Junctions / Q000502:physiology; D006168:Guinea Pigs; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009116:Muscarine / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology; D009420:Nervous System / Q000378:metabolism; D009433:Neural Inhibition / Q000502:physiology; D026902:Potassium Channel Blockers; D011930:Reaction Time / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D014018:Tissue Distribution
D026902:Potassium Channel Blockers; D009116:Muscarine