Roles of extrajunctional receptors in the response of guinea-pig mesenteric and rat tail arteries to adrenergic nerves.
Studies of the electrical response of isolated guinea-pig mesenteric and rat tail arteries to perivascular nerve stimulation were made by micro-electrodes inserted from the outer surface of the vessels. Membrane potential of both arteries was -68 to -69 mV and usually stable, though with occasional miniature excitatory junction potentials (m.e.j.p.s). Perivascular nerve stimulation produced excitatory junction potentials (e.j.p.s) which usually increased in size with repetitive stimulation, particularly in the mesenteric artery, but rarely triggered a spike or other regenerative response. Phentolamine and yohimbine in low concentrations increased the size of the e.j.p.s in both arteries, and increased the mechanical response of the mesenteric artery, probably by blocking prejunctional alpha 2 receptors which depress release of noradrenaline by the nerves; they reduced the mechanical response of the tail artery, probably by blocking alpha 2 receptors of the smooth muscle. Prazosin in low concentration had no effect on the e.j.p.s but inhibited contraction in both arteries, probably by blocking alpha 1 receptors of the smooth muscle. In the tail artery, but not the mesenteric artery, e.j.p.s produced by repetitive perivascular nerve stimulation were followed by a slow depolarization reaching a maximum at about 20 s and then decaying over 1-3 min; it did not reach the threshold for contraction, assessed by K depolarization. Yohimbine reduced the size and duration of the slow depolarization. High concentrations of noradrenaline (10(-5) M) caused depolarization and contraction of the mesenteric artery, both of which were blocked by prazosin and little affected by yohimbine. In the tail artery, yohimbine did but prazosin did not block the depolarization produced by any concentration of noradrenaline, although yohimbine was almost as effective as prazosin in blocking the contraction produced by low concentrations of noradrenaline. Extrajunctional adrenoceptors in the mesenteric artery therefore included high sensitivity types of alpha 1 receptor, and in the tail artery high sensitivity types of alpha 1 and alpha 2 receptor. Some of the extrajunctional receptors, as well as the junctional receptors responsible for e.j.p.s in both arteries, produced depolarization. Most of the contraction induced by either nerves or exogenous noradrenaline was produced by the extrajunctional receptors, and was not dependent on the depolarization which some of these receptors induced.
D000200:Action Potentials / Q000187:drug effects; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001158:Arteries / Q000294:innervation; D005260:Female; D006168:Guinea Pigs; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008638:Mesenteric Arteries / Q000294:innervation / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D013623:Tail / Q000098:blood supply
D000317:Adrenergic alpha-Antagonists; D000959:Antihypertensive Agents; D011941:Receptors, Adrenergic; D009543:Nifedipine; D011188:Potassium; D009638:Norepinephrine