Characterization of a neurogenic and a direct smooth muscle component in the contractile response to electrical field stimulation in rat tail artery.
1. The extent to which neuronal transmitter release contributes to the contractions induced by transmural nerve stimulation of the rat tail artery at various stimulus intensities was characterized. 2. Using tetrodotoxin, which blocks conduction of the action potential along the nerves, and omega-conotoxin GVIA, a blocker of transmitter release from the nerve terminals, as well as chemical and surgical denervations of the perivascular sympathetic nerves, a neurogenic and a direct smooth muscle component could be clearly separated. 3. The neurogenic component was fast in onset, rise and decline (after the end of stimulus), and showed a voltage dependency only at lower stimulus intensities. The non-neurogenic component was slower in onset, rise and decline, and showed a strict voltage dependency throughout the whole stimulus range. This implies that the non-neurogenic component becomes increasingly prominent at high, non-physiological voltages. Mechanisms underlying the declining neurogenic contractile response at the stronger stimulus intensities are discussed. 4. We found no evidence supporting the existence of a possible tetrodotoxin- or omega-conotoxin GVIA-resistant contractile component originating from the perivascular nerves (sympathetic or non-sympathetic). Thus, in order to get a purely neurogenic response stimulus intensities should be minimized to give a contraction that is fully sensitive to these two agents. 5. Transmitter release from the perivascular sympathetic nerves was fully responsible for the purely neurogenic contractions. Activation of postjunctional alpha 1-adrenergic receptors was mainly involved, with a substantial contribution from alpha 2-receptors, and a minor contribution from neuropeptide Y receptors. There was no evidence for a contractile component linked to activation of so-called gamma-adrenergic receptors. 6. Beta-adrenergic receptors, serotonergic, cholinergic, prostanoic or purinergic mechanisms do not appear to contribute to the neurogenic (or the non-neurogenic) response. The neurogenic contraction does not utilize potential-sensitive calcium channels.
Szabó
C
C
Department of Medical Cell Research, University of Lund, Sweden.
Hardebo
J E
JE
D000109:Acetylcholine / Q000502:physiology; D000818:Animals; D001158:Arteries / Q000294:innervation / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004558:Electric Stimulation; D006892:Hydroxydopamines / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000294:innervation / Q000502:physiology*; D009478:Neuropeptide Y / Q000502:physiology; D016627:Oxidopamine; D010456:Peptides, Cyclic / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology; D011687:Purines / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D012701:Serotonin / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D013623:Tail / Q000098:blood supply*; D013779:Tetrodotoxin / Q000494:pharmacology; D020866:omega-Conotoxin GVIA
D002121:Calcium Channel Blockers; D006892:Hydroxydopamines; D009478:Neuropeptide Y; D010456:Peptides, Cyclic; D011453:Prostaglandins; D011687:Purines; D011942:Receptors, Adrenergic, alpha; D012701:Serotonin; D013779:Tetrodotoxin; D016627:Oxidopamine; D020866:omega-Conotoxin GVIA; D000109:Acetylcholine; D011188:Potassium