Tyramine-Induced Contractions in the Rabbit Ear and Basilar Arteries

Lee, Tony J-F.; Araki, Harumi; Su, Chin Chang

doi:10.1097/00005344-198109000-00006

Cited by 9 publications

(6 citation statements)

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“…Consistent with previous findings in several spe cies (Duckles and Bevan, 1976;Lee et al, 1981), the NE contractile dose-response curves in cerebral arteries of the dog and cat were composed of two phases: an initial phase of smaller contractions in duced by NE in concentrations from 10 -6 to 3 X 10-4 M, followed by a second phase of sharply el evated contractile responses induced by higher con centrations ofNE 00-3 -3 x 10-3 M) ( sponses may be mediated by non-u-adrenergic receptors (Edvinsson and Owman, 1974;Bevan, 1981), the effect of bilirubin on the initial phase of NE dose-response curves was examined. In the presence of bilirubin (3 x 10-5 M), NE-induced contractions were usually similar to or smaller than the contractions induced before addition of bilirubin (Fig.…”

Section: Effects Of Bilirubin On Vasoconstriction Induced By Nesupporting

confidence: 93%

Effects of Bilirubin on Cerebral Arterial Tone in vitro

Miao

Lee

1989

J Cereb Blood Flow Metab

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Hemoglobin and its metabolite, bilirubin, have been shown to be present in high concentrations in CSF following subarachnoid hemorrhage (SAH). Several reports have indicated that hemoglobin is a potent cerebral vasoconstrictor and therefore is considered to be an active principle in the genesis of cerebral vasospasm. The possible role of bilirubin on the genesis of cerebral vasospasm, however, has not been clarified. The effect of bilirubin on cerebral vessel tone was therefore examined using in vitro tissue bath techniques. Bilirubin (10−5-3 × 10−5 M) induced strong constriction of cerebral arteries from the cat, dog, and pig. The vasoconstriction returned to baseline after bilirubin was washed by prewarmed Krebs solution. Vasomotor responses to various vasoactive substances were then examined after bilirubin was washed away (the bilirubin postwash effect). Norepinephrine (NE)–induced but not serotonin- or acetylcholine (ACh)–induced constrictions were significantly potentiated by bilirubin postwash effect. The potentiated NE-induced constriction was attenuated by yohimbine but not by prazosin. This enhanced vasoconstriction was mimicked by clonidine but not by phenylephrine, suggesting that the potentiation of NE-induced constriction by the bilirubin postwash effect was mediated by the α2-adrenoceptor subtype. The bilirubin postwash effect also resulted in blockade of endothelium-dependent vasodilations induced by A-23147, ACh, and ATP without affecting relaxations induced by direct muscle relaxants such as β-adrenoceptors, papaverine, and sodium nitroprusside. These results indicate that bilirubin induces direct vasoconstriction, potentiates α2-adrenoceptormediated vasoconstriction, and inhibits endothelium-dependent vasodilation. These actions of bilirubin may promote an enhanced overall vasoconstriction in vivo. Bilirubin, therefore, may be involved in the genesis of cerebral vasospasm following SAH.

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Section: Effects Of Bilirubin On Vasoconstriction Induced By Nesupporting

confidence: 93%

Effects of Bilirubin on Cerebral Arterial Tone in vitro

Miao

Lee

1989

J Cereb Blood Flow Metab

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“…This lack of an adrenergic component is substantiated in this experiment by the fact that tyramine, which produced a contraction in control arteries, did not cause any response in reserpine-treated arteries. Tyramine often causes contraction of vessels by acting indirectly on sympathetic nerves to release noradrenaline which in turn acts postjunctionally to produce a vasoconstriction (Vanhoutte et al, 1981), such a response is abolished or is far less potent in the reserpinepretreated vessel (Lee et al, 1981;Muramatsu et al, 1984). This evidence suggests that in the dog mesenteric artery the prazosin-resistant contraction is caused by substance(s) other than noradrenaline.…”

Section: Discussionmentioning

confidence: 99%

The effect of reserpine on sympathetic, purinergic neurotransmission in the isolated mesenteric artery of the dog: a pharmacological study

Muramatsu

1987

British J Pharmacology

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1 Electrical transmural stimulation evoked a transient contraction in the isolated mesenteric artery of the dog. This contraction was abolished by guanethidine or tetrodotoxin and was partially inhibited by prazosin. Noradrenaline was competitively antagonized by prazosin. 2 Similarly, in the reserpine-treated artery, electrical transmural stimulation produced a transient contraction which was abolished by guanethidine or tetrodotoxin. However, prazosin failed to inhibit this contraction. The contraction to noradrenaline was not significantly different from the response it produced in control vessels. 3 Tyramine (10-5M), which acts on sympathetic nerves to release noradrenaline, evoked a tonic contraction in the untreated artery. This contraction was abolished or markedly attenuated by prazosin or guanethidine. The response was not observed in the reserpine-treated artery, indicating that reserpine had depleted the nerves of noradrenaline. 4 In the control vessel a,-methylene-ATP produced a transient contraction which was followed by a complete relaxation to the basal level. This contractile response was not significantly different in the presence of guanethidine or prazosin or in the reserpine-treated artery.5 After desensitization of the vessel to a,p-methylene ATP (5 x 10-6M) the prazosin-resistant contractions induced by electrical transmural stimulation were abolished both in reserpine-treated and untreated arteries. Also the contractile responses to ATP and z,4-methylene-ATP were abolished but the responses to tyramine (control vessels), noradrenaline and KCI were not affected. 6 8-Phenyltheophylline (10-M) showed no inhibitory effect on the contractile responses to electrical transmural stimulation, tyramine, ATP or a,p-methylene-ATP.7 Neuropeptide Y, peptide YY, vasoactive intestinal polypeptide, bombesin and substance P (10-7 and 10-6 M for each peptide) caused no contractile response in the dog mesenteric artery. 8 These experiments provide further evidence that the sympathetic contraction of the isolated mesenteric artery of the dog induced by electrical transmural stimulation consists of an adrenergic and a purinergic component and that the latter component is mediated through postsynaptic P2-purinoceptors.

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“…This result would not support the possibility that a presynaptic cholinergic feedback mechanism (Kilbinger, 1978) is participating in neurogenic vasodilation. These results further suggest that the nerve-released ACh may not play an important role in direct control of cerebral vascular tone like that of norepinephrine from the sympathetic nerve (Aim and Bill, 1973;Heistad et al, 1978;Lee et al, 1978Lee et al, , 1981.…”

Section: Figure 7 Effect Of Cold Storage On Transmural Nerve Stimulamentioning

confidence: 96%

Cholinergic mechanism in the large cat cerebral artery.

Lee¹

1982

Circulation Research

101

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The isolated cat cerebral arteries (basilar, middle cerebral, anterior cerebral, and internal carotid) were studied in vitro. ACh at low concentration (3 x 10(-8) to 3 x 10(-6) M) induced relaxation, and at high concentration (10(-5) to 3 x 10(-3) M) induced constriction of the arteries with endothelial cells. In contrast, concentration of any magnitude (10(-6) to 3 x 10(-3) M) induced constriction exclusively in arteries without endothelium. Atropine (3 x 10(-6) to 3 x 10(-5) M) blocked and physostigmine (3 x 10(-6) M) potentiated both ACh-induced relaxation and constriction. These results suggest that the relaxation induced by exogenous ACh is solely dependent on the endothelial cells and that the primary effect of the direct action of ACh on the smooth muscle cells is constriction. Transmural nerve stimulation (TNS) induced a frequency-dependent relaxation in the arteries with or without endothelium. Neither atropine nor physostigmine affected the TNS-induced dilator response in either preparation. This, together with the wide separation between the nerve and endothelium in the vessel wall, suggests that ACh is not involved in TNS-induced vasodilation. Furthermore, the TNS-induced relaxation at any frequency is not smaller but greater in the arteries without endothelial cells than in those with endothelial cells. Blockade of the TNS-induced vasodilation by tetrodotoxin (TTX) or cold storage denervation did not prevent the arteries from relaxing in response to ACh or methacholine (MCh). It is suggested that the TNS-induced vasodilation is independent of the endothelial cells and that the vasodilation is due to the direct action of a yet-to-be identified dilator transmitter on the smooth muscle cells. Results of the present study support our previous finding that, in the cat cerebral artery. ACh is more likely to be a constrictor transmitter than a dilator transmitter.

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Tyramine-Induced Contractions in the Rabbit Ear and Basilar Arteries

Cited by 9 publications

References 0 publications

Effects of Bilirubin on Cerebral Arterial Tone in vitro

Effects of Bilirubin on Cerebral Arterial Tone in vitro

The effect of reserpine on sympathetic, purinergic neurotransmission in the isolated mesenteric artery of the dog: a pharmacological study

Cholinergic mechanism in the large cat cerebral artery.

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