Cholinergic mechanism in the large cat cerebral artery.

Lee, T J

doi:10.1161/01.res.50.6.870

Cited by 101 publications

(71 citation statements)

References 24 publications

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“…The vasocon striction may result from activation of muscarinic receptors located directly on the smooth-muscle cells (Lee, 1982). These findings suggest a direct link between the hyperpolarization and the dilation in response to ACh and imply that the endothelial cell-mediated response to exogenous ACh normally dominates the overall effect of muscarinic activa tion, even at high concentrations of ACh.…”

Section: Discussionmentioning

confidence: 84%

Endothelium-Dependent Dilation of Feline Cerebral Arteries: Role of Membrane Potential and Cyclic Nucleotides

Brayden

Wellman

1989

J Cereb Blood Flow Metab

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Summary: The objective of this study was to characterize the role of membrane potential and cyclic nucleotides in endothelium-dependent dilation of cerebral arteries. Mid dle cerebral arteries isolated from cats were depolarized and constricted in response to serotonin or when sub jected to transmural pressures >50 mm Hg. Acetylcho line (ACh) and ADP caused vasodilation and a sustained, dose-dependent hyperpolarization of up to 20 m V in this artery. The membrane potential change preceded the va sodilation by -6 s. Hyperpolarizations and dilations to ACh and ADP did not occur in preparations without en dothelium. The hyperpolarizations were abolished by ouabain (10-5 M), which also blocked the dilator re sponse to ACh. However, dilations to ADP were unaf fected by ouabain. Methylene blue (5 x 10-5 M), a guaVasodilation in response to many agents occurs through release of a factor or factors from the vas cular endothelium (Furchgott, 1983). However, the mechanisms by which such endothelial factors cause vasodilation have not been fully elucidated. In the aorta (Rapoport and Murad, 1983), pulmo nary artery (Ignarro et al., 1987), and coronary ar tery (Holzmann, 1982), among others, endothelium dependent vasodilation is associated with increased formation of cyclic guanosine monophosphate (cGMP). Changes in cGMP may lead to phosphor ylation and altered function of proteins involved in the mechanisms of contraction and relaxation (Rap oport et aI., 1982). In addition, several laboratoriesReceived August 1,1988; accepted November 15,1988. Address correspondence and reprint requests to Dr. J. E. Brayden at Department of Pharmacology, Given Medical Build ing, The University of Vermont, Burlington, VT 05405, U.S.A.Abbreviations used: ACh, acetylcholine; cAMP, cyclic ade nosine monophosphate; cGMP, cyclic guanosine monophos phate. 256nylate cyclase inhibitor, had no effect on the responses to ACh or ADP in the presence or absence of ouabain. Cy clic guanosine monophosphate (cGMP) levels were not altered in cerebral arteries exposed to ACh or ADP. However, ADP did increase cyclic adenosine monophos phate levels in these blood vessels. We conclude that although membrane hyperpolarizations may be adequate to cause vasodilation, at least one other pathway of en dothelium-dependent vasodilation also is present in feline cerebral arteries. Cyclic GMP does not appear to be in volved in this alternate pathway of dilation.

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Section: Discussionmentioning

confidence: 84%

Endothelium-Dependent Dilation of Feline Cerebral Arteries: Role of Membrane Potential and Cyclic Nucleotides

Brayden

Wellman

1989

J Cereb Blood Flow Metab

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“…The platinum wire was bent into a U shape and anchored to a gate. The stainless-steel rod was connected to a strain gauge (UC2; Gould) for isometric recording of changes in force, as described in our previous report (Lee, 1982). The temperature of the Krebs solution equilibrated with 95% 02/5% CO2 was maintained at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…The endothelial cells of the arterial ring segments were mechanically removed by a standard brief gentle rubbing of the intimal surface with a stainless-steel rod having a diameter (25-30 gauge) equivalent to the lumen of the arteries (Lee, 1982). The successful removal of endothe lial cells was verified by lack of acetylcholine (3 ILM) induced relaxation (Furchgott and Zawadzki, 1980;Lee, 1980).…”

Section: Removal Of Endothelial Cellsmentioning

confidence: 99%

Endotoxin Decreases the Contractile Responses of the Porcine Basilar Artery to Vasoactive Substances

Ueno

Lee

1993

J Cereb Blood Flow Metab

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Summary: The effects of endotoxin (lipopolysaccharide; LPS) on the reactivity of isolated porcine basilar artery were examined using in vitro tissue bath techniques. The active muscle tone of the basilar arterial rings with or without endothelial cells induced by U46619 (1 fl-M) reached a plateau in 15 min, which was stable for the first hour and gradually decreased during the next 5 h. This time-dependent decrease in tone was significantly poten tiated in the presence of LPS (20 fl-g/ml). Gram-negative bacteria are pathogens commonly involved in infections of the CNS (Tunkel and Scheld, 1991) and in endotoxic shock, which is characterized by hypotension, vascular injury, and resistance to vasoconstrictors in various species (Miller et aI., 1987; Van Deventer et aI., 1988; Suf fredini et aI., 1989; Auguet et ai., 1991; Dal N ogare, 1991). A marked decrease in CBF resulting from hypotension following exposure to endotoxin has been reported (Miller et aI., 1987; N ishijima et ai., 1988). The exact mechanisms responsible for endo toxin-induced hypotension and the decrease in CBF remain unclear.Endotoxin (lipopolysaccharide; LPS), which is the toxic moiety of the gram-negative bacterial outer membrane, has been shown to induce vascu- 712U46619 and KCI were decreased following incubation with LPS (20 fl-g/ml) for 4 h. Similar hyporeactivity was observed in cold storage-denervated cerebral arteries in cubated with LPS for 4 h. This decrease in contractile responses in LPS-treated rings was reversed by 60 fl-M L-NNA and 1 fl-M dexamethasone. These results indicate that LPS treatment renders the porcine basilar arteries hyporesponsive to vasoconstrictors. Since effects of LPS were not modified by the presence of endothelial cells and perivascular neurons, the alteration in cerebral arterial reactivity may be due in part to an enhanced formation of nitric oxide from L-arginine in the vascular smooth mus cle cells.

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“…In our developed method, we believe that it is rather easy to make a preparation by means of a variety of diameter sizes of cannulae even in the relatively small vessels, and it is easy to insert a cannula from one side. Lee (1982) reported that ACh caused a vasodilatation in the isolated cerebral arteries with endothelium and a vasoconstriction without endothelium. Busse et al (1983) suggested that prostaglandin I2 might be involved in the hypoxic endothelium-induced dilatation.…”

Section: Monkey Basilar Arterymentioning

confidence: 99%

Vascular responsiveness of isolated, perfused basilar arteries in dogs and monkeys.

Chiba

Tsuji

1985

Tohoku J. Exp. Med.

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A new model of isolated basilar arterial preparation was developed in the dog and monkey. Isolated arteries were perfused at a constant flow rate with Krebs solution and suspended in a bath at 3TC. By inserting the steel cannula into the artery, the space between the luminal wall of the artery and the cannula was narrowed enough to obtain a suitable perfusion pressure during the perfusion. The resting perfusion pressure was maintained at a constant level of 50-100 mmHg. The drug solution was intraluminally administered, and the response was obtained as changes in the perfusion pressure. Responses to 6 vasoactive substances (norepinephrine, 5-HT, PGF2a, histamine, ATP and KCl) were compared between simian and canine basilar arteries. It was demonstrated that in simian arteries, PGF2a was the strongest but 5-HT and norepinephrine induced slight vasoconstriction to the same degree, and in canine basilar arteries, 5-HT induced the strongest constriction but norepinephrine did not produce significant vasoconstriction, and KC1 induced marked constriction to the same degree at extremely large doses in both species. It was demonstrated that the cannula inserting method is useful to observe the responses of isolated basilar arteries. cannula inserting method ; isolated basilar artery ; simian cerebral artery ; dog cerebral artery Recently, a new model of isolated and perfused vascular preparation was developed by Hongo and Chiba (1983) and modified by Tsuji and Chiba (1984). In their preparation, the resting perfusion pressure was maintained between 50-100 mm Hg which was close to physiological arterial blood pressure throughout the experiment. The drug administration was performed on the endothelial side of the artery. By using this method, vascular responses to vasoactive substances were studied in several parts of relatively large arteries isolated (Hongo and Chiba 1983;Tsuji and Chiba 1984; Chiba and Tsukada 1984a, b ; Ito and Chiba 1984a, b). In the present experiments, we made an attempt to apply this method to the isolated cerebral artery in the dog and monkey, by using a modified cannula inserting method, and to compare effects of 6 different vasoactive substances

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Cholinergic mechanism in the large cat cerebral artery.

Cited by 101 publications

References 24 publications

Endothelium-Dependent Dilation of Feline Cerebral Arteries: Role of Membrane Potential and Cyclic Nucleotides

Endothelium-Dependent Dilation of Feline Cerebral Arteries: Role of Membrane Potential and Cyclic Nucleotides

Endotoxin Decreases the Contractile Responses of the Porcine Basilar Artery to Vasoactive Substances

Vascular responsiveness of isolated, perfused basilar arteries in dogs and monkeys.

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