摘要:

The possible modulation of adenosine-induced relaxation by endogenous prostaglandins was studied in isolated porcine, bovine and canine coronary arteries. Artery rings were mounted for isometric tension recording in organ bath filled with Krebs-Ringer-bicarbonate solution (37 °C). Increasing concentrations (10-6–10–4 M) of adenosine relaxed contractions induced by 35 mM KC1. The cyclo-oxygenase inhibitor indomethacin (5 × 10–6 M) significantly augmented the relaxations in response to adenosine in coronary arteries isolated from all three species. In the porcine coronary artery (which was most sensitive to exogenous adenosine) the mixed lipoxygenase/cyclo-oxygenase inhibitor phenidone augmented, while exogenous arachidonic acid (3 × 10–5 M) or a decrease in bath O2-level from 95 to 20% depressed adenosine-induced relaxations. Indomethacin completely prevented the inhibitory effect of decreasing bath O2, but only partially antagonized the suppression caused by arachidonic acid. The data demonstrate that arachidonic acid and its cyclo-oxygenase metabolites modulate (depress) adenosine responsiveness in isolated coronar

ISSN:1018-1172    

DOI:10.1159/000158603

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The intracellular sodium content, unidirectional radiosodium efflux, and unidirectional radiosodium influx were studied in whole rat tail arteries and in rat tail artery strips. The tissues were allowed to come to a steady condition while immersed in physiological salt solution at 37 °C, then were subjected to a small transient mechanical disturbance or to a larger disturbance of 5–20 min duration. The small transient disturbance caused a large transient increase in the sodium content of the cells, in the radiosodium influx, and in the radiosodium efflux. The sustained disturbance caused a sustained increase in sodium content. All effects of a mechanical disturbance were prevented by blockade of α-adrenoreceptors with 1 µM phenoxybenzamine. Pre-treatment of the rat with reserpine was as effectice as acute treatment of the artery with phenoxybenzamine in preventing the transient increase in the radiosodium efflux. It is hypothesized that mechanical disturbances cause norepinephrine release from terminal adrenergic plexuses in the artery wall, and that the binding of norepinephrine to α-adrenoreceptors in the smooth muscle cells causes an increase in the sodium permeability of the cell mem

ISSN:1018-1172    

DOI:10.1159/000158604

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effects of 5’-methylthioadenosine (MTA) and adenosine analogues on isolated rabbit thoracic aorta strips were studied in vitro. High concentrations (500–1,000 µM) of adenosine analogues produced dose-dependent relaxation in isolated rabbit thoracic aorta strips. The relative potencies of relaxant effect were MTA& > N6-phenylisopropyladenosine& > 2-chloroadenosine on a molar basis. MTA (50–1,000 µM) suppressed the contraction induced by norepinephrine in isolated rabbit thoracic aorta strips in a concentration-dependent manner. Nucleoside uptake inhibitor dipyridamole did not impair the MTA actions. Pretreatment of the aorta strips with theophylline, an adenosine receptor antagonist, blocked the actions of MTA. MTA showed a relaxant effect in KCl-contracted aorta suggesting that MTA did not affect the metabolism or reuptake of norepinephrine. The present experiments suggest that MTA has a pharmacological action on the arterial smooth muscle cells mediated through adenosine re

ISSN:1018-1172    

DOI:10.1159/000158606

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effects of α-adrenergic stimulation and high K+-induced membrane depolarization on 45Ca2+ uptake and tension generation in the rabbit aorta were investigated. Tension and unidirectional 45Ca2+ uptake were increased by both stimulants. Moreover, this ‘steady-state’ uptake remained elevated for as long as the stimulants were present. When tissues were preincu-bated in 45Ca2+-containing PSS prior to the Ne or high K+ challenge the resulting Ca2+ uptake showed an ‘initial burst’ of uptake which was not observed in the ‘steady-state’ experiments. The magnitude of the ‘initial burst’ increased with time displaying a t½ for exchange of 1.25 min for both high K+ and Ne, suggesting that this Ca2+ source is shared by both stimulants. The ‘initial burst’ became Ca2+ saturated when [Ca2+]o was between 0.5 and 1.5 mM, was enhanced by 45Ca2+ preincubation in a solution of lowered ionic strength and was inhibited (∼70%) by D600 (5 × 10–6 M). In contrast, the ‘steady-state’ uptake was linearly dependent on [Ca2+]o up to 6.4 mM, was 90% inhibited by 5 × 10–6 M D600 and was unaffected by lowered ionic strength. It is concluded that the properties displayed by the Ca2+ source responsible for the ‘initial burst’ and ‘steady-state’ uptake suggest that they are of distinct origin; the ‘initial burst’ being derived from a bound extracellular Ca2+ pool and the ‘steady-state’ uptake resulting from the uptake of free Ca<

ISSN:1018-1172    

DOI:10.1159/000158607

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158608

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158609

出版商:S. Karger AG    

年代:1985

数据来源: Karger

ISSN:1018-1172    

DOI:10.1159/000158610

出版商:S. Karger AG    

年代:1985

数据来源: Karger