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R G Bogle

Publications and source records attributed to R G Bogle.

24 records · Page 2Linked to original sources
PubMed1991

Bradykinin and ATP stimulate L-arginine uptake and nitric oxide release in vascular endothelial cells.

The effects of bradykinin and ATP on L-arginine transport and nitric oxide (NO) production were studied in porcine aortic endothelial cells cultured and perfused on microcarriers and deprived of L-arginine for 24 h. Stimulation of cells with bradykinin (100 nM) or ATP (100 microM) resulted in a rapid increase in L-arginine uptake and NO release. In the presence of nitro-L-arginine (100 microM), an inhibitor of NO synthase, the stimulatory effect of bradykinin on L-arginine uptake was partially inhibited while NO release was completely abolished. Nitro-L-arginine alone was not an inhibitor of basal L-arginine transport, suggesting that its inhibitory action was not directly on the L-arginine transporter but a result of the inhibition of NO generation. These data indicate that during agonist-stimulated NO production there is a concomitant increase in the transport of L-arginine into endothelial cells providing a mechanism for the continual generation of NO.

Adenosine Triphosphate↗
PubMed1991

Spiking of intracellular calcium ion concentration in single cultured pig aortic endothelial cells stimulated with ATP or bradykinin.

Single pig aortic endothelial cells in culture loaded with the Ca(2+)-sensitive fluorescent dye Indo-1 were stimulated with ATP (0.1-100 microM) or bradykinin (0.1-5.0 nM). Spiking or oscillations of [Ca2+]i were seen in approx. 50% of cells stimulated with either agonist. Non-spiking or transient responses in which [Ca2+]i returned to pre-stimulation levels rapidly 9120-250 s), or sustained responses in which [Ca2+]i remained elevated for many minutes, were seen in a further 20% of cells in each case, stimulated with either agonist. There was a marked variation between individual cells in the latency, magnitude, frequency and overall pattern of oscillations induced by ATP and bradykinin, although the patterns of response to bradykinin were less variable. In cells where repetitive spikes were seen, a relation between concentration of ATP and the latency of the response and the frequency of spiking was evident. Effects of removal of extracellular Ca2+, elevation of extracellular K+ concentration (35 or 70 mM) or exposure to phorbol 12,13-dibutyrate or 1,2-dioctanoyl-sn-glycerol were tested on the spiking Ca2+ responses. Each of these procedures reversibly slowed or prevented Ca2+ spiking evoked by ATP or bradykinin. In contrast, the inactive phorbol ester 4 alpha-phorbol didecanoate had no effect on Ca2+ spiking evoked by these hormones. Our results thus indicate that the responses of single cells to ATP or bradykinin exhibit marked heterogeneity, and suggest that secretory events driven by extracellular Ca2+ may be regulated by repetitive spikes or oscillations of Ca2+.

Adenosine Triphosphate↗
PubMed1990

Evidence that central 5-HT1A-receptors play a role in the von Bezold-Jarisch reflex in the rat.

1. The effects of intracisternal (i.c.) application of putative 5-hydroxytryptamine (5-HT)1A antagonists on the reflex bradycardia evoked by injection of phenylbiguanide (i.v.) were investigated in anaesthetized, atenolol-pretreated rats. 2. Intracisternal application of spiperone (100 micrograms kg-1) reversibly attenuated the reflex bradycardia whilst the same dose given i.v. had no effect. The bradycardia was also attenuated by i.c. methiothepin (200 micrograms kg-1), (+/-)-pindolol (100 micrograms kg-1) and buspirone (200 micrograms kg-1) but was not attenuated by antagonists selective for alpha 1-adrenoceptors (alfuzosin; 100 micrograms kg-1), 5-HT2-receptors (BW 501C67; 100 micrograms kg-1) or dopamine D2-receptors ((-)-sulpiride; 100 micrograms kg-1) given i.c. 3. It is concluded that the 5-HT1A-receptor antagonist action of intracisternally applied spiperone, methiothepin, (+/-)-pindolol and buspirone is responsible for the ability of these drugs to attenuate reversibly the excitation of cardiac vagal motoneurones caused by activation of the von Bezold-Jarisch reflex.

Anesthesia↗