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Biomedical subjects

R Wadsworth

Publications and source records attributed to R Wadsworth.

At least 55 records · Page 3Linked to original sources
PubMed1994

Effect of hypoxia on contraction and 45Ca2+ uptake induced by the thromboxane mimetic U46619 in sheep coronary artery.

The thromboxane mimetic U46619 (11 alpha,9 alpha-epoxymethano PGH2) increased 45Ca2+ uptake in sheep coronary artery rings. A larger increase occurred in endothelium-denuded than in endothelium-inact rings (increase in 45Ca2+ uptake: endothelium intact = 9.6 +/- 3.8, endothelium-denuded = 33.2 +/- 8.1 nmol g-1), in agreement with the increase in U46619 contraction produced by endothelium denudation. Hypoxia (PO2 = 4 mm Hg) inhibited both the U46619 contraction (at the U46619 EC50, contraction under oxygenated conditions = 158 +/- 35, under hypoxic conditions = 105 +/- 40 g cm-2) and the U46619-stimulated 45Ca2+ uptake. It is concluded that inhibition, by hypoxia, of the U46619 contractile effect on sheep coronary artery rings may be in part due to inhibition of U46619-stimulated 45Ca2+ uptake.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Regulation by hypoxia of endothelin-1-stimulated phospholipase D activity in sheep pulmonary artery cultured smooth muscle cells.

1. The aim of the study was to characterize the effects of hypoxia on agonist-stimulated phospholipase D (PLD) and phospholipase C activity of sheep pulmonary artery cultured smooth muscle cells. 2. Endothelin-1 (ET-1), 5-hydroxytryptamine (5-HT) and the protein kinase C (PKC) activator tetradecanoylphorbol acetate (TPA), stimulated a time- and concentration-dependent increase in [3H]-phosphatidylbutanol accumulation. This was abolished by pretreatment of the cells with the PKC inhibitor, Ro-318220, suggesting that agonist-stimulated phospholipase D activity is dependent upon the activation of PKC. 3. Hypoxia (PO2 20 mmHg for 30 min) stimulated basal [3H]-phosphatidylbutanol accumulation by approximately 2 fold and this activity was abolished by preincubation of the cells with 10 microM Ro-318220. 4. In cells preincubated in low O2 containing medium for 30 min, the subsequent agonist-stimulated accumulation of [3H]-phosphatidylbutanol was reduced. However, the decrease in stimulation was greater for ET-1 and 5-HT than for TPA. 5. ET-1 and TPA stimulated a time-dependent increase in protein kinase C- mediated psuedosubstrate phosphorylation. Following preincubation for 30 min in low O2 containing media, basal pseudosubstrate phosphorylation increased whilst the fold stimulation by TPA and ET-1 decreased. 6. In cells preincubated in low O2 containing medium, ET-1-stimulated [3H]-inositol phosphate accumulation was reduced by approximately 30-40%. This reduction was reversed by preincubation of the cells with Ro-318220. 7. These results suggest a role for PKC in the effects of hypoxia on PLD in pulmonary artery smooth muscle cells.

Amino Acid Sequence↗
PubMed1994

Phosphoinositide metabolism and aging in aorta from SHR and WKY rats: effects of endothelin-1 and noradrenaline.

Inositol phosphate formation in aortic rings from SHR and WKY rats of different ages (6, 14, and 40 weeks) was examined. Both basal and agonist (noradrenaline and endothelin-1) stimulated levels of inositol phosphates were studied. No differences in basal levels of inositol phosphate formation were observed between SHR and WKY nor were differences in agonist stimulated levels found in 6 week old animals. However, at 14 and 40 weeks both noradrenaline and endothelin-1 stimulated levels were reduced in SHR compared to WKY. Both endothelin and noradrenaline stimulated inositol phosphate formation decreased with age in SHR. In WKY there was a decrease in endothelin but not noradrenaline stimulated levels with age. Age related decreases were consistently greater in SHR than WKY. Thus, both age and rat strain modulated agonist stimulated inositol phosphate formation.

Aging↗