Affirmative action.
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Biomedical subjects
Publications and source records attributed to W Sunman.
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1. Small arteries were isolated from either rat mesentery or human subcutaneous fat, and mounted in a myograph for the measurement of isometric force. 2. Superoxide dismutase, either in the presence or absence of catalase, relaxed noradrenaline-induced tone. This effect was abolished by removal of the endothelium or incubation with an inhibitor of NO synthase, N-omega-nitro-L-arginine methyl ester. Catalase alone had a negligible effect on noradrenaline-induced tone. 3. Captopril, an angiotensin-converting enzyme inhibitor and putative free-radical scavenger, did not relax pre-contracted isolated vessels. N-Acetylcysteine caused an endothelium-independent relaxation of rat vessels. Similar effects were observed in human vessels. 4. Acetylcholine induced a concentration-dependent relaxation of isolated resistance arteries, which was inhibited by removal of the endothelium or N-omega-nitro-L-arginine methyl ester, but unaffected by indomethacin. Preincubation with captopril, N-acetylcysteine or catalase alone did not alter the acetylcholine concentration-response relationship, but superoxide dismutase in combination with catalase enhanced responses to acetylcholine, causing a six-fold increase in potency. 5. Superoxide dismutase causes endothelium-dependent relaxation of resistance arteries and potentiates responses to acetylcholine. This action is probably due to the ability of the enzyme to scavenge superoxide anions which inhibit endothelium-dependent relaxation. 6. N-Acetylcysteine causes an endothelium-independent relaxation of resistance arteries which is probably unrelated to the putative ability of this compound to scavenge superoxide radicals and may reflect a direct action on vascular smooth muscle.
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Small resistance arteries were isolated from human subcutaneous fat and omentum and studied using a myograph. Endothelin-1 induced a concentration-dependent contraction in both type of arteries. In subcutaneous arteries preincubation with calcium antagonists partially inhibited responses to endothelin-1. The effectiveness of the calcium antagonists was nisoldipine > nimodipine > verapamil = flunarizine > diltiazem. In omental arteries nimodipine and diltiazem had no significant effect on endothelin-1-induced contraction and removal of extracellular calcium also had little effect on responses to endothelin-1. The role of influx of extracellular calcium through voltage operated calcium channels in endothelin-1-induced contraction appear to differ between subcutaneous and omental resistance arteries.
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We present a case in which a patient, having already sustained an episode of malignant hypertension, was subsequently found to have an underlying Conn's adenoma. Ablation of the adenoma improved control of her hypertension. When a second adenoma developed in her remaining adrenal gland, control of her hypertension deteriorated.