Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of cooling on the isometric response of rabbit isolated central ear (cutaneous) and femoral (non-cutaneous) arteries to histamine were determined at 37 degrees C and 24 degrees C (cooling). Under resting tension, both types of arteries contracted to histamine (10(-7)-10(-3) M), and the sensitivity of ear arteries, but not of femoral arteries was lower at 24 than at 37 degrees C. Chlorpheniramine (10(-7) M) blocked the contraction of both types of arteries to histamine at both temperatures. In ear arteries, endothelium removal or treatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-5) M) did not affect the contraction to histamine at 37 degrees C, but it reversed the decreased contraction at 24 degrees C. In femoral arteries, endothelium removal or L-NAME (10(-5) M) did not affect the response to histamine at 37 and 24 degrees C. Ear and femoral arteries precontracted with endothelin-1 (10(-8)-10(-7) M) and pretreated with chlorpheniramine (10(-5) M) relaxed to histamine (10(-7)-10(-4) M), and the sensitivity of this relaxation in ear arteries, but not in femoral arteries, increased at 24 degrees C. The relaxation of ear and femoral arteries to histamine was not modified by endothelium removal, L-NAME (10(-5) M) or meclofenamate (10(-5) M), but it was blocked by cimetidine (10(-6) M) at 37 degrees C and 24 degrees C. These results suggest: (1) ear and femoral arteries have contracting H1 and relaxing H2 receptors, probably located on smooth musculature, and (2) cooling reduces the contraction and increases the relaxation of cutaneous arteries to histamine: the reduction of this contraction could be caused by an augmented availability of endothelial nitric oxide, and the increment of this relaxation could be caused by an augmented sensitivity of H2 receptors of smooth musculature induced by cooling. These features do not seem to occur in deep vessels.
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PMID:Cooling effects on the histaminergic response of rabbit ear and femoral arteries: role of the endothelium. 797 17

Superoxide plays a role in blood pressure regulation in certain vascular diseases, however, its involvement in regulating basal blood pressure is uncertain. Vascular superoxide concentrations are limited by extracellular superoxide dismutase (EC-SOD), which is highly expressed in the vasculature of most animal species. Metalloporphyrins are low molecular weight, synthetic, redox-active, catalytic antioxidants that act as SOD mimetics. We evaluated the effects of metalloporphyrins on blood pressure in different animal species. The metalloporphyrin AEOL10113 (5-10 micro /kg iv), but not native or polyethylene glycol-CuZnSOD, caused a dose-dependent reduction in blood pressure in anesthetized rats. AEOL10113 had no effect on blood pressure in mice (wild-type or EC-SOD knockouts), guinea pigs, dogs, or baboons at doses up to 5 mg/kg iv Structure-activity studies indicated that metalloporphyrins with high SOD activity were more effective in lowering rat blood pressure than low-activity analogs. The blood pressure effect of AEOL10113 was not attributable to the release of manganese, nor was it affected by inhibitors of nitric oxide synthase (L-NAME) and guanylate cyclase (ODQ, 8-bromo-cGMP, and methylene blue) or nitric oxide scavengers (HbAo). Chlorpheniramine attenuated the effect, suggesting that the blood pressure response in rats is related to histamine release rather than the protection of nitric oxide.
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PMID:Hemodynamic effects of metalloporphyrin catalytic antioxidants: structure-activity relationships and species specificity. 1248 34