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Biomedical subjects

S Moncada

Publications and source records attributed to S Moncada.

531 records · Page 30Linked to original sources
PubMedDate not supplied

Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factor.

Endothelium-derived vascular relaxing factor (EDRF) is a humoral agent that is released by vascular endothelium and mediates vasodilator responses induced by various substances including acetylcholine and bradykinin. EDRF is very unstable, with a half-life of between 6 and 50 s, and is clearly distinguishable from prostacyclin. The chemical structure of EDRF is unknown but it has been suggested that it is either a hydroperoxy- or free radical-derivative of arachidonic acid or an unstable aldehyde, ketone or lactone. We have examined the role of superoxide anion (O-2) in the inactivation of EDRF released from vascular endothelial cells cultured on microcarrier beads and bioassayed using a cascade of superfused aortic smooth muscle strips. With this system, we have now demonstrated that EDRF is protected from breakdown by superoxide dismutase (SOD) and Cu2+, but not by catalase, and is inactivated by Fe2+. These findings indicate that O-2 contributes significantly to the instability of EDRF.

Animals↗
PubMedDate not supplied

Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor.

Endothelium-derived relaxing factor (EDRF) is a labile humoral agent which mediates the action of some vasodilators. Nitrovasodilators, which may act by releasing nitric oxide (NO), mimic the effect of EDRF and it has recently been suggested by Furchgott that EDRF may be NO. We have examined this suggestion by studying the release of EDRF and NO from endothelial cells in culture. No was determined as the chemiluminescent product of its reaction with ozone. The biological activity of EDRF and of NO was measured by bioassay. The relaxation of the bioassay tissues induced by EDRF was indistinguishable from that induced by NO. Both substances were equally unstable. Bradykinin caused concentration-dependent release of NO from the cells in amounts sufficient to account for the biological activity of EDRF. The relaxations induced by EDRF and NO were inhibited by haemoglobin and enhanced by superoxide dismutase to a similar degree. Thus NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator. We suggest that EDRF and NO are identical.

Animals↗
PubMedDate not supplied

Nightly peritoneal dialysis (NPD): six years of experience.

From the 84 patients who initiated PD from 1990 to 1996, 15 did NPD, 3 changed from CAPD to NPD. In general the reason for choosing NPD were: 10/18 clinical motivations, 8/18 social and economical. From our experience and based on nurses' opinions, a patient who chooses NPD is a balanced person with good family support, accepts the treatment and benefits from this modality. On the other hand patients who withdraw from NPD for clinical reasons have no strong motivations and have different problems. Working to improve patient adaptation and improving patient treatment modality selection should be a must.

Adult↗
PubMedDate not supplied

[Nitric oxide: from endogenous vasodilator to biologic mediator].

This paper review the actual knowledges about the physiological role of nitric oxide, sintetized from amino acid L-arginine. The nitric oxide sintetized in the vascular endothelium has a fundamental role in vascular tone, blood flow and arterial pressure control, acting stimulating guanylate cyclase on vascular smooth muscle. Nitric oxide could be considered the endogenous nitrovasodilator. Its action on the cardiovascular system are imitated by nitroglycerine, sodium nitroprusside and related compounds. Probably the disturbance in the synthesis or release of nitric oxide may be involved in the pathophysiology of hypertension, vasospasm and atherosclerosis. Recently has been shown that nitric oxide synthesis from L-arginine also occurs in other different cells like macrophages, central nervous system, liver, neutrophils, adrenal glands, playing different biological effects. Changes in nitric oxide synthesis or action in those systems, could be related to different pathological disorders as inflammation, atherosclerosis and cancer. The found of a substance as simple as nitric oxide, let suppose that we are in the presence of a biological mediator with a very early evolutionary origin, probably widespread in all the animal kingdom, and which represents the universal transduction system for activation of the soluble guanylate cyclase enzyme.

Epoprostenol↗
PubMedDate not supplied

Nitric oxide--from mediator to medicines.

Nitric oxide is involved in a wide range of physiological processes in humans and in animals. It controls vascular tone, acts as a neurotransmitter and neuromodulator in the central and peripheral nervous systems and influences the activity of the immune system. Substances that selectively enhance or inhibit its synthesis or removal and modify its effects, are likely to yield interesting therapeutic agents.

Amino Acid Oxidoreductases↗