Dermal application of GSNO may be an effective treatment for promoting the local vasodilation in both healthy and diabetic states, without inducing protein nitration or alterations in blood pressure or heart rate.
SummaryTobacco smoking is associated with alterations in several factors considered to be important in the atherosclerotic process. Thirty chronic smokers were studied 2 weeks before and 2 weeks after complete tobacco withdrawal. Significant reductions in fibrinogen, haematocrit, plasma viscosity and whole blood viscosity as well as a significant increase in HDLcholesterol were observed. As these factors are important in both atherogenesis and thrombogenesis, these observations may give insight into tobacco-induced atherosclerotic disease and may be responsible for the more rapid reduction in the incidence of cardiovascular disease that is believed to occur after stopped smoking.
IntroductionTobaccosmoking is a well described independent risk factor for several cardiovascular events including heart attack and stroke. Epidemiological studies have shown the strong synergistic effects of smoking with other risk factors such as hypertension and hypercholesterolaemia on cardiovascular disease-". Recently, several studies have shown that smokers who abstain after myocardial infarction have a significant reduction in mortality over several years compared with those who continue to smokev". Atherosclerotic disease is a consequence of atherogenic and thrombogenic mechanismsv-P and smokers often have identifiable abnormalities in both atherogenic and thrombogenic factors 13 -20 • However, little is known about the timescale over which withdrawal of tobacco affects these atherogenic and thrombogenic factors. The aim of the present study was to assess,
Protease inhibitors are increasingly recognized as causing significant metabolic abnormalities including hypertriglyceridaemia, hypercholesterolaemia, insulin resistance, diabetes, and lipodystrophy. Considerable concern has been generated by recent reports of premature coronary artery disease occurring in HIV-1 infected patients on protease inhibitor containing regimens.
Low-density lipoproteins activate isolated human platelets. The mechanism of this activation is unknown, but may involve increased phosphoinositide turnover. We have examined the effect of low-density lipoproteins on intracellular calcium concentrations in platelets loaded with the photoprotein aequorin. The lipoproteins induced concentration-dependent increases in intracellular calcium, associated with shape change and aggregation.These responses could be partially inhibited by the removal of extracellular calcium and by pre-incubation with acetylsalicylic acid. They were also antagonised by agents which increase cellular concentrations of cyclic adenosine and guanosine monophosphates. It is not clear whether the platelet-lipoprotein interaction involves a 'classical' lipoprotein receptor.
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