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Silvia V. Conde

Researcher at Universidade Nova de Lisboa

Publications -  87
Citations -  1518

Silvia V. Conde is an academic researcher from Universidade Nova de Lisboa. The author has contributed to research in topics: Carotid body & Insulin resistance. The author has an hindex of 19, co-authored 70 publications receiving 1154 citations. Previous affiliations of Silvia V. Conde include University of Valladolid & Nova Southeastern University.

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Carotid body denervation prevents the development of insulin resistance and hypertension induced by hypercaloric diets

TL;DR: It is proposed that CB overstimulation is involved in the etiology of IR and HT, core metabolic and hemodynamic disturbances of highly prevalent diseases like the metabolic syndrome, type 2 diabetes, and obstructive sleep apnoea and may represent a novel therapeutic target in these diseases.
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Chronic caffeine intake decreases circulating catecholamines and prevents diet-induced insulin resistance and hypertension in rats

TL;DR: It is concluded that long-term caffeine intake prevented the development of insulin resistance and hypertension in HF and HSu models and that this effect was related to a decrease in circulating catecholamines.
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Hypoxia induces adenosine release from the rat carotid body.

TL;DR: It is concluded that CB chemoreceptor sensitivity could be related to its low threshold for the release of adenosine in response to hypoxia here quantified for the first time.
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Caffeine inhibition of rat carotid body chemoreceptors is mediated by A2A and A2B adenosine receptors.

TL;DR: It is concluded that endogenous adenosine, via presynaptic A1/A2B and postsynaptic A2A receptors, can exert excitatory effects on the overall output of the rat CB chemoreceptors.
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Hypoxic intensity: a determinant for the contribution of ATP and adenosine to the genesis of carotid body chemosensory activity

TL;DR: It is demonstrated that ATP and adenosine are key neurotransmitters involved in hypoxic CB chemotransduction, with a more relevant contribution ofadenosine during mild hypoxia, while vesicular ATP release constitutes the preferential origin of extracellularAdenosine in high-intensity hypoxIA.