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Luis M. Ruilope

Researcher at European University of Madrid

Publications -  891
Citations -  109166

Luis M. Ruilope is an academic researcher from European University of Madrid. The author has contributed to research in topics: Blood pressure & Renal function. The author has an hindex of 94, co-authored 841 publications receiving 97778 citations. Previous affiliations of Luis M. Ruilope include Lund University & Mayo Clinic.

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Obesity and hypertension in Latin America: Current perspectives.

TL;DR: The current status for the prevalence and consequences of obesity and hypertension in Latin America is summarized, with the aim of initiating a call to action to all stakeholders for greater implementation of primary prevention strategies, particularly in the young.
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Comparison of Agents That Affect Aldosterone Action

TL;DR: The first aldosterone blocker, spironolactone, initially was used as a diuretic but was accompanied by a significant amount of side effects that necessitated the withdrawal of the drug in a relevant number of patients as discussed by the authors.
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Hypertension in Latin America: Current perspectives on trends and characteristics.

TL;DR: The epidemiological and management trends and patterns in hypertension that may be specific or more common to Latin-American populations - what the authors term 'Latin American characteristics' of hypertension - are discussed via a review of the recent literature.
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Effects of long-term treatment with indomethacin on renal function.

TL;DR: Prolonged treatment with indomethacin induced chronic hyporeninism and hypoaldosteronism, and some of the symptoms of a syndrome of hypoprostaglandinism, such as decreased plasma renin activity, plasma aldosterone, and urinary prostaglandsin E2 in association with increases in plasma potassium levels and diastolic pressure.
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Effects of antihypertensive therapy on factors mediating endothelium-dependent relaxation in rats treated chronically with L-NAME.

TL;DR: The administration of L-NAME in Sprague-Dawley rats increased the production of endothelium-derived hyperpolarizing factor as a compensatory mechanism to maintain acetylcholine-induced relaxation.