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Gema Ruiz-Hurtado

Researcher at Complutense University of Madrid

Publications -  135
Citations -  2479

Gema Ruiz-Hurtado is an academic researcher from Complutense University of Madrid. The author has contributed to research in topics: Albuminuria & Kidney disease. The author has an hindex of 24, co-authored 117 publications receiving 1802 citations. Previous affiliations of Gema Ruiz-Hurtado include University of Paris & University of Paris-Sud.

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Journal ArticleDOI

Relationship between Clinic and Ambulatory Blood-Pressure Measurements and Mortality

José R. Banegas, +9 more
- 18 Apr 2018 - 
TL;DR: Ambulatory blood‐pressure measurements were a stronger predictor of all‐cause and cardiovascular mortality than clinic blood‐ pressure measurements, and these relationships were consistent across subgroups of age, sex, and status with respect to obesity, diabetes, cardiovascular disease, and antihypertensive treatment.
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Lifestyle interventions for the prevention and treatment of hypertension

Pedro L. Valenzuela, +7 more
- 01 Apr 2021 - 
TL;DR: Strong evidence supports the benefits of regular physical activity and exercise for the prevention and management of hypertension, and the Dietary Approaches to Stop Hypertension diet is the most effective dietary approach to prevent hypertension and to reduce blood pressure in individuals with pre-hypertension or hypertension.
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TNF-α downregulates transient outward potassium current in rat ventricular myocytes through iNOS overexpression and oxidant species generation

María Fernández-Velasco, +4 more
- 02 Mar 2007 - 
TL;DR: TNF-alpha exposure, through iNOS induction and generation of oxidant species, promotes electrophysiological changes in rat ventricular myocytes, providing new insights into how cytokines modulate K(+) channels in the heart.
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Epac enhances excitation-transcription coupling in cardiac myocytes.

Laetitia Pereira, +15 more
- 01 Jan 2012 - 
TL;DR: These data provide the first evidence that the cAMP-binding protein Epac modulates cardiac nuclear Ca(2+) signaling by increasing [Ca(2+)](n) through PLC, IP(3)R and CaMKII activation, and initiates a prohypertrophic program via HDAC5 nuclear export and subsequent activation of the transcription factor MEF2.
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Calcium signaling in diabetic cardiomyocytes.

Laetitia Pereira, +5 more
- 01 Nov 2014 - 
TL;DR: A brief overview of Ca(2+) fluxes alteration reported on diabetes is given, and some new data on differential modulation of Ca (2+) handling alteration in males and females type 2 diabetic mice is provided to promote further research.