ACE Inhibition, p300, Serum Nitrite and Lipid Peroxidation in Newly Diagnosed Hypertensives

Authors: Akhtar, Nasreen; Babbar, Rashmi; Agarwal, Sarita

Source: Vascular Disease Prevention, Volume 5, Number 2, May 2008 , pp. 145-149(5)

Publisher: Bentham Science Publishers

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Abstract:

Hypertension related decrements in cognitive functioning have been documented in those without clinical evidence of vascular disease and in individuals unaware of their hypertension. Impaired cognition in asymptomatic hypertensives may or may not be altered by antihypertensive therapy. We have examined the effect of three months of ramipril therapy on ambulatory blood pressure, cognitive function, lipid peroxidation and nitric oxide levels. Thirty male asymptomatic, newly diagnosed hypertensives were administered ramipril 5mg daily orally. Ambulatory blood pressure was recorded before and after three months of therapy. Cognitive function was assessed using event related potentials (N2 and P300 waveforms). Malondialdehyde was used as a marker of lipid peroxidation and serum nitrite levels were used as an index of nitric oxide levels. Along with the antihypertensive effect, three months of ramipril therapy improved the P300 but not the N2 latency. There was a positive correlation between the P300 latency and the systolic blood pressure parameters of the ambulatory blood pressure. The serum nitrite levels were increased and the malondialdehyde levels were decreased after therapy. Thus ramipril may improve some aspects of cognitive function by affecting the serum nitrite and lipid peroxidation pathways.

Keywords: Ramipril; cognition; P300; serum nitrite; hypertension

Document Type: Research article

DOI: http://dx.doi.org/10.2174/156727008784223972

Publication date: 2008-05-01

More about this publication?
  • Vascular Disease Prevention publishes reviews as well as original papers to update all those concerned with this topic at the clinical or scientific level. In addition to clinically relevant topics, we consider reviews and original papers dealing with the more scientific aspects of vascular disease prevention. This includes the evaluation of emerging vascular risk factors, research dealing with the pathogenesis of atherosclerosis and the investigation of new treatment options both at the clinical and scientific level (e.g. epidemiology, patient-based studies, experimental models, in vitro experiments or molecular research). Therefore, another function of Vascular Disease Prevention is to bridge the gap between clinical practice and ongoing laboratory-based research.

    In particular, we welcome critical reviews and comments on recent trials. This is a topic that requires regular updates because of the large number of trials published every year.

    Debates are encouraged in the correspondence section of this journal.
    The editorial structure of Vascular Disease Prevention is set up with the aim of dealing with the submitted material as rapidly as possible. Specialist editors will provide a more expert and rapid assessment unlike a more centralized editorial structure.
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