Journal of hypertension
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Journal of hypertension · Nov 1999
Randomized Controlled Trial Clinical TrialPROGRESS - Perindopril Protection Against Recurrent Stroke Study: characteristics of the study population at baseline. Progress Management Committee.
The primary aim of the Perindopril Protection Against Recurrent Stroke Study (PROGRESS) is to determine the effects of a long-term angiotensin converting enzyme (ACE)-inhibitor-based blood-pressure-lowering regimen on the risk of stroke among patients with a history of stroke or transient ischaemic attack (TIA). Secondary aims include investigation of the effects of treatment on total cardiovascular events, dementia and disability. ⋯ The successful completion of recruitment, together with current indicators of statistical power, suggest that PROGRESS should achieve its primary aim on schedule.
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Journal of hypertension · Aug 1999
Randomized Controlled Trial Clinical TrialEvaluation of the potential interaction between NaCl and prostaglandin inhibition in elderly individuals with isolated systolic hypertension.
To evaluate whether prostaglandin inhibition with the non-steroidal anti-inflammatory drug (NSAID), indomethacin (I) interacts synergistically with different doses of salt (NaCl) in elevating systolic blood pressure (SBP). ⋯ Chronic high salt diet elevated blood pressure more than I in the total cohort of elderly individuals. No interaction was demonstrated and their effects were additive. In the ISH group, chronic high salt diet significantly increased SBP and DBP while I failed to alter blood pressure. In the normotensive group, I, but not salt, elevated SBP. Patients with ISH are sensitive to the pressor effect of NaCl but resistant to the pressor effect of prostaglandin inhibition in contrast to elderly normotensive control individuals where the reverse was found.
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Journal of hypertension · Jun 1999
Comparative StudyHyper-responsiveness to angiotensin II is related to cardiac structural adaptation in hypertensive subjects.
Angiotensin II has been found to be a growth stimulating factor for myocardial cells. In humans, angiotensin II infusion causes vasoconstriction in systemic and renal vasculature and leads to aldosterone secretion. Our hypothesis was that hyper-responsiveness to angiotensin II is related to left ventricular mass in human essential hypertension. ⋯ Hyper-responsiveness to angiotensin II is related to an increased left ventricular mass in hypertensive subjects independent of blood pressure.
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In human subjects, the assessment of renal function and of its changes by interventions is limited to the measurement of glomerular filtration rate (GFR), renal blood flow and the estimation of proteinuria. In humans, GFR can be determined exactly by measuring the clearance of an ideal filtration marker, such as inulin. The classic method of measuring inulin clearance in humans includes constant intravenous infusion of the compound and timed collections of urine. ⋯ Quantitative measurements of marker proteins can be used to estimate the extent and the site of damage in the nephron. These measurements may be used to estimate the progression of renal disease and the response to therapeutic interventions. Of particular interest is the degree of albuminuria which indicates nephropathy in diabetic patients and end-organ damage in patients with hypertension.
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Journal of hypertension · Feb 1999
Comparative StudyEffects of antihypertensive therapy on factors mediating endothelium-dependent relaxation in rats treated chronically with L-NAME.
To evaluate the relative participation of endothelium-derived factors mediating relaxation in response to acetylcholine in isolated mesenteric vascular beds from rats treated chronically with N(G)-nitro-L-arginine methylester (L-NAME); and to compare the consequences of prolonged treatment with either an angiotensin converting enzyme inhibitor or a calcium channel blocker on the components of acetylcholine-induced relaxation in this vascular preparation. ⋯ 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. Antihypertensive therapy with either quinapril or diltiazem produced a selective redistribution of the endothelial factors mediating acetylcholine-induced relaxation.