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1995
DOI: 10.1097/00004872-199502000-00012
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Proximal and distal pulse pressure after acute antihypertensive vasodilating drugs in Wistar-Kyoto and spontaneously hypertensive rats

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Cited by 16 publications
(12 citation statements)
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“…In healthy humans 25,26 or rodents, 27 owing to the mechanical properties of the vasculature along the arterial tree, SBP is higher at peripheral sites, the brachial or tail artery compared with a central site such as the thoracic aorta. Direct SBP measurements in cats were performed in the distal abdominal aorta, whereas HDO measurements were performed at the level of the coccygeal artery.…”
Section: Discussionmentioning
confidence: 99%
“…In healthy humans 25,26 or rodents, 27 owing to the mechanical properties of the vasculature along the arterial tree, SBP is higher at peripheral sites, the brachial or tail artery compared with a central site such as the thoracic aorta. Direct SBP measurements in cats were performed in the distal abdominal aorta, whereas HDO measurements were performed at the level of the coccygeal artery.…”
Section: Discussionmentioning
confidence: 99%
“…Selective and nonselective aldosterone blockers attenuate cfPWV and AIx (185;186) in select patient groups by increasing nitric oxide (NO) bioactivity and improving endothelial vasodilator dysfunction (187). Vasodilating drugs, such as hydralazine and dipyridamole, primarily increase arteriolar caliber and therefore decrease peripheral resistance and mean arterial pressure via their action on arteriolar smooth-muscle cells with little effect on aortic wave reflections (188). Nitrates primarily relax smooth muscle cells in large conduit muscular arteries and therefore decrease arterial stiffness, aortic wave reflection amplitude and duration and reduce central systolic and PP with little change in brachial cuff systolic and PP (189191).…”
Section: Section 4: Arterial Stiffness Wave Reflections and LV Aftermentioning
confidence: 99%
“…27 In genetically hypertensive rats that have equal central and peripheral pressures, giving ACE inhibitors or calcium-channel blockers restores the pulse pressure gradient but hydralazine does not. 18 However, there is evidence that ACE inhibitors, by causing an equal decrease in brachial and aortic PP may not actually increase PP amplification, despite reducing wave reflection in patients with essential hypertension 14 although some studies have shown a restoration of pulse pressure gradient in patients with end-stage renal disease. 13 In the present study, we have observed that valsartan when added to an ACE inhibitor, preferentially decreased central pulse pressure, favourably modifying pulse pressure amplification, restoring it to normal values.…”
Section: Pulse Pressure Amplificationmentioning
confidence: 99%
“…[10][11][12][13][14][15] Attention is being directed at drugs that reduce early AWR and arterial stiffness, as not all antihypertensives have a beneficial effect on arterial stiffness and AWR despite the same level of blood pressure reduction. 16,17 Angiotensin-converting enzyme (ACE) inhibitors, in particular, have been shown to delay AWR and increase the pulse pressure gradient between the central and peripheral circulation in both animal 18 and human studies. 13 We hypothesised that combined angiotensin II (ATII) antagonism, by adding an AT 1 receptor antagonist to an ACE inhibitor, might provide a more complete block of the renin-angiotensin system.…”
Section: Introductionmentioning
confidence: 99%