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Assessment of arterial distensibility by automatic pulse wave velocity
measurement. Validation and clinical application studies. Hypertension,
1995. 26:485-490.
- Low molecular weight heparins : a guide to their optimum use in pregnancy.
Drugs, 2002. 62:463-477.
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Influence of L-NAME, acetylcholine
and adenosine on mean blood pressure, pulse pressure and pulse pressure amplification
in rats. Journal of Cardiovascular Pharmacology, 2003.
41:210-8.
- Heart rate and pulse pressure
amplification in hypertensive subjects. American Journal of Hypertension
2003. May;16(5):363-70.
- Gender influence on the relation
between heart rate and aortic stiffness. Journal of Hypertension
2003. 21:555-562
- Pulse pressure and arterial
stiffness in rats: comparison with humans. American Journal of
Physiology - Heart and Circulatory Physiology, 2003. 285(4):H1363-9.
Laurent P, Safar
M.E, Meaune S, Blacher J. Influence
of L-NAME, acetylcholine and adenosine on mean blood pressure, pulse
pressure and pulse pressure amplification in rats. J
Cardiovasc Pharmacol 2003. 41: 210-8
Abstract :
The blood pressure pattern in spontaneously hypertensive rats (SHRs)
involves three main characteristics: increase in mean blood pressure
(MBP); increase in thoracic aorta (proximal) and iliac (distal) pulse
pressure (PP); disappearance of the normal PP amplification between
the proximal and the distal arteries.
Whether pharmacologic agents may reduce MBP with different or even
opposite effects regarding PP and PP amplification has been poorly
investigated. In SHRs and Wistar-Kyoto (WKY) anesthetized rats, the
NO inhibitor l-nitro-arginine methyl ester (l-NAME) was infused at
the dosage of 1 mg/kg for 30 min. Before and after infusion, 7 microg/kg/min
acetylcholine (Ach) and 200 mg/kg adenosine (Ado) were perfused for
4 min. Proximal and distal intra-arterial BP was monitored throughout
the procedure. In both WKYs and SHRs, l-NAME increased proximal and
distal systolic (SBP), diastolic (DBP), and MBP but not PP. Before
l-NAME, SBP, DBP, and MBP were significantly reduced by Ado and Ach.
After l-NAME, such blood pressure reductions were abolished with Ach
but not Ado.
In both strains, the proximal and distal PP, when expressed in percent
reduction of MBP, were significantly higher under Ado than under Ach.
The Ado but not Ach changed PP amplification, causing a reduction in
WKYs and an increase in SHRs independent of l-NAME. Vasodilating agents
may reduce MBP with significantly different effects on PP.
The Ado alters PP amplification,
an effect not obtained with the nitric oxide endothelium-dependent
vasorelaxing agent Ach. Tail SBP measurements cannot predict such
dissociated changes.
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last modified on : 25 oct 2005 |
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