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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.
- 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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