title: Role of arterial compliance in the physiopharmacological approach to human hypertension.
abstract: Arterial compliance in humans is generally measured by modeling analysis of pulse tracing or of pulse wave propagation in the arterial tree. It is decreased in hypertension in part because elevation of blood pressure stiffens the arteries by stretching the rigid collagen fibres of their walls. Using a modeling evaluation of the compliance-pressure relationship in large arteries, it is possible to correct compliance from the mechanical effect (passive effect) due to pressure elevation. This makes it possible to show that, at the same pressure as in normal controls, hypertensive patients maintain decreased arterial compliance. This finding suggests that functional and/or structural changes other than pressure-mediated stretching of arteries (active effect) contribute toward reducing arterial compliance. Thus, the response of compliance to antihypertensive drugs must be studied by differentiating between passive and active effects. The diameter and compliance-pressure relationship in arteries allow differentiation of a passive arterial effect due to the pressure-lowering action of the drug, and an active pharmacological effect calculated at the same pressure before and after drug administration. Four drugs--ketanserin, urapidil, nitrendipine, and nicardipine (acute administration)--are given as examples. No active or passive compliance changes are observed with urapidil and ketanserin. In contrast, an active increase in compliance is observed in isobaric conditions with calcium antagonists, together with large-artery dilation due to a potent smooth muscle-relaxing effect. This active increase in compliance is potentiated by a passive increase due to the pressure-lowering effect that reduces the mechanical stretch exerted by blood pressure on arterial bioelastomers. Finally, an optimum increase in arterial compliance is achieved by drugs that vasodilate large arteries by smooth muscle relaxation and concomitantly decrease blood pressure. This may be of importance because low compliance has adverse effects on the cardiovascular system by contributing to the pathogenesis of systolic hypertension and left ventricular hypertrophy. Loss of arterial compliance may also be an early marker of atherosclerosis.
authors.affiliation: Centre de Médecine Préventive Cardiovasculaire, Hôpital Broussais, Paris, France.
authors.forename: A C
authors.initials: AC
authors.lastname: Simon
authors.forename: J
authors.initials: J
authors.lastname: Levenson
authors.forename: N P
authors.initials: NP
authors.lastname: Chau
authors.forename: I
authors.initials: I
authors.lastname: Pithois-Merli
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology*; D001161:Arteriosclerosis / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D006332:Cardiomegaly / Q000503:physiopathology; D003198:Computer Simulation; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008955:Models, Cardiovascular; D009126:Muscle Relaxation; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D014664:Vasodilation
chemical_list: D000959:Antihypertensive Agents