Ageing and disease states associated with an increase in cardiovascular events alter the physical characteristics of blood vessel walls and impair the pulsatile function of arteries. An accumulating body of evidence indicates that impaired pulsatile function of arteries provides important prognostic and therapeutic information beyond that provided by traditional blood pressure measurements. A variety of techniques are currently employed to evaluate the mechanical properties of arteries. All techniques have theoretical, technical and practical limitations that impact on their widespread application in the clinical setting and use as measurement tools to improve cardiovascular risk stratification. A detailed discussion of these issues forms the basis of this review.

Traditionally, nitric oxide-mediated alteration in blood vessel tone has been inferred from changes in flow in response to physical and pharmacological interventions using plethysmographic or ultrasonic techniques. We hypothesized that alteration in pulsatile arterial function may represent a more sensitive measure to detect and monitor nitric oxide-mediated modulation of arterial smooth muscle tone. Healthy male volunteers ( n = 15) had radial artery pressure pulse waveforms recorded using a calibrated tonometer device. A computer-based assessment of the diastolic pressure decay was employed to quantify changes in arterial waveform morphology in terms of altered pulsatile (arterial compliance) and steady-state (peripheral resistance) haemodynamics. N G -nitro- L -arginine methyl ester ( L -NAME), a stereospecific inhibitor of nitric oxide synthesis, was infused intravenously in incrementally increasing doses of 0.25, 0.5 and 0.75 mg/kg for 8 min each. Subjects then received either L -arginine or D -arginine (200 mg/kg over 15 min) intravenously in a blinded fashion. On a separate day, subjects had radial artery pressure pulse waveforms recorded before and after the sublingual administration of glyceryl trinitrate, an exogenous donor of nitric oxide. Cardiac output and heart rate decreased and mean arterial blood pressure increased significantly ( P < 0.01 for all) in response to the incremental intravenous infusion of L -NAME. Small artery compliance decreased, whereas systemic vascular resistance increased in response to nitric oxide synthesis inhibition ( P < 0.01 for both). The intravenous infusion of L -arginine restored the pulsatile and steady-state haemodynamic parameters to pre-treatment values, whereas D -arginine had no effect. Sublingual glyceryl trinitrate decreased systemic vascular resistance by 11%, whereas large artery- and small artery-compliance increased by 25% and 44% respectively. Pressure pulse contour analysis represents a sensitive and convenient technique capable of tracking changes in the pulsatile function of arteries accompanying nitric oxide-mediated alteration in arterial smooth muscle tone.