Whether the decrease in large-artery distensibility observed in hypertensive patients is due primarily to an increase in distending pressure or to hypertension-induced changes in structural properties has been much debated. We determined noninvasively the diameter-pressure curve of the common carotid artery over the systolic-diastolic range by continuously recording both the pulsatile changes in internal diameter (high-resolution echo-tracking system) and, simultaneously on the contralateral artery, the pressure waveform (high-fidelity applanation tonometry). We then derived the distensibility/pressure curve and compared arterial distensibility in 14 normotensive subjects and 15 age-and sex-matched hypertensive subjects at their respective mean arterial pressures (MAP) and at a common distending pressure: 100 mm Hg. Distensibility decreased as blood pressure increased, and distensibility at MAP was significantly lower in hypertensive than in normotensive subjects (7.8±0.7 versus 11.7±1.7 kPa"'-10" 3 , mean±SEM; P<.05). In hypertensive subjects,

This study used a precise noninvasive method in normotensive humans to determine the effects of sympathetic activation on arterial compliance. A recently developed, high-resolution echo-tracking system capable of measuring systolic/diastolic variations of arterial diameter was coupled to a Finapres system and used to calculate instantaneous systolic/diastolic pressure-diameter and compliance-pressure curves for a muscular medium-sized artery, the radial artery. Two standardized tests of sympathetic system activation, a cold pressor test (2 min) and a mental stress test (2 min of mental arithmetic), were performed at an interval of 8 days in random order in nine healthy volunteers [30 +/- 9 (SD) yr]. Radial arterial parameters were recorded every 30 s for 9 min, which included 2 min of cold pressor test or mental stress test. During both tests, radial arterial mean diameter did not change despite t he increase in mean arterial pressure (P < 0.001); stroke change in diameter decreased (P < 0.01), whereas pulse pressure increased (P < 0.01). Arterial compliance, calculated for the instantaneous level of mean arterial pressure, decreased significantly (P < 0.01). Compliance (C) calculated at 100 mmHg (C100) was arbitrarily chosen as a reference point for comparing compliance among the different periods of the test. C100 decreased significant (P < 0.05) during both tests (from 2.93 +/- 1.27 to 2.04 +/- 0.94 and from 3.29 +/- 1.73 to 2.63 +/- 1.55 mm2.mmHg-1.10(-3) during mental stress and the cold pressor test, respectively). These results indicate that sympathetic activation is able to decrease radial arterial compliance in healthy subjects. The reduction in arterial compliance probably resulted from complex interactions between changes in distending blood pressure and changes in radial arterial smooth muscle tone.

Hypertension is known to decrease arterial distensibility and systemic compliance. However, the arterial tree is not homogeneous, and it has been shown that the mediumsize radial artery does not behave like the proximal, elastic, large, common carotid artery. Indeed, radial artery compliance in hypertensive patients (HTs) has been shown to be paradoxically increased when compared with that in normotensive control subjects (NTs) at the same blood pressure level. To determine whether this increase was due to hypertension-related hypertrophy of the arterial wall, radial artery functional and geometric parameters from 22 NTs (mean±SD, 44±11 years) were compared with those from 25 age-and sex-matched never-treated essential HTs (48 ±12 years) by using a high-precision ultrasonic, echo-tracking system coupled to a photoplethysmograph (Finapres system),

The role of intravenously administered recombinant human transforming growth factor-fl (rhTGF-fl1) on the healing of incisional wounds in rats with impaired healing due to age or glucocorticoid administration was investigated. The administration of methylprednisolone to young adult rats decreased wound breaking strength to 50% of normal control.

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