OBJECTIVE In a previous study (J Hypertens 1993, 11:135-139) our group showed that in anaesthetized rats, although pulse pressure increased from the proximal (common carotid artery) to the distal (terminal aorta) portion of the aorta in normotensive Wistar-Kyoto (WKY) rats, such a pulse pressure gradient was not observed in spontaneously hypertensive rats (SHR) which had identical values of proximal and distal pulse pressure. The purpose of the present study was to show, in awake SHR, in comparison with awake WKY rats, that the lack of pulse pressure gradient might be functionally reversed after acute administration of vasodilating agents. METHODS The drugs (administered intra-arterially) were an angiotensin converting enzyme inhibitor (perindoprilat; 2 mg/kg), a calcium antagonist (nicardipine; 30 micrograms/kg), a peripheral vasodilator (hydralazine; 200 micrograms/kg) and placebo (isotonic saline). Blood pressure was evaluated invasively. RESULTS In untreated rats it was noticed that pulse pressure increased physiologically from the proximal to the distal part of the aorta for the same mean arterial pressure in WKY rats, whereas no pulse pressure gradient was observed in SHR. With acute drug administration, marginal modifications were observed in WKY rats, but mean arterial pressure was reduced significantly in SHR (hydralazine > perindoprilat > nicardipine). Proximal pulse pressure was decreased significantly with perindoprilat or nicardipine but was unchanged with hydralazine. Distal pulse pressure was unchanged, except for an increase in the nicardipine-treated group. Heart rate was increased significantly by hydralazine. CONCLUSIONS The results show that, although all of the drugs studied decreased mean arterial pressure in SHR, only the calcium antagonist nicardipine and the angiotensin converting enzyme inhibitor perindoprilat reduced proximal pulse pressure. This dissociation between the effects on mean arterial pressure and proximal and distal pulse pressure can be explained by the preferential action of the different antihypertensive agents on large arteries and wave reflections, producing different patterns in the pulsatile component of the heart load.