In the anesthetized rat, acute increases in heart rate are accompanied by a
reduction in arterial distensibility, which is a significant phenomenon in
elastic-type vessels such as the common carotid but much less evident in m
uscle-type vessels such as the femoral artery. Because the sympathetic nerv
ous system importantly reduces arterial distensibility, the present study a
imed to determine whether sympathetic influences (1) are involved in the he
art rate-dependent changes in arterial distensibility and (2) exert differe
ntial effects on elastic-type versus muscle-type arteries, To address this
issue, 9 sympathectomized (6-hydroxydopamine) and 10 vehicle-treated, 12-we
ek-old, pentobarbitone-anesthetized Wistar-Kyoto rats were subjected to atr
ial pacing via a transjugular catheter at 5 different randomly sequenced ra
tes (280, 310, 340, 370, and 400 bpm). After each step, spontaneous sinus r
hythm was allowed to return to normal, Common carotid and femoral artery di
ameters were measured by an echo Doppler device (NIUS 01), and blood pressu
re was measured via catheter inserted into the contralateral vessel, Arteri
al distensibility was calculated over the systolic-diastolic pressure range
according to the Langewouters formula, In the common carotid artery, progr
essive increases in heart rate determined progressive and marked reductions
of distensibility (range, 15% to 43%) in sympathectomized and intact rats.
In the femoral artery, the stiffening effect of tachycardia was present in
sympathectomized rats (range, 21% to 42%), at variance with the inconsiste
nt changes observed in intact rats, In conclusion, our experiments support
the notions (1) that in predominantly elastic-type arteries, the stiffening
effect of tachycardia is exerted independently of sympathetic modulation o
f the vessel wall properties and (2) that in predominantly muscle-type arte
ries, removal of sympathetic influences unmasks the stiffening effect of ta
chycardia.