Abstract
The arterial baroreflex system may be analyzed by dividing it into neural arc and peripheral arc subsystems. The central and peripheral effects of a given drug can be assessed by changes in the neural and peripheral arcs, respectively. First generation dihydropyridine calcium blockers (DHPs) exert a strong and rapid arterial pressure (AP)-lowering effect via vasodilatation but may evoke baroreflex-mediated sympathetic excitation, leading to increased heart rate (HR). Second and third generation DHPs have slow-onset and reduce AP while either maintaining or actually decreasing HR, indicating possible sympathoinhibitory effect. We examined the acute effect of intravenous nifedipine, cilnidipine, and azelnidipine (1st, 2nd, and 3rd generation DHP, respectively) on sympathetic nerve activity (SNA) in anesthetized Wistar Kyoto rats. When the baroreceptor input pressure was controlled at predefined pressure levels, nifedipine, cilnidipine, and azelnidipine did not significantly affect the SNA response. The acute hypotensive effects of intravenous DHPs may be chiefly attributable to the peripheral vasodilator action but not to the direct inhibition of the sympathetic outflow.
