Relative contribution of aortic and carotid baroreflexes to heart rate control in man during steady state and dynamic increases in arterial pressure.

Abstract

We studied the contribution of carotid vs. extracarotid baroreceptors in control of heart rate in normal humans. We measured heart interval (HI) and arterial pressure during steady-state infusion of phenylephrine (PE). PE increased mean arterial pressure (MAP) by 13±2 mmHg (mean±SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors. Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure. PE infusion alone prolonged HI by 230±24 ms (P < 0.05). Application of NP attenuated the HI response to 65±22 ms above control (P < 0.05 vs. PE alone). During these steady-state increases in arterial pressure, elimination of the carotid baroreflex contribution reduced the HI prolongation by 41-70% in five subjects and by >93% in five subjects.We also measured the HI response to dynamic ramp elevation of systolic arterial pressure (SAP) using bolus administrations of PE. Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation). During PE alone, the baroreflex slope was 20.2±2.9 ms/mmHg (a = 10). During PE plus NP, the baroreflex slope was reduced by 30% to 14.1±2.8 ms/mmHg (P < 0.02 vs. during PE alone). Thus, during dynamic increases in arterial pressure, eliminating the carotid baroreflex contribution reduced the HI response by 30%.These studies indicate that extracarotid (presumably aortic) and carotid baroreflexes both participate in control of heart rate in humans. Extracarotid (aortic) baroreflexes appear to have the greater role in control of heart rate during dynamic increases in arterial pressure.

Baroreflex Control of Muscle Sympathetic Nerve Activity After Carotid Body Tumor Resection

“…Experiments on selective (un)loading of aortic baroreceptors by simultaneous infusion of vasoactive substances and application of neck suction/ pressure to maintain a stable carotid sinus transmural pressure indicated that aortic baroreceptors are dominant in the baroreflex control of heart rate, with the carotid baroreceptors contributing only Ϸ30%. 28,29 In line with these observations, baroreflex control of heart rate in mainly determined by the distensibility of the aortic arch than of the carotid sinus. 30 In contrast, combined neck suction/pressure with nonpharmacological (de)loading of aortic baroreceptors indicate that carotid baroreceptors are the principal contributors to baroreflex control of heart rate.…”

Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans.

“…In any event, any effects of phenylephrine on the baroreflex itself is unlikely to have influenced our findings, since any such effect would be present during both the hypoxic and hypercapnic stresses. With regard to possible effects of phenylephrine on the baroreflexes, the doses of phenylephrine used in this study do not sensitize the arterial baroreceptors to graded levels of neck pressure (14).…”

Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

“…7 Under these conditions, baroreceptor reflex impairments are transient rather than permanent, presumably because there is marked redundancy of baroreceptor afferents, particularly in the control of sympathetic nerve activity. 8 " 10 Thus, the loss of carotid baroreceptor input does not appear to cause a long-term impairment in baroreceptor reflex control of sympathetic vasoconstrictor outflow so long as the aortic baroreceptors remain intact.…”