Human sympathetic and vagal baroreflex responses to sequential nitroprusside and phenylephrine

Abstract

We evaluated a method of baroreflex testing involving sequential intravenous bolus injections of nitroprusside followed by phenylephrine and phenylephrine followed by nitroprusside in 18 healthy men and women, and we drew inferences regarding human sympathetic and vagal baroreflex mechanisms. We recorded the electrocardiogram, photoplethysmographic finger arterial pressure, and peroneal nerve muscle sympathetic activity. We then contrasted least squares linear regression slopes derived from the depressor (nitroprusside) and pressor (phenylephrine) phases with 1) slopes derived from spontaneous fluctuations of systolic arterial pressures and R-R intervals, and 2) baroreflex gain derived from cross-spectral analyses of systolic pressures and R-R intervals. We calculated sympathetic baroreflex gain from integrated muscle sympathetic nerve activity and diastolic pressures. We found that vagal baroreflex slopes are less when arterial pressures are falling than when they are rising and that this hysteresis exists over pressure ranges both below and above baseline levels. Although pharmacological and spontaneous vagal baroreflex responses correlate closely, pharmacological baroreflex slopes tend to be lower than those derived from spontaneous fluctuations. Sympathetic baroreflex slopes are similar when arterial pressure is falling and rising; however, small pressure elevations above baseline silence sympathetic motoneurons. Vagal, but not sympathetic baroreflex gains vary inversely with subjects’ ages and their baseline arterial pressures. There is no correlation between sympathetic and vagal baroreflex gains. We recommend repeated sequential nitroprusside followed by phenylephrine doses as a simple, efficientmeans to provoke and characterize human vagal and sympathetic baroreflex responses.

Asymmetric features of short-term blood pressure variability

“…1,[3][4][5][6][7]9,14,16,[18][19][20][21]27,31 The baroreflex sensitivity is different for blood pressure increases and reductions, which is evident by comparing phenylephrine with nitroprusside infusion, or neck pressure with neck suction methods. [18][19][20] Heart rate asymmetry, although independent of blood pressure asymmetry, is probably related to baroreflex, which is supported by the observation that heart rate asymmetry is correlated with measures of baroreflex function. 32 Porta et al 33 showed that asymmetrical features of HRV change during sympathetic provocation like head-up tilting and that heart rate asymmetry expression increases during the day compared with night, both in healthy people and patients with congestive heart failure.…”

“…However, in most physiological and clinical studies continuous noninvasive recordings of blood pressure signal at the finger level are most commonly used. [4][5][6][7][8][9]14,[18][19][20][21]27,35 Studies on blood pressure asymmetry can develop in different directions. First, the explanation of the mechanisms responsible for this phenomenon like the influence of respiration, autonomic provocations or blockade is necessary.…”

“…9,[18][19][20][21] As both HRV and baroreflex function are asymmetric, it can be expected that a similar phenomenon may be found in BPV. The primary aim of this study is to establish the existence of asymmetric features of short-term blood pressure asymmetry, in short, blood pressure asymmetry, by separately analyzing the information from systolic blood pressure (SBP) increases and reductions.…”

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

“…These drugs were administered via a catheter placed in an antecubital vein. After a 10-min baseline period, 100 g of sodium nitroprusside were administered, followed ϳ60 s later by 150 g of phenylephrine HCl (21). These doses decreased arterial pressure 10-15 mmHg below baseline levels and then increased blood pressure 5-10 mmHg above the baseline levels, respectively.…”

“…The sensitivity of arterial baroreflex control of MSNA was identified from the linear relationship between MSNA and diastolic pressure during pharmacologically induced changes in blood pressure (11,21). Diastolic pressure was used because MSNA correlates closely with diastolic pressure but not with systolic pressure (23).…”