Importance of left atrial baroreceptors in the cardiopulmonary baroreflex of normal humans

1993 ◽  
Vol 74 (6) ◽  
pp. 2672-2680 ◽  
Author(s):  
R. M. Oren ◽  
H. P. Schobel ◽  
R. M. Weiss ◽  
W. Stanford ◽  
D. W. Ferguson
Keyword(s):  
Computed Tomography ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Left Atrial ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Cardiopulmonary Baroreflex ◽  
Normal Humans ◽  
Cardiac Filling ◽  
Forearm Vascular Resistance

In animals, sympathetic responses to orthostasis are regulated in part by cardiopulmonary afferents arising from atrial and ventricular baroreceptors. To determine the relative importance of these baroreceptor regions in the cardiopulmonary baroreflex of normal humans, simultaneous measurements of left atrial and right and left ventricular volumes (cine computed tomography), invasive hemodynamics, forearm vascular resistance (plethysmography), and efferent sympathetic nerve activity to muscle (microneurography) were obtained under control conditions and with nonhypotensive lower body negative pressure (-10 mmHg, LBNP-10) in nine normal human subjects. LBNP-10 did not alter heart rate or mean systemic arterial pressure, but it did produce significant decreases in pulmonary artery diastolic and right atrial pressures. This reduction in cardiac filling pressures resulted in efferent sympathoexcitation evidenced by increases in forearm vascular resistance and efferent sympathetic nerve activity to the muscle. LBNP-10 did not alter end-diastolic volume of the left or the right ventricle. Similarly, ventricular stroke volume was unchanged during LBNP-10, as assessed by cine computed tomography or thermodilution techniques. In contrast, LBNP-10 resulted in a significant decrease in left atrial volume. Thus, LBNP produced a significant decrease in cardiac filling pressures and left atrial volumes with resultant reflex sympathoexcitation, whereas ventricular volumes were unchanged. These observations suggest an important role for left atrial (nonventricular) baroreceptor afferents in the cardiopulmonary baroreflex of normal humans.

Directionally opposite left atrial and ventricular volume changes during lower body suction

1994 ◽  
Vol 77 (3) ◽  
pp. 1569-1570
Author(s):  
D. L. Eckberg
Keyword(s):  
Computed Tomography ◽  
Sympathetic Nerve ◽  
Left Atrial ◽  
Sympathetic Nerve Activity ◽  
Lower Body ◽  
Nerve Activity ◽  
Cardiopulmonary Baroreflex ◽  
Normal Humans ◽  
Cardiac Filling ◽  
Forearm Vascular Resistance

In animals, sympathetic responses to orthostasis are regulated in part by cardiopulmonary afferents arising from atrial and ventricular baroreceptors. To determine the relative importance of these baroreceptor regions in the cardiopulmonary baroreflex of normal humans, simultaneous measurements of left atrial and right and left ventricular volumes (cine computed tomography), invasive hemodynamics, forearm vascular resistance (plethysmography), and efferent sympathetic nerve activity to muscle (microneurography) were obtained under control conditions and with nonhypotensive lower body negative pressure (-10 mmHg, LBNP-10) in nine normal human subjects. LBNP-10 did not alter heart rate or mean systemic arterial pressure, but it did produce significant decreases in pulmonary artery diastolic and right atrial pressures. This reduction in cardiac filling pressures resulted in efferent sympathoexcitation evidenced by increases in forearm vascular resistance and efferent sympathetic nerve activity to the muscle. LBNP-10 did not alter end-diastolic volume of the left or the right ventricle. Similarly, ventricular stroke volume was unchanged during LBNP-10, as assessed by cine computed tomography or thermodilution techniques. In contrast, LBNP-10 resulted in a significant decrease in left atrial volume. Thus, LBNP produced a significant decrease in cardiac filling pressures and left atrial volumes with resultant reflex sympathoexcitation, whereas ventricular volumes were unchanged. These observations suggest an important role for left atrial (nonventricular) baroreceptor afferents in the cardiopulmonary baroreflex of normal humans.

Modulation of cardiovascular reflexes by arginine vasopressin

1987 ◽  
Vol 65 (8) ◽  
pp. 1717-1723 ◽  
Author(s):  
John S. Floras ◽  
Philip E. Aylward ◽  
Badri N. Gupta ◽  
Allyn L. Mark ◽  
Francois M. Abboud
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Normal Humans ◽  
Forearm Vascular Resistance

Arginine vasopressin (AVP), a potent vasoconstrictor, does not raise arterial pressure in normal humans or neurally intact animals, even during infusions that achieve pathophysiological plasma concentrations. It has been proposed that this is because AVP facilitates the baroreflex control of the circulation. We performed a series of investigations to test this hypothesis, and to determine sites at which AVP might act to augment the baroreflex. In anesthetized rabbits, vasopressin (36 pmol∙kg−1∙min−1) increased discharge from both medullated and nonmedullated single fibres from aortic baroreceptor nerves during elevations in aortic arch pressure. Similarly, vasopressin (36 pmol∙kg−1∙min−1) increased the response of left ventricular mechanoreceptor single fibre discharge to elevations of left ventricular end-diastolic pressure. These observations suggest that sensitization of high and low pressure baroreceptors is one mechanism by which vasopressin may facilitate baroreflexes. In a further series of experiments in sinoaortic denervated anesthetized rabbits, vasopressin (18 pmol∙kg−1∙min−1) facilitated vagally mediated reflex inhibition of renal sympathetic nerve activity during volume expansion. In humans, AVP (0.37 pmol∙kg−1∙min−1) raised plasma AVP to an antidiuretic level (22 ± 4 fmol/mL), but did not change blood pressure or the baroreflex control of heart rate or forearm vascular resistance. A higher dose (3.7 pmol∙kg−1∙min−1) raised plasma levels to 268 ± 38 fmol/mL, decreased pulse pressure, increased central venous pressure (from 2.6 ± 0.5 to 4.1 ± 0.4 mmHg) (1 mmHg = 133.3 Pa) and suprisingly, in view of its direct vasoconstrictor effect, increased forearm blood flow by 30% and decreased forearm vascular resistance from 24 ± 4 to 18 ± 3 units (p < 0.05); mean arterial pressure was unchanged. The reflex vasodilator response to the sudden release of lower body negative pressure was augmented by AVP, whereas reflex changes in heart rate were unaltered. To test the hypothesis that vasopressin caused this resting vasodilation through inhibition of sympathetic nerve activity, we recorded postganglionic efferent muscle sympathetic nerve activity directly from the peroneal nerve before, during, and after intravenous infusion of AVP, 3.7 pmol∙kg−1∙min−1. Forearm vascular resistance again fell; sympathetic nerve activity decreased abruptly on starting AVP, from 254 ± 40 to 163 ± 34 units (p < 0.05), and remained below control throughout the infusion. This decrease did not appear to be due to a ganglionic action of AVP. The inhibition of sympathetic nerve activity probably resulted principally from mechanical stimulation of cardiac and arterial baroreceptors. However, since the marked reduction of nerve activity was not consistently associated with increases in arterial pressure or central venous pressure, we cannot exclude the possibility that vasopressin decreased sympathetic nerve activity in part by sensitizing baroreceptor afferents or by a central neural action. Sympathoinhibition would appear to be an important mechanism by which the potent pressor effects of AVP are countered in normal humans.

Sympathetic and Hemodynamic Effects of Moderate and Deep Sedation with Propofol in Humans

2005 ◽  
Vol 103 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Thomas J. Ebert
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Deep Sedation ◽  
Infusion Pump ◽  
Random Order ◽  
Mean Blood Pressure ◽  
Nerve Activity ◽  
Forearm Vascular Resistance

Background The objective of this study was to determine the mechanisms involved in the hypotension associated with sedative doses of propofol in humans. Methods Ten healthy volunteers (aged 21-37 yr) participated on two occasions and in random order received placebo or propofol infusions. Standard monitoring and radial artery blood pressure were combined with measurement of forearm blood flow (plethysmography) and derivation of forearm vascular resistance, recording of peroneal nerve sympathetic activity, and blood sampling for norepinephrine concentrations. A computer-controlled infusion pump delivered placebo or two concentrations of propofol, adjusted to achieve moderate and deep sedation based on the Observer Assessment of Alertness/Sedation score (responsiveness component) of 4 and 3. Level of sedation was quantitated using bispectral analysis of the electroencephalogram. Baroreflexes were assessed with a hypotensive challenge via administration of sodium nitroprusside. Results Baseline neurocirculatory and respiratory parameters did not differ between sessions. Progressive infusions to achieve moderate and deep sedation resulted in average Bispectral Index values of 70 and 54, respectively. Propofol significantly reduced sympathetic nerve activity at both levels of sedation and decreased norepinephrine and forearm vascular resistance at deep sedation. These effects resulted in significant decreases in mean blood pressure of 9% and 18% at moderate and deep sedation, respectively. Propofol also reduced reflex increases in sympathetic nerve activity. Conclusions These data from healthy subjects indicate that sedation doses of propofol, which did not compromise respiratory function, had substantial inhibitory effects on sympathetic nerve activity and reflex responses to hypotension resulting in vasodilation and significant decreases in mean blood pressure.

Muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation

2020 ◽  
Vol 128 (1) ◽  
pp. 1-7
Author(s):  
Keisho Katayama ◽  
Thales C. Barbosa ◽  
Jasdeep Kaur ◽  
Benjamin E. Young ◽  
Damsara Nandadeva ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Muscle Metaboreflex ◽  
Muscle Pump ◽  
Low Intensity ◽  
Leg Cycling ◽  
Cardiopulmonary Baroreflex

Muscle sympathetic nerve activity (MSNA) decreases during leg cycling at low intensity because of muscle pump-induced increases in venous return and loading of the cardiopulmonary baroreceptors. However, MSNA increases during leg cycling when exercise is above moderate intensity or for a long duration, suggesting that the sympathoinhibitory effect of the cardiopulmonary baroreflex can be overridden by a powerful sympathoexcitatory drive, such as the skeletal muscle metaboreflex. Therefore, we tested the hypothesis that high-intensity muscle metaboreflex activation attenuates muscle pump-induced inhibition of MSNA during leg cycling. MSNA (left radial nerve) was recorded during graded isolation of the muscle metaboreflex in the forearm with postexercise ischemia (PEI) after low (PEI-L)- and high (PEI-H)-intensity isometric handgrip exercise (20% and 40% maximum voluntary contraction, respectively). Leg cycling (15–20 W) was performed alone and during each PEI trial (PEI-L+Cycling, PEI-H+Cycling). Cycling alone induced a significant decrease in MSNA burst frequency (BF) and total activity (TA). MSNA BF and TA also decreased when cycling was performed during PEI-L. However, the magnitude of decrease in MSNA during PEI-L+Cycling [∆BF: –19 ± 2% ( P < 0.001), ∆TA: –25 ± 4% ( P < 0.001); mean ± SE] was less than that during cycling alone [∆BF: –39 ± 5% ( P = 0.003), ∆TA: –45 ± 5% ( P = 0.002)]. More importantly, MSNA did not decrease during cycling with PEI-H [∆BF: –1 ± 2% ( P = 0.845), ∆TA: +2 ± 3% ( P = 0.959)]. These results suggest that muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation in an intensity-dependent manner. NEW & NOTEWORTHY There are no available data concerning the interaction between the sympathoinhibitory effect of muscle pump-induced cardiopulmonary baroreflex loading during leg cycling and the sympathoexcitatory influence of the muscle metaboreflex. In this study, muscle metaboreflex activation attenuated the inhibition of muscle sympathetic nerve activity (MSNA) during leg cycling. This may explain, in part, the response of MSNA to graded-intensity dynamic exercise in which low-intensity leg cycling inhibits MSNA whereas high-intensity exercise elicits graded sympathoexcitation.

Effect of vasopressin on baroreflex control of lumbar sympathetic nerve activity and hindquarter resistance

1996 ◽  
Vol 270 (6) ◽  
pp. H1963-H1971 ◽  
Author(s):  
D. A. Scheuer ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Resistance Index ◽  
Inhibitory Influence ◽  
Nerve Activity ◽  
Baroreflex Control

Arginine vasopressin (AVP) has been shown to increase the inhibitory influence of the baroreflex on sympathetic nerve activity by a mechanism involving receptors located in the area postrema. The purpose of these experiments was to study the functional effect of this action of AVP by testing the hypothesis that AVP can buffer its own vasoconstrictor effect by facilitating baroreflex-mediated withdrawal of sympathetic nerve activity. Specifically, we determined 1) if AVP can attenuate increases in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine, and 2) whether the effects of AVP on vascular resistance are associated with appropriate corresponding changes in lumbar sympathetic nerve activity (LSNA). In pentobarbital-anesthetized New Zealand White rabbits the baroreflex was stimulated by phenylephrine-induced elevations in arterial pressure. Baroreflex-mediated changes in heart rate (HR), calculated hindquarter vascular resistance index (R), and LSNA were determined during the simultaneous intravertebral infusion of AVP (0, 0.5, or 1.0 ng.kg-1, min-1). Intravertebral infusion of AVP alone had no effect on resting mean arterial pressure (MAP) but reduced baseline values for LSNA and HR. Intravenous infusion of phenylephrine alone produced dose-dependent increases in MAP and R and decreases in LSNA and HR. The simultaneous infusion of AVP (0.5 or 1.0 ng.kg-1 min-1) and phenylephrine (1.25, 2.5, 5.0, 7.5, and 10.0 micrograms.kg-1.min-1) had no effect on the increase in MAP but attenuated the increases in R and facilitated the reductions in LSNA at all doses of phenylephrine. The higher dose of AVP also enhanced the phenylephrine-induced reductions in HR. In contrast, the intravenous infusion of AVP (1.0 ng.kg-1.min-1) did not alter baroreflex-mediated changes in R, LSNA, or HR. Therefore, we conclude that the action of AVP to increase baroreflex-mediated sympathoinhibition results in an attenuated rise in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine.

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