Impact of Acute Mental Stress on Sympathetic Nerve Activity and Regional Blood Flow in Advanced Heart Failure

We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

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Blunted muscle vasodilatation during chemoreceptor stimulation in patients with heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00156.2007 ◽

2007 ◽

Vol 293 (1) ◽

pp. H846-H852 ◽

Cited By ~ 16

Author(s):

Andrea Di Vanna ◽

Ana Maria F. W. Braga ◽

Mateus C. Laterza ◽

Linda M. Ueno ◽

Maria Urbana P. B. Rondon ◽

...

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Muscle Sympathetic Nerve Activity ◽

Muscle Blood Flow ◽

Heart Association ◽

Functional Class ◽

Nerve Activity ◽

Normal Controls

Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure (HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptor activation in patients with HF are unknown. We tested the hypothesis that the muscle blood flow responses during peripheral and central chemoreflex stimulation would be blunted in patients with HF. Sixteen patients with HF (49 ± 3 years old, Functional Class II-III, New York Heart Association) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O2 and 90% N2 for 3 min. The central chemoreflex control was evaluated by inhalation of 7% CO2 and 93% O2 for 3 min. Muscle sympathetic nerve activity (MSNA) was directly evaluated by microneurography. Forearm blood flow was evaluated by venous occlusion plethysmography. Baseline MSNA were significantly greater in HF patients (33 ± 3 vs. 20 ± 2 bursts/min, P = 0.001). Forearm vascular conductance (FVC) was not different between the groups. During hypoxia, the increase in MSNA was significantly greater in HF patients than in normal controls (9.0 ± 1.6 vs. 0.8 ± 2.0 bursts/min, P = 0.001). The increase in FVC was significantly lower in HF patients (0.00 ± 0.10 vs. 0.76 ± 0.25 units, P = 0.001). During hypercapnia, MSNA responses were significantly greater in HF patients than in normal controls (13.9 ± 3.2 vs. 2.1 ± 1.9 bursts/min, P = 0.001). FVC responses were significantly lower in HF patients (−0.29 ± 0.10 vs. 0.37 ± 0.18 units, P = 0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptor stimulation is blunted in HF patients. This vascular response seems to be explained, at least in part, by the exaggerated MSNA responses during hypoxia and hypercapnia.

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Renal responses to mental stress and epinephrine in humans

AJP Renal Physiology ◽

10.1152/ajprenal.1989.257.4.f682 ◽

1989 ◽

Vol 257 (4) ◽

pp. F682-F689 ◽

Cited By ~ 7

Author(s):

B. Tidgren ◽

P. Hjemdahl

Keyword(s):

Blood Flow ◽

Sympathetic Nerve ◽

Mental Stress ◽

Sympathetic Nerve Activity ◽

Renin Release ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Arterial Plasma ◽

Renal Sympathetic ◽

Venous Plasma

Renal blood flow, renal sympathetic nerve activity, and renin release responses to mental stress (Stroop's color-word conflict test; CWT) and intravenously infused epinephrine (Epi) were evaluated in 12 healthy volunteers. The overflows of norepinephrine (NE) and dopamine (DA) to renal venous plasma were measured as indexes of nerve activity; the fractional extraction of Epi was used to assess renal catecholamine extraction from arterial plasma. At rest, NE and DA levels were higher in renal venous plasma than in arterial plasma. Arterial Epi levels were 0.26 +/- 0.04 nmol/l, and the fractional extraction of Epi by the kidney was 46 +/- 4%. CWT increased renal vascular resistance (RVR) by 48%, renal venous NE overflow by 214% (to 708 +/- 79 pmol/min), and DA overflow by 42% (to 34 +/- 4 pmol/min). Arterial Epi increased by 197%. The vasoconstrictor response was correlated with the NE overflow response. The increased renin release (from 75 to 247 U/min, median values; P less than 0.001) was correlated to increases in mean arterial pressure and NE and DA overflows. Epi infusion increased arterial plasma Epi and renin release dose dependently to 6.43 +/- 0.27 nmol/l and by 664%, respectively. RVR and NE and DA overflows were unchanged. Renal venous DA data support the existence of a subset of renal dopaminergic nerves. Mental stress causes renal vasoconstriction, apparently due to increased renal sympathetic nerve activity. Physiological increments of circulating Epi do not affect renal blood flow but enhance renin release markedly without apparent activation of the renal nerves in humans.

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Role of the hypothalamic PVN in the regulation of renal sympathetic nerve activity and blood flow during hyperthermia and in heart failure

AJP Renal Physiology ◽

10.1152/ajprenal.00734.2009 ◽

2010 ◽

Vol 298 (4) ◽

pp. F839-F846 ◽

Cited By ~ 39

Author(s):

Emilio Badoer

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Paraventricular Nucleus ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic

The hypothalamic paraventricular nucleus is a key integrative area in the brain involved in influencing sympathetic nerve activity and in the release of hormones or releasing factors that contribute to regulating body fluid homeostasis and endocrine function. The endocrine and hormonal regulatory function of the paraventricular nucleus is well studied, but the regulation of sympathetic nerve activity and blood flow by this region is less clear. Here we review the critical role of the paraventricular nucleus in regulating renal blood blow during hyperthermia and the evidence pointing to an important pathophysiological role of the paraventricular nucleus in the elevated renal sympathetic nerve activity that is a characteristic of heart failure.

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