Erythrocyte Catechol-O-Methyltransferase Activity and Indices of Sympathetic Activity in Man

1980 ◽  
Vol 58 (5) ◽  
pp. 423-425 ◽  
Author(s):  
G. A. Fitzgerald ◽  
C. A. Hamilton ◽  
D. H. Jones ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Interindividual Variability ◽  
Population Sample ◽  
Plasma Noradrenaline ◽  
Methyltransferase Activity ◽  
Urinary Catecholamines ◽  
Wide Interindividual Variability ◽  
Inactivation Of Noradrenaline

1. Erythrocyte catechol-O-methyltransferase was studied in a population sample of 147 subjects. 2. There was a wide interindividual variability of catechol-O-methyltransferase activity, which was not unimodally distributed. Catechol-O-methyltransferase activity was not influenced by blood pressure, age or sex, nor was it related to plasma noradrenaline or urinary catecholamines or metanephrines. 3. It is not likely that inactivation of noradrenaline by O-methylation at least by erythrocytes is an important mechanism determining plasma noradrenaline, let alone arterial pressure.

Arterial pressure and muscle sympathetic nerve activity are increased after two hours of sustained but not cyclic hypoxia in healthy humans

2005 ◽  
Vol 98 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Renaud Tamisier ◽  
Amit Anand ◽  
Luz M. Nieto ◽  
David Cunnington ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sustained Hypoxia

Sustained and episodic hypoxic exposures lead, by two different mechanisms, to an increase in ventilation after the exposure is terminated. Our aim was to investigate whether the pattern of hypoxia, cyclic or sustained, influences sympathetic activity and hemodynamics in the postexposure period. We measured sympathetic activity (peroneal microneurography), hemodynamics [plethysmographic forearm blood flow (FBF), arterial pressure, heart rate], and peripheral chemosensitivity in normal volunteers on two occasions during and after 2 h of either exposure. By design, mean arterial oxygen saturation was lower during sustained relative to cyclic hypoxia. Baseline to recovery muscle sympathetic nerve activity and blood pressure went from 15.7 ± 1.2 to 22.6 ± 1.9 bursts/min ( P < 0.01) and from 85.6 ± 3.2 to 96.1 ± 3.3 mmHg ( P < 0.05) after sustained hypoxia, respectively, but did not exhibit significant change from 13.6 ± 1.5 to 17.3 ± 2.5 bursts/min and 84.9 ± 2.8 to 89.8 ± 2.5 mmHg after cyclic hypoxia. A significant increase in FBF occurred after sustained, but not cyclic, hypoxia, from 2.3 ± 0.2 to 3.29 ± 0.4 and from 2.2 ± 0.1 to 3.1 ± 0.5 ml·min−1·100 g of tissue−1, respectively. Neither exposure altered the ventilatory response to progressive isocapnic hypoxia. Two hours of sustained hypoxia increased not only muscle sympathetic nerve activity but also arterial blood pressure. In contrast, cyclic hypoxia produced slight but not significant changes in hemodynamics and sympathetic activity. These findings suggest the cardiovascular response to acute hypoxia may depend on the intensity, rather than the pattern, of the hypoxic exposure.

Plasma Noradrenaline Concentration and α-Adrenoceptor-Mediated Vasoconstriction in Normotensive and Hypertensive Man

1981 ◽  
Vol 60 (5) ◽  
pp. 483-489 ◽  
Author(s):  
W. Kiowski ◽  
F. R. Bühler ◽  
P. Vanbrummelen ◽  
F. W. Amann
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Vascular Resistance ◽  
Sympathetic Activity ◽  
Plasma Noradrenaline ◽  
Arterial Infusion ◽  
Hypertensive Patients ◽  
Noradrenaline Concentration ◽  
Normotensive Subjects ◽  
Control Plasma

1. Plasma noradrenaline concentrations and blood pressure were measured in 45 patients with essential hypertension and 34 matched normotensive subjects. Plasma noradrenaline was similar in both groups, but in the hypertensive patients plasma noradrenaline correlated with blood pressure. 2. The increase in forearm flow in response to an intra-arterial infusion of phentolamine was determined in 12 of the hypertensive and 14 of the normotensive subjects to assess the α-adrenoceptor-mediated component of vascular resistance. Although the dilator response to phentolamine was similar in both groups, in the hypertensive patients it was correlated with the control plasma noradrenaline (r = 0.83, P<0.01) as well as the height of mean blood pressure (r = 0.73, P<0.01). 3. These results suggest that in hypertensive patients plasma noradrenaline can be a marker for both sympathetic activity and the α-adrenoceptor-mediated component of vascular resistance.

Plasma Catecholamines do Not Invariably Reflect Sympathetically Induced Changes in Blood Pressure in Man

1983 ◽  
Vol 65 (3) ◽  
pp. 227-235 ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
Luisa Gregorini ◽  
G. Leonetti ◽  
G. Parati ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Plasma Noradrenaline ◽  
Carotid Baroreceptor ◽  
Induced Changes ◽  
Neck Chamber ◽  
Noradrenaline And Adrenaline

1. Plasma concentrations of noradrenaline and adrenaline were measured radioenzymatically in nine subjects during 4 min pressor and depressor responses (intra-arterial measurements) induced by increasing and reducing sympathetic vasoconstrictor tone via carotid baroreceptor deactivation and stimulation (neck chamber technique). 2. During the pressor response (15 ± 3 mmHg, mean ± se) plasma noradrenaline and adrenaline showed various changes in the different subjects and on average were not significantly increased above control. During the depressor response (−9 ± 2 mmHg) plasma noradrenaline and adrenaline also showed various changes in the subjects and were on average not significantly reduced below control. 3. In contrast the same subjects all showed an increase in noradrenaline and adrenaline (average 76 and 117%) at the fourth minute of a tilting manoeuvre with- a return to pretilting values no more than 4 min after resumption of the supine position. 4. These results suggest that the moderate and/or restricted alterations in sympathetic tone produced by manipulating a single baroreflex, though capable of affecting blood pressure, are not reflected by alterations in plasma catecholamines. To modify these humoral indices significantly, the more drastic or more diffuse alterations in sympathetic activity that may be produced by manipulating low as well as high pressure reflexogenic areas are needed.

Nervous System and Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 45s-56s ◽  
Author(s):  
J. P. Chalmers
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Nervous System ◽  
Arterial Pressure ◽  
High Blood Pressure ◽  
Sympathetic Activity ◽  
Experimental Hypertension ◽  
Primary Role ◽  
Noradrenergic Nerves ◽  
Peripheral Sympathetic Activity

1. Presynaptic regulation. The regulation of noradrenaline release by a wide variety of substances acting on presynaptic receptors suggests that local factors may play a greater role in the control of blood pressure than was previously believed and that a number of new approaches to the drug treatment of hypertension could be developed. It also raises the possibility that there might be differences in the presynaptic receptor populations of hypertensive and normotensive subjects or animals. 2. Central nerve pathways. There is a need for more precise delineation of central nerve tracts subserving a cardiovascular function and for greater use of morphological techniques to confirm the reliability of biochemical and physiological experiments in the central nervous system. Two appropriate techniques are described. 3. Models of experimental hypertension. (a) Neurogenic hypertension: interference with baroreceptor afferents can cause a permanent elevation of arterial pressure mediated by increased activity of peripheral sympathetic nerves and of descending noradrenergic nerves terminating in the spinal cord. Catecholamine nerve connections of the nucleus tractus solitarius serve mainly to modulate rather than to mediate baroreceptor reflexes. (b) DOCA—salt hypertension: increased peripheral sympathetic activity is important in both the initiation and the maintenance of this form of hypertension. The decrease in brain-stem noradrenaline turnover found in this model could play a determinant role in the development of the high blood pressure. (c) Renal hypertension: both central and peripheral nervous mechanisms contribute to the development and the early phase of ‘one-kidney’ hypertension in animals. Their role in the maintenance of this form of hypertension is still controversial. (d) Spontaneously hypertensive rats: peripheral and central mechanisms do not appear to have a major role in the maintenance of this form of hypertension. However, it seems possible that centrally evoked increases in peripheral sympathetic activity could be important in the initiation of the high blood pressure. (e) Central catecholamines and blood pressure control; central catecholaminergic nerves do not make up a single homogeneous system. For example, the activity of descending noradrenergic nerves in the spinal cord contributes to an elevation of arterial pressure, whereas the activity of catecholaminergic nerves in the dorsomedial medulla appears to have a depressor effect. 4. Human essential hypertension. (a) There is no good evidence that the nervous system plays the major primary role in the development or maintenance of essential human hypertension. (b) Effective treatment of raised blood pressure through nervous mechanisms requires an understanding of the factors that normally control the pressure and does not necessarily depend on reversing specific nervous processes responsible for producing the increase in pressure.

scholarly journals Sympathetic baroreflex gain in normotensive pregnant women

2015 ◽  
Vol 119 (5) ◽  
pp. 468-474 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Rachel J. Skow ◽  
Brittany A. Matenchuk ◽  
Radha S. Chari ◽  
Colleen G. Julian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Pregnant Women ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Sequence Method ◽  
Normotensive Pregnancy ◽  
Dependent Mechanism

Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting. We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls. Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m2) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m2). Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls. Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy. Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (−3.7 ± 0.5 vs. −5.4 ± 0.5 bursts·100 heart beats−1·mmHg−1, P = 0.03), as was baroreflex gain calculated with total sympathetic activity (−294 ± 24 vs. −210 ± 24 au·100 heart beats−1·mmHg−1; P = 0.03). Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2). However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women ( R = −0.7; P = 0.02). Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism.

Plasma Noradrenaline Concentrations in Experimental Renovascular Hypertension in the Rat

1977 ◽  
Vol 52 (5) ◽  
pp. 477-483 ◽  
Author(s):  
H. J. Dargie ◽  
S. S. Franklin ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Plasma Noradrenaline ◽  
Experimental Hypertension ◽  
Hydroxylase Activity ◽  
Goldblatt Rat ◽  
Arterial Constriction ◽  
The One ◽  
6 Hydroxydopamine ◽  
Peripheral Sympathetic Activity

1. Plasma noradrenaline concentrations and dopamine β-hydroxylase activity have been measured at various stages in the development of hypertension in the one-kidney Goldblatt rat (unilateral renal arterial constriction and contralateral nephrectomy). 2. Although plasma noradrenaline concentrations were significantly elevated from control values at 7, 14 and 28 days, plasma dopamine β-hydroxylase activity was not significantly different from control values except at 24 h. 3. These findings suggest that peripheral sympathetic activity is increased in the one-kidney Goldblatt model of experimental hypertension but that plasma dopamine β-hydroxylase activity is a poor index of this increase. 4. Both the rise in blood pressure and the rise in plasma noradrenaline concentrations were prevented by pretreatment with intracisternal 6-hydroxydopamine, suggesting that the increased sympathetic activity is at least in part centrally mediated.

scholarly journals Sustained suppression of sympathetic activity and arterial pressure during chronic activation of the carotid baroreflex

2010 ◽  
Vol 299 (2) ◽  
pp. H402-H409 ◽  
Author(s):  
Thomas E. Lohmeier ◽  
Radu Iliescu ◽  
Terry M. Dwyer ◽  
Eric D. Irwin ◽  
Adam W. Cates ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Vascular Reactivity ◽  
Carotid Sinus ◽  
Plasma Norepinephrine ◽  
Carotid Baroreflex ◽  
Chronic Activation ◽  
Norepinephrine Spillover ◽  
The Brain

Following sinoaortic denervation, which eliminates arterial baroreceptor input into the brain, there are slowly developing adaptations that abolish initial sympathetic activation and hypertension. In comparison, electrical stimulation of the carotid sinus for 1 wk produces sustained reductions in sympathetic activity and arterial pressure. However, whether compensations occur subsequently to diminish these responses is unclear. Therefore, we determined whether there are important central and/or peripheral adaptations that diminish the sympathoinhibitory and blood pressure-lowering effects of more sustained carotid sinus stimulation. To this end, we measured whole body plasma norepinephrine spillover and α1-adrenergic vascular reactivity in six dogs over a 3-wk period of baroreflex activation. During the first week of baroreflex activation, there was an ∼45% decrease in plasma norepinephrine spillover, along with reductions in mean arterial pressure and heart rate of ∼20 mmHg and 15 beats/min, respectively; additionally, plasma renin activity did not increase. Most importantly, these responses during week 1 were largely sustained throughout the 3 wk of baroreflex activation. Acute pressor responses to α-adrenergic stimulation during ganglionic blockade were similar throughout the study, indicating no compensatory increases in adrenergic vascular reactivity. These findings indicate that the sympathoinhibition and lowering of blood pressure and heart rate induced by chronic activation of the carotid baroreflex are not diminished by adaptations in the brain and peripheral circulation. Furthermore, by providing evidence that baroreflexes have long-term effects on sympathetic activity and arterial pressure, they present a perspective that is opposite from studies of sinoaortic denervation.

Baroreflex Control of Blood Pressure and Plasma Noradrenaline during Exericse in Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 169s-171s ◽  
Author(s):  
P. Sleight ◽  
J. S. Floras ◽  
M. O. Hassan ◽  
J. V. Jones ◽  
B. A. Osikowska ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Bicycle Ergometer ◽  
Plasma Noradrenaline ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Resting Blood Pressure ◽  
Mean Pressure

1. Twelve subjects (mean age 46·3 ± 12·5 years) with mild to moderate hypertension were studied before, during and after bicycle ergometer exercise. 2. Baroreflex sensitivity was determined by the Oxford phenylephrine method; sensitivity at rest was inversely related to intra-arterial pressure and age. Age and resting arterial pressure were not related. 3. Exercise for 5 min at 50 W and 5 min at 75 W raised the mean arterial pressure from 116·4 ± 18·0 to 150·0 ± 25·4 mmHg, the heart rate from 73·2 to 126·7 beats/min and the plasma noradrenaline from 541 ± 142·7 to 1309·8 ± 543·5 pg/ml (P &lt; 0·001). 4. The increase in noradrenaline during exercise and the maximum mean pressure achieved were inversely related to resting baroreflex sensitivity (r = −0·68 and −0·77 respectively). Resting values of noradrenaline were not related to baroreflex sensitivity, age, or resting blood pressure. 5. It is possible that the rise in both plasma noradrenaline and arterial blood pressure produced by exercise is controlled by the baroreceptor reflexes; these are less effective in hypertensive subjects and thus the increases in noradrenaline and arterial pressure during exercise are greater in subjects with raised blood pressure.

Sequential Changes in Plasma Noradrenaline during Bicycle Exercise

1980 ◽  
Vol 58 (1) ◽  
pp. 37-43 ◽  
Author(s):  
R. D. S. Watson ◽  
C. A. Hamilton ◽  
D. H. Jones ◽  
J. L. Reid ◽  
T. J. Stallard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Supine Position ◽  
Sympathetic Activity ◽  
Plasma Noradrenaline ◽  
Bicycle Exercise ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Exercise Blood Pressure ◽  
Venous Plasma

1. Forearm venous plasma noradrenaline, heart rate and intra-arterial blood pressure were measured sequentially during and after upright bicycle exercise in five normotensive and six hypertensive patients. 2. Plasma noradrenaline increased significantly between 4 and 8 min during exercise. 3. On stopping exercise blood pressure and heart rate decreased rapidly whilst plasma noradrenaline increased in each subject to reach a maximum at a median time of 108 s after exercise. 4. Plasma noradrenaline decreased in five of six normotensive patients between the end of exercise and 2 min after exercise performed in the supine position. 5. Evidence in favour of a reflex increase in sympathetic activity after upright exercise is discussed.

scholarly journals The Effects of Gallamine and a Mixture of Pancuronium and Alcuronium on the Pressor and Plasma Catecholamine Responses to Tracheal Intubation

1984 ◽  
Vol 12 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Mary F. Cummings ◽  
W. J. Russell ◽  
D. B. Frewin ◽  
Wendy A. Miller
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Tracheal Intubation ◽  
Arterial Pressure ◽  
Plasma Noradrenaline ◽  
Plasma Catecholamine ◽  
Plasma Adrenaline ◽  
Noradrenaline Concentration ◽  
Noradrenaline And Adrenaline

Tracheal intubation can be accompanied by significant increases in arterial pressure, heart rate and the plasma levels of noradrenaline and adrenaline. The drugs used at induction can enhance or attenuate these responses. In nine patients who had received gallamine, intubation was associated with a 45% rise in mean arterial pressure, a twofold rise in plasma adrenaline and a 49% rise in plasma noradrenaline concentration. When a mixture of pancuronium and alcuronium (in a ratio of 4:10 by weight) was used in ten patients, blood pressure fell 24% after induction and rose 49% after intubation. A 24% rise in plasma noradrenaline in response to intubation was also observed. Compared with pancuronium alone, the use of the mixture attentuates the rise in blood pressure and noradrenaline concentration associated with intubation but does not abolish them. In addition, the mixture was associated with a significant fall in blood pressure between induction and intubation, whereas this was not found with gallamine.

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