Sympathetic Nervous Regulation in Patients with Cirrhosis: Pathogenesis of Fluid Retention and Formation of Ascites

Increased circulating noradrenaline in patients with cirrhosis is due to enhanced sympathetic nervous activity and is not merely the result of decreased clearance of catecholamines. There is a direct relation between the level of arterial norndrenaline and severity of cirrhosis, increased portal pressure and fluid accumulation; patients with the hepatorenal syndrome exhibit the highest values of plasma noradrenaline. In patients with cirrhosis, the kidneys have been identified as an important source of noradrenaline ‘spillover’ into plasma, which indicates enhanced sympathetic nervous activity in these organs. Moreover, the level of plasma noradrenaline is inversely related to renal bloodflow and urinary excretion of sodium, and directly related to plasma renin, vasopressin and aldosterone. An increased spillover of noradrenaline has recently been demonstrated in the splanchnic system and superior portosystemic collaterals. Reduced central and arterial blood volume and low arterial blood pressure secondary to peripheral vasodilation are probably important afferent stimuli for enhanced sympathetic nervous activity, although a nonvolume-dependent hepatic baroreceptor may also be present. The authors conclude that the sympathetic nervous system, in concert with other regulatory systems, plays an important role in sodium-water homeostasis and fluid retention, as well as in the systemic and hepatosplanchnic circulatory derangement seen in patients with cirrhosis.

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Renin Release during Head-up Tilt Occurs Independently of Sympathetic Nervous Activity in Tetraplegic Man

Clinical Science ◽

10.1042/cs0590251 ◽

1980 ◽

Vol 59 (4) ◽

pp. 251-256 ◽

Cited By ~ 59

Author(s):

C. J. Mathias ◽

N. J. Christensen ◽

H. L. Frankel ◽

W. S. Peart

Keyword(s):

Blood Pressure ◽

Plasma Renin Activity ◽

Nervous Activity ◽

Plasma Renin ◽

Normal Subjects ◽

Renin Activity ◽

Plasma Noradrenaline ◽

Sympathetic Nervous Activity ◽

Head Up Tilt ◽

Sympathetic Nervous

1. The role of the sympathetic nervous system in the release of renin during head-up tilt has been studied in five normal subjects and in four tetraplegic patients with cervical spinal-cord transection above the sympathetic outflow. Blood pressure, heart rate and concentrations of plasma noradrenaline, plasma adrenaline and plasma renin activity were measured during head-up tilt to 45° before and after acute β-adrenoreceptor blockade with intravenous propranolol. 2. In the normal subjects there were minimal changes in blood pressure during head-up tilt and there was a rise in both plasma noradrenaline concentration and plasma renin activity. After propranolol values of plasma renin activity at rest fell with little change occurring during head-up tilt. 3. In the tetraplegic patients there was a substantial fall in blood pressure during head-up tilt. Concentrations of plasma noradrenaline and adrenaline did not change but there was a marked increase in plasma renin activity. Values of plasma renin activity both at rest and during head-up tilt were unaffected by propranolol. 4. We conclude that in tetraplegic patients renin release during head-up tilt may occur independently of sympathetic nervous activity and is probably largely dependent on activation of renal vascular receptors.

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Variations in Individual Organ Release of Noradrenaline Measured by An Improved Radioenzymatic Technique; Limitations of Peripheral Venous Measurements in the Assessment of Sympathetic Nervous Activity

Clinical Science ◽

10.1042/cs0610585 ◽

1981 ◽

Vol 61 (5) ◽

pp. 585-590 ◽

Cited By ~ 84

Author(s):

M. J. Brown ◽

D. A. Jenner ◽

D. J. Allison ◽

C. T. Dollery

Keyword(s):

Renal Artery ◽

Renal Artery Stenosis ◽

Nervous Activity ◽

Artery Stenosis ◽

Plasma Noradrenaline ◽

Sympathetic Nervous Activity ◽

Release Of Noradrenaline ◽

Noradrenaline Concentration ◽

Sympathetic Nervous ◽

Noradrenaline And Adrenaline

1. The validity of plasma noradrenaline as an index of sympathetic nervous activity was assessed by estimating variation in individual organ contribution to circulating concentrations. 2. Arteriovenous (A—V) differences in noradrenaline and adrenaline concentration were measured across several organs in nine patients with mild essential hypertension, in five with renal artery stenosis and 15 phaeochromocytoma patients. 3. In patients with phaeochromocytomas the percentage extraction of noradrenaline and adrenaline (estimated from the A—V differences) was similar across all organs, suggesting that adrenaline extraction could be used as a marker for noradrenaline extraction. 4. In the non-tumour patients the A—V difference for noradrenaline was less than that for adrenaline across most organs studied, reflecting the net result of noradrenaline release and extraction. The estimated contribution of various organs to the noradrenaline concentrations in their venous effluent was: heart. 21%; kidney 47%; legs 68%. 5. This pattern of A—V difference proved a positive diagnostic feature for non-tumour patients since it was not found even in the patients with small phaeochromocytomas, whose peripheral venous noradrenaline concentration alone did not distinguish them. 6. The venous-arterial difference across the adrenal glands of non-tumour patients was more than 10-fold greater for adrenaline than that for noradrenaline. Since the mean arterial concentration of noradrenaline was more than fivefold higher than that of adrenaline, the normal adrenal contribution to circulating noradrenaline is likely to be less than 2%. 7. In the patients with renal artery stenosis renal venous concentrations of noradrenaline (from the ischaemic kidney) were higher than arterial values, but mean arterial values were no higher than in the essential hypertensive patients. 8. Local variations in sympathetic activity may occur without altering the plasma noradrenaline concentration measured in peripheral plasma.

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Choice of Control Groups in the Appraisal of Sympathetic Nervous Activity in Essential Hypertension

Clinical Science ◽

10.1042/cs0570339 ◽

1979 ◽

Vol 57 (4) ◽

pp. 339-344 ◽

Cited By ~ 29

Author(s):

D. H. Jones ◽

Carlene A. Hamilton ◽

J. L. Reid

Keyword(s):

Essential Hypertension ◽

Nervous Activity ◽

Plasma Noradrenaline ◽

Sympathetic Nervous Activity ◽

Urinary Catecholamine ◽

Control Groups ◽

Laboratory Staff ◽

Metabolite Concentrations ◽

Vanillyl Mandelic Acid ◽

Sympathetic Nervous

1. Plasma noradrenaline concentrations were similar in normotensive and hypertensive outpatients, but were significantly lower in laboratory control subjects. 2. Standing plasma noradrenaline concentrations were similar in all three groups. 3. Urinary vanillyl mandelic acid, catecholamines and metanephrines were also similar in the normotensive and hypertensive groups. 4. Laboratory controls, possibly because of familiarity with the techniques of sphygmomanometry and blood sampling, may attain a ‘basal’ resting level of sympathetic nervous discharge more readily and rapidly than subjects who are unfamiliar with such procedures. 5. After orthostatic stimulation by standing for 2 min, the activity of the sympathetic nervous system, as determined by pulse rate and plasma noradrenaline concentrations, was similar in the three groups, despite the lower starting values in the laboratory staff. 6. The absence of differences in plasma noradrenaline or urinary catecholamine and metabolite concentrations does not support the hypothesis of excessive sympathetic nervous activity in essential hypertension.

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Angiotensin converting enzyme inhibition lowers blood pressure in patients with primary autonomic failure independently of plasma renin levels and sympathetic nervous activity

Journal of Hypertension ◽

10.1097/00004872-198900076-00018 ◽

1989 ◽

Vol 7 ◽

pp. S42-43 ◽

Cited By ~ 5

Author(s):

Jaspal S. Kooner ◽

Sarah Raimbach ◽

Roger Bannister ◽

Stanley Peart ◽

Christopher J. Mathias

Keyword(s):

Blood Pressure ◽

Angiotensin Converting Enzyme ◽

Autonomic Failure ◽

Nervous Activity ◽

Plasma Renin ◽

Sympathetic Nervous Activity ◽

Angiotensin Converting Enzyme Inhibition ◽

Converting Enzyme ◽

Converting Enzyme Inhibition ◽

Sympathetic Nervous

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787-6 Hypotension Induced by Captopril in Patients with Primary Autonomic Failure Occurs Independently of Plasma Renin Levels and Sympathetic Nervous Activity

Journal of the American College of Cardiology ◽

10.1016/0735-1097(95)92862-y ◽

1995 ◽

Vol 25 (2) ◽

pp. 338A-339A

Author(s):

J.S. Kooner ◽

R. Baliga ◽

W.S. Peart ◽

C.J. Mathias

Keyword(s):

Autonomic Failure ◽

Nervous Activity ◽

Plasma Renin ◽

Sympathetic Nervous Activity ◽

Sympathetic Nervous

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Sympathetic nervous activity and arterial blood pressure control in conscious rat during rest and behavioral stress

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.267.5.r1241 ◽

1994 ◽

Vol 267 (5) ◽

pp. R1241-R1249 ◽

Cited By ~ 14

Author(s):

D. C. Randall ◽

D. R. Brown ◽

L. V. Brown ◽

J. M. Kilgore

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Neural Control ◽

Nervous Activity ◽

Sympathetic Nervous Activity ◽

Initial Increase ◽

Conditional Response ◽

Arterial Blood ◽

Behavioral Stress ◽

Sympathetic Nervous

The object of this experiment is to analyze the neural control of arterial blood pressure (BP) during rest and a sudden behavioral stress. Sprague-Dawley rats were classically conditioned by following a 15-s tone (CS+) with a 0.5-s tail shock. Bipolar renal nerve electrodes and a caudal artery catheter were implanted. Two days later BP and sympathetic nervous activity (SNA) were recorded in the behaviorally trained animals. The CS+ evoked a large initial increase in BP (peak, 14 +/- 5 mmHg, mean +/- SD; n = 12) that lasted 3.9 +/- 0.8 s. An abrupt (latency = 0.16 +/- 0.03 s), short (duration = 0.58 +/- 0.12 s), and intense (4.09 +/- 1.02 times average control) burst in sympathetic activity preceded this first component (C1) of the BP conditional response. The size of C1 was related to the magnitude of the SNA burst. SNA then fell below control; this quiet period preceded a fall in BP after the C1 peak. Pressure rose again (C2; peak = 6 +/- 3 mmHg, average increase = 3 +/- 3 mmHg) for the remainder of the CS+. SNA increased to 1.24 +/- 0.14 of control during this second component of the BP conditional response. Ganglionic blockade eliminated the BP and SNA conditional response (n = 3). The C1 pressure increase appears to result from an “open-loop” process in which a brief barrage of nerve activity governs BP changes lasting several seconds. The quite period probably results from a negative feedback (i.e., baroreflex) relationship between SNA and BP.(ABSTRACT TRUNCATED AT 250 WORDS)

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Postprandial Sympatho-Adrenal Activity: Its Relation to Metabolic and Cardiovascular Events and to Changes in Meal Frequency

Clinical Science ◽

10.1042/cs0890349 ◽

1995 ◽

Vol 89 (4) ◽

pp. 349-357 ◽

Cited By ~ 32

Author(s):

Mario Vaz ◽

Andrea Turner ◽

Bronwyn Kingwell ◽

Jaye Chin ◽

Elizabeth Koff ◽

...

Keyword(s):

Heart Rate ◽

Cardiovascular Events ◽

Peak Plasma ◽

Nervous Activity ◽

Systolic Pressure ◽

Plasma Noradrenaline ◽

Whole Body ◽

Sympathetic Nervous Activity ◽

Insulin Levels ◽

Sympathetic Nervous

1. Sympatho-adrenal activity was measured after the consumption of a 3.15 MJ mixed meal. Whole-body noradrenaline spillover rates, forearm plasma noradrenaline spillover and adrenaline secretion rates were derived using isotope dilution methodology. Heart rate and blood pressure spectral analysis measurements were also made. The relation of sympatho-adrenal activity to thermogenic and cardiovascular events was studied. Sympathetic nervous and thermogenic responses were measured for 120 min after the single 3.15 MJ meal and compared with those after three 1.05 MJ meals, given 30 min apart. 2. Whole-body and forearm plasma noradrenaline spillover, and the 0.1 Hz component of systolic pressure power all increased significantly postprandially, while the 0.1 Hz component of heart rate variability, an indirect index of cardiac sympathetic nervous activity, remained unaltered. Adrenaline secretion was unaltered postprandially. Whole-body plasma noradrenaline spillover and thermogenesis during the 120 min postprandial period were 37% and 36% higher after the single meal as compared with the multiple meals, although this was not statistically significant. 3. The sympathetic neural responses were delayed in relation to peak plasma insulin levels and sustained in the face of declining insulin levels. Energy expenditure increased significantly postprandially, but there was no direct quantitative relationship to plasma noradrenaline spillover. Forearm oxygen consumption did not increase postprandially despite significant increases in regional noradrenaline spillover. Thus, no close relation was demonstrated between postprandial sympathetic nervous activation and either insulin secretion or thermogenesis.

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Effects of Clonidine on Biochemical Indices of Sympathetic Function and Plasma Renin Activity in Normotensive Man

Clinical Science ◽

10.1042/cs0530045 ◽

1977 ◽

Vol 53 (1) ◽

pp. 45-53 ◽

Cited By ~ 13

Author(s):

L. M. H. Wing ◽

J. L. Reid ◽

C. A. Hamilton ◽

P. Sever ◽

D. S. Davies ◽

...

Keyword(s):

Blood Pressure ◽

Plasma Renin Activity ◽

Nervous Activity ◽

Plasma Renin ◽

Renin Activity ◽

Plasma Noradrenaline ◽

Sympathetic Nervous Activity ◽

Angiotensin I ◽

Sympathetic Function ◽

Normotensive Subjects

1. A single oral dose of clonidine hydrochloride (300 μg) lowered systolic blood pressure by 20 ± 2 mmHg and diastolic blood pressure by 15 ± 2 mmHg in seven healthy normotensive subjects. 2. Resting supine plasma noradrenaline concentration fell from 2·42 ± 0·47 nmol/l before dosing to a minimum of 0·59 ± 0·18 nmol/l at 6 h. The value subsequently rose and was not significantly different from that before the dose at 12 h. There was a significant reduction in urinary free catecholamine excretion in the first 12 h after dosing. 3. Resting supine plasma renin activity before dosing was 0·95 ± 0·16 pmol of angiotensin I h−1 ml−1 of plasma and rose significantly after clonidine to 3·50 ± 0·39 pmol of angiotensin I h−1 ml−1 of plasma at 6 h. By 12 h plasma renin activity had returned to control values. 4. When the same subjects were studied on a control, drug-free, day under the same conditions, there was no significant change in blood pressure or plasma noradrenaline. Although plasma renin activity rose during this control day, it was significantly lower than after clonidine. 5. In normotensive subjects single doses of clonidine lower blood pressure and are associated with a reduction of sympathetic nervous activity. Delayed elevation of plasma renin activity may be secondary to the fall in blood pressure. There is no evidence for an overshoot of sympathetic activity after a single dose of clonidine.

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