Plasma Noradrenaline as a Measure of Baroreflex Sensitivity in Hypertensive Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 165s-168s ◽  
Author(s):  
A. M. M. Shepherd ◽  
M.-S. Lin ◽  
T. K. Keeton ◽  
J. L. McNay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Clinical Investigation ◽  
Plasma Noradrenaline ◽  
Chronotropic Response ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Lower Blood ◽  
Noradrenaline Levels

1. Changes in plasma noradrenaline levels and heart rate were used as measures of baroreflex sensitivity in six hypertensive subjects given serial incremental doses of sodium nitroprusside (intravenously) to lower blood pressure. 2. The rises in both heart rate and plasma noradrenaline concentration were linearly related to the decrement in blood pressure and inversely related to the severity of the hypertension. 3. A positive correlation between rise in heart rate and rise in plasma noradrenaline was found for each subject. With increasing severity of hypertension, a greater increase in heart rate occurred for each increment in plasma noradrenaline concentration. 4. Baroreflex sensitivity can be assessed by relating changes in heart rate to change in arterial pressure; however, this method does not distinguish the relative contributions of the vagal and sympathetic components of the autonomic neural response or variations in the chronotropic response to sympathetic stimulation. 5. Changes in plasma noradrenaline levels in response to graded reductions in blood pressure may be a more appropriate measure of baroreflex sensitivity than the methods currently used in clinical investigation.

Plasma Noradrenaline Concentration and Blood Pressure in Essential Hypertension, Phaeochromocytoma and Depression

1974 ◽  
Vol 48 (s2) ◽  
pp. 239s-242s ◽  
Author(s):  
W. J. Louis ◽  
A. E. Doyle ◽  
S. N. Anavekar
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Endogenous Depression ◽  
Plasma Noradrenaline ◽  
Lower Blood Pressure ◽  
Normal Range ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Lower Blood ◽  
Blood Pressures

1. Mean plasma noradrenaline concentration was elevated in forty-four patients with established essential hypertension. Eighteen of these hypertensive patients had resting plasma noradrenaline concentrations in the normal range. 2. Patients with endogenous depression had higher mean plasma noradrenaline concentrations but significantly lower blood pressure than patients with essential hypertension. 3. Patients with phaeochromocytoma had plasma noradrenaline concentrations twenty-eight times greater than those found in essential hypertension, but blood pressures were less than 20% higher. 4. It is concluded that excess of sympathetic drive only partly explains the level of the blood pressure in essential hypertension.

Cardiovascular and Autonomic Reflexes in Haemodialysis Patients

1981 ◽  
Vol 60 (2) ◽  
pp. 165-170 ◽  
Author(s):  
R. B. Naik ◽  
C. J. Mathias ◽  
C. A. Wilson ◽  
J. L. Reid ◽  
D. J. Warren
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Noradrenaline ◽  
Valsalva Manoeuvre ◽  
Induced Hypotension ◽  
Autonomic Nervous ◽  
Control Subjects ◽  
Head Up Tilt ◽  
And Control ◽  
Noradrenaline Levels

1. Blood pressure and heart rate responses to head-up tilt, standing, the Valsalva manoeuvre, sustained handgrip and cutaneous cold were measured in 27 haemodialysis patients (10 of whom had episodes of haemodialysis-induced hypotension) and 15 control subjects to assess autonomic nervous function. Plasma nor-adrenaline levels were measured at rest and during head-up tilt. 2. Mean resting supine blood pressure, heart rate and plasma noradrenaline levels were higher in haemodialysis patients than in the control subjects. There was no fall in blood pressure during head-up tilt or standing. The ratio of the R-R intervals of the thirtieth and the fifteenth heart beat after standing (30: 15) was lower in the patients; this may be related to their higher resting heart rate. Head-up tilt raised plasma noradrenaline levels in both groups. Heart rate responses to the Valsalva manoeuvre were similar in the patients and control subjects. 3. Systolic blood pressure and heart rate responses to sustained handgrip were similar in both groups. Diastolic and mean blood pressure changes, however, were lower in the patients. The blood pressure and heart rate responses to cutaneous cold were similar in the patients and control subjects. 4. We conclude that generalized autonomic nervous dysfunction does not appear to cause haemodialysis-induced hypotension in patients with chronic renal failure on maintenance haemodialysis.

Studies on the Mechanism of Mineralocorticoid-Induced Blood Pressure Increase in Man

1979 ◽  
Vol 57 (s5) ◽  
pp. 303s-305s ◽  
Author(s):  
A. Distler ◽  
T. Philipp ◽  
B. Lüth ◽  
G. Wucherer
Keyword(s):  
Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Pressure Rise ◽  
Sympathetic Tone ◽  
Plasma Noradrenaline ◽  
Steroid Administration ◽  
Arterial Blood ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration

1. To gain insight into the mechanism of mineralocorticoid-induced blood pressure rise in man we performed haemodynamic studies in six normotensive volunteer subjects before and during administration of the synthetic steroid 9α-fluorocortisol (0·8 mg daily) for a period of 6 weeks. In a further study, performed in seven subjects, plasma noradrenaline concentration and reactivity to exogenous noradrenaline were determined before and during administration of the mineralocorticoid. 2. Within the first week of steroid administration an increase in mean arterial blood pressure could be demonstrated, which was due to an increase in cardiac output. After the sixth week the elevated blood pressure was the consequence of an increased total peripheral resistance. 3. Plasma noradrenaline concentration decreased and reactivity to exogenous noradrenaline increased during steroid administration. 4. The mechanism underlying the increase in total peripheral resistance during long-term mineralocorticoid administration remains unclear. Increased sympathetic tone does not seem to be a factor since plasma noradrenaline decreased considerably. Pressor response to noradrenaline increased probably due to decreased sympathetic tone.

Plasma and platelet free catecholamine concentrations in patients with familial hypercholesterolaemia

1992 ◽  
Vol 82 (1) ◽  
pp. 113-116 ◽  
Author(s):  
C. C. T. Smith ◽  
B. N. C. Prichard ◽  
D. J. Betteridge
Keyword(s):  
Familial Hypercholesterolaemia ◽  
Plasma Cholesterol ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Cholesterol Concentration ◽  
Plasma Cholesterol Concentration ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Heterozygous Familial Hypercholesterolaemia ◽  
Noradrenaline Levels

1. Plasma and platelet free catecholamine concentrations were measured in 22 normal subjects and in 10 treated and 11 untreated patients with heterozygous familial hypercholesterolaemia. 2. Plasma noradrenaline concentrations were significantly higher in both treated and untreated hypercholesterolaemic patients than in normal subjects. Adrenaline concentrations did not differ. 3. Platelet noradrenaline levels were higher in untreated hypercholesterolaemic patients than in normal subjects. 4. Positive correlations between the plasma noradrenaline concentration and the platelet noradrenaline concentration were observed in both normal subjects and hypercholesterolaemic patients. 5. Combining the data for normal subjects and hypercholesterolaemic patients revealed that the plasma noradrenaline concentration correlated positively with the plasma cholesterol concentration. The platelet noradrenaline concentration was also found to correlate with the plasma cholesterol concentration. 6. Our results suggest that an increased plasma cholesterol concentration may be associated with increased sympathetic nervous system activity as indicated by elevated plasma and platelet noradrenaline levels. Increases in circulating catecholamines may contribute to the platelet hyperaggregability seen in familial hypercholesterolaemia.

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.

Plasma Noradrenaline Correlates with α-Adrenoreceptor-Mediated Vasoconstriction and Blood Pressure in Patients with Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 177s-180s ◽  
Author(s):  
W. Kiowski ◽  
P. Van Brummelen ◽  
F. R. Bühler
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Essential Hypertension ◽  
Forearm Blood Flow ◽  
Blocking Agent ◽  
Plasma Noradrenaline ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Blood Pressures ◽  
Normotensive Subjects

1. The relationships between plasma noradrenaline concentration at rest and blood pressure, as well as increase in forearm blood flow in response to a brachial artery infusion of the α-adrenoreceptor-blocking agent phentolamine, were investigated in hypertensive and normotensive subjects of similar age. 2. In 44 hypertensive patients plasma noradrenaline correlated with systolic, diastolic and mean blood pressures, but no difference in the mean plasma noradrenaline concentration was found. 3. In 11 patients and 14 normotensive subjects α-adrenoreceptor blockade resulted in a similar increase in forearm blood flow. Only in the patients, however, was this increase related to plasma noradrenaline and blood pressure. 4. In patients with established essential hypertension plasma noradrenaline can be considered to be a marker of α-adrenoreceptor-mediated vasoconstriction, which, in part, determines the height of the blood pressure.

Changes in plasma free 3,4-dihydroxyphenylethylene glycol and noradrenaline levels after acute alcohol administration

1985 ◽  
Vol 69 (4) ◽  
pp. 423-428 ◽  
Author(s):  
L. G. Howes ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Major Effect ◽  
Plasma Noradrenaline ◽  
Normal Male ◽  
Alcohol Administration ◽  
Reflex Tachycardia ◽  
Transient Rise ◽  
Blood Pressures ◽  
Noradrenaline Levels

1. The effects of alcohol (0.9 g/kg) compared with placebo (400 ml of orange juice) on plasma noradrenaline and 3,4-dihydroxyphenylethylene glycol levels, and on erect and supine blood pressures and heart rates, were studied in eight normal male volunteers. 2. Alcohol caused a rise in noradrenaline levels that commenced approximately 30 min after drinking and lasted about 4h. In contrast, 3,4-dihydroxyphenylethylene glycol levels fell immediately after alcohol administration and remained low for at least 6h. Acute alcohol administration alters noradrenaline catabolism, and may have a dual effect of increasing noradrenaline release and decreasing noradrenaline clearance. 3. Alcohol caused a transient rise in erect and supine blood pressures that preceded the rise in plasma noradrenaline. Thereafter erect blood pressures fell compared with control. This fall was associated with a progressive rise in both supine and erect rates, and reached a maximum several hours after the maximum levels of blood alcohol. 4. The major effect of acute alcohol administration is to lower blood pressure and induce a reflex tachycardia. Changes in noradrenaline and 3,4-dihydroxyphenylethylene glycol levels did not readily explain changes in blood pressure or heart rate, suggesting that alcohol induced changes in noradrenaline metabolism occur largely independent of changes in blood pressure and heart rate.

Effects of desmethylimipramine and normetanephrine on calorigenic response and plasma noradrenaline concentration in warm- and in cold-acclimated rats exposed to cold

1983 ◽  
Vol 61 (10) ◽  
pp. 1177-1184 ◽  
Author(s):  
Chi-Chung Chan ◽  
Florent Depocas
Keyword(s):  
Oxygen Consumption ◽  
Cold Exposure ◽  
Plasma Noradrenaline ◽  
Extraneuronal Uptake ◽  
Physiological Conditions ◽  
Plasma Noradrenaline Concentration ◽  
Noradrenaline Concentration ◽  
Time Required ◽  
Noradrenaline Levels

Oxygen consumption and plasma noradrenaline concentration were increased significantly above resting levels in warm-acclimated and in cold-acclimated rats exposed to an ambient temperature of 4 °C. Administration of normetanephrine (1 μg∙min−1∙g body weight−0.74), but not of desmethylimipramine (1 mg∙kg−1), resulted in higher resting plasma noradrenaline levels at 24 °C and increased the length of time required for the oxygen consumption to return to resting levels after cold exposure in both acclimation groups. These observations support a significant role of extraneuronal uptake in noradrenaline inactivation under normal physiological conditions. Calorigenic responses to cold exposure were not affected at all by treatment of animals with desmethylimipramine and (or) normetanephrine in either warm-acclimated or cold-acclimated rats, although an enhancing effect of these uptake inhibitors on plasma noradrenaline was evident in cold-acclimated rats. It is suggested that a peripheral–central thermoregulatory mechanism adjusts activation of thermogenic effectors so as to maintain a steady calorigenic response, appropriate to the thermal demand of the environment, to compensate for changes in perineuronal concentration of noradrenaline in sympathetic thermoeffectors owing to blockade of extraneuronal uptake.

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