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.

Plasma Catecholamines and Blood Pressure Responses to the Carotid Baroreceptor Reflex in Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 165s-167s ◽  
Author(s):  
G. Mancia ◽  
G. Leonetti ◽  
G. B. Picotti ◽  
A. Ferrari ◽  
M. D. Galva ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Plasma Catecholamines ◽  
Variable Pressure ◽  
Carotid Baroreceptor ◽  
Pressure Variable ◽  
Blood Pressure Responses ◽  
Neck Chamber ◽  
Noradrenaline And Adrenaline

1. Slight decreases and increases in carotid baroreceptor activity were induced in subjects with essential hypertension by slight alterations in carotid transmural pressure (variable pressure neck-chamber technique) in order to obtain limited increases and reductions in sympathetic adrenergic activity. 2. When sympathetic activity was reflexly increased there was a rise in arterial pressure but no significant increase in plasma catecholamines. Likewise when sympathetic activity was reflexly reduced there was a fall in arterial pressure but no significant reduction in plasma catecholamines. 3. Plasma noradrenaline and adrenaline significantly and markedly increased in the same subjects when sympathetic activity was increased by activation of both arterial and low pressure baroreceptor reflexes with tilting. 4. It is suggested that measurements of catecholamines in systemic plasma may reveal marked degrees of sympathetic activation but may not be a sensitive index of more moderate changes in sympathetic tone.

Plasma Catecholamines and Plasma Renin Activity at Birth and during the First Days of Life

1980 ◽  
Vol 59 (s6) ◽  
pp. 319s-321s ◽  
Author(s):  
G. Leonetti ◽  
C. Bianchini ◽  
G. B. Picotti ◽  
A. Cesura ◽  
Letizia Caccamo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Umbilical Cord Blood ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Plasma Adrenaline ◽  
Noradrenaline And Adrenaline ◽  
Noradrenaline Levels

1. Plasma noradrenaline and adrenaline concentrations and plasma renin activity were measured in 21 mothers at delivery and in their babies at birth (umbilical cord blood) and on days 1 and 5 of extrauterine life. 2. At birth plasma renin activity was significantly higher in the newborn than in mothers. Plasma renin activity increased further, but not significantly, on day 1 of life and significantly decreased on day 5. On day 5, 10 min head-up tilting caused no change in plasma renin activity. 3. Plasma noradrenaline in the newborn was higher than in mothers at birth and significantly decreased thereafter. Plasma adrenaline levels at birth were similar in the newborn and their mothers and significantly lower in the newborn in subsequent days. Tilting caused no increase in either plasma adrenaline or noradrenaline levels. 4. No correlation was found between plasma noradrenaline and adrenaline levels and plasma renin activity, or between noradrenaline, adrenaline or plasma renin activity and blood pressure.

Differential cardiovascular effects of central clonidine and B-HT 920 in conscious rats

1988 ◽  
Vol 66 (11) ◽  
pp. 1455-1460 ◽  
Author(s):  
Kathryn A. King ◽  
Catherine C. Y. Pang
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Cardiovascular Effects ◽  
Plasma Noradrenaline ◽  
Adrenoceptor Agonists ◽  
Noradrenaline And Adrenaline ◽  
Prior Administration

The effect of intracerebroventricular (i.c.v.) injection of the α2-adrenoceptor agonists clonidine and B-HT 920 on mean arterial pressure (MAP), heart rate (HR), and plasma concentrations of noradrenaline and adrenaline was examined in conscious unrestrained rats. The injection of 1.0 μg clonidine significantly decreased MAP and slightly decreased HR. Plasma noradrenaline and adrenaline levels were slightly but not significantly decreased after the injection of 1 μg clonidine. In contrast, the injection of 0.1–10.0 μg B-HT 920 increased MAP and decreased HR. Plasma noradrenaline and adrenaline levels were slightly increased after the injection of the 1- and 10-μg doses. The i.c. v. injection of the α2-antagonist rauwolscine slightly but not significantly increased MAP and plasma noradrenaline and adrenaline levels. The responses to i.c. v. injection of clonidine and B-HT 920 were not changed by prior administration of rauwolscine. Neither the pressor response to B-HT 920 nor the depressor response to clonidine was abolished by rauwolscine, suggesting that neither response was mediated by α2-adrenoceptors.

Plasma catecholamines in pregnancy induced hypertension

1986 ◽  
Vol 71 (1) ◽  
pp. 111-115 ◽  
Author(s):  
Peter C. Rubin ◽  
Lucy Butters ◽  
Rosemary McCabe ◽  
John L. Reed
Keyword(s):  
Blood Pressure ◽  
Post Partum ◽  
Plasma Concentrations ◽  
Plasma Noradrenaline ◽  
Pregnancy Induced Hypertension ◽  
Noradrenaline Concentration ◽  
Induced Hypertension ◽  
Sympathetic Nervous ◽  
Noradrenaline And Adrenaline ◽  
In Pregnancy

1. Increased activity of the sympathetic nervous system has been implicated in the genesis of early hypertension in young people. Studies in pregnancy allow observations to be made on evolving, recently established and resolving hypertension in the human. We describe the results of two studies involving women who developed hypertension during pregnancy. 2. In the first study, plasma concentrations of noradrenaline and adrenaline were measured in 17 women with pregnancy induced hypertension (PIH) and 17 normotensive pregnant control subjects. Plasma noradrenaline (nmol/l) was lower in the PIH group compared with control patients in both semi-recumbent (1.11 ± 0.53 vs 1.98 ± 0.96, P < 0.001) and standing positions (1.31 ± 0.65 vs 2.57 ± 1.27, P < 0.005). Five days post partum, plasma noradrenaline had risen in the PIH group compared with pregnant values in semi-recumbent (1.65 ± 1.0 vs 1.11 ± 0.52, P < 0.05) and standing positions (2.46 ± 1.5 vs 1.31 ± 0.65, P < 0.05). In the normotensive patients plasma noradrenaline did not differ between post partum and pregnant values (1.51 ± 0.73 vs 1.98 ± 0.96 semi-recumbent; 2.00 ± 1.16 vs 2.57 ± 1.7 standing). 3. Logarithmic transformation of the noradrenaline concentration data resulted in a significant (P < 0.02) negative correlation with diastolic blood pressure in the pregnant patients but not post partum. Plasma adrenaline concentration was the same in both groups. 4. In the second study, plasma concentrations of noradrenaline and adrenaline were measured sequentially through pregnancy in five women who developed PIH and five control subjects who remained normotensive. There was no difference in catecholamine concentrations between groups at any stage, but noradrenaline concentration tended to fall as blood pressure rose in the PIH patients. 5. We conclude that the sympathetic nervous system does not contribute to the development of PIH but responds to the increased blood pressure with decreased activity.

Brain Angiotensin II Stimulates Release of Pituitary Hormones, Plasma Catecholamines and Increases Blood Pressure in Dogs

1980 ◽  
Vol 59 (s6) ◽  
pp. 53s-56s ◽  
Author(s):  
B. A. Schölkens ◽  
W. Jung ◽  
W. Rascher ◽  
A. Schömig ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Antidiuretic Hormone ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Pressure Effects ◽  
Conscious Dogs ◽  
Arterial Blood

1. The mechanisms of central angiotensin II blood pressure effects in conscious dogs on normal or sodium-deficient diets were examined. 2. The biosynthesis of brain angiotensin II in cerebrospinal fluid from its local precursor angiotensinogen was induced in vivo by injection of 0.5 unit of hog kidney renin through a chronically implanted cannula into the third brain ventricle in conscious dogs. 3. Intracerebroventricular administration of renin induced an increase of arterial blood pressure and a marked drinking response under both dietary regimens. Sodium restriction had no effect on the magnitude of the central angiotensin pressor response. 4. Plasma concentrations of renin and angiotensin II decreased, and plasma antidiuretic hormone, noradrenaline, adrenaline and corticosterone increased, in both groups of dogs. 5. Simultaneous intraventricular administrations of captopril with renin inhibited the central renin effects. Intracerebroventricular injections of [Sar1, Val5, Ala8] angiotensin II alone increased plasma renin and angiotensin II concentrations. 6. It is concluded that endogenous brain angiotensin II participates in central mechanisms of blood pressure regulation by the stimulation of the release of antidiuretic hormone, adrenocorticotrophic hormone, adrenaline and noradrenaline.

Plasma Catecholamines and the Pressor Response to Sar1-Ala8-Angiotensin II in Man

1977 ◽  
Vol 53 (4) ◽  
pp. 341-348
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham ◽  
C. R. Benedict
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Dialysis Patients ◽  
Anephric Patients ◽  
Change In Mean

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemodialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5–6 min, occurred in all normal subjects, patients with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P < 0·02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P < 0·05) and was similar to the response to 5 min of a 40° head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P < 0·005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P < 0·001) and angiotensin II (P < 0·001), directly related to blood volume (P < 0·001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.

Antihypertensive Effects of Clonidine in Tetraplegic Subjects Devoid of Central Sympathetic Control

1979 ◽  
Vol 57 (s5) ◽  
pp. 425s-428s ◽  
Author(s):  
C. J. Mathias ◽  
J. L. Reid ◽  
L. M. H. Wing ◽  
H. L. Frankel ◽  
N. J. Christensen
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Cervical Spinal Cord ◽  
Pressor Response ◽  
Plasma Noradrenaline ◽  
Marked Rise ◽  
Indwelling Catheters ◽  
Oral Clonidine ◽  
Noradrenaline And Adrenaline

1. The effects of 300 μg of oral clonidine on blood pressure, heart rate, plasma noradrenaline and adrenaline concentrations were studied in seven tetraplegic subjects with physiologically complete cervical spinal cord transections. 2. Clonidine did not significantly change resting blood pressure during the 8 h of the study. Resting heart rate fell. Resting plasma noradrenaline and adrenaline concentrations, when measured 2 h after clonidine, were not significantly lower. 3. Urinary bladder stimulation resulted in a marked rise in blood pressure accompanied by an elevation in plasma noradrenaline but not adrenaline. The hypertensive response to bladder stimulation was substantially reduced by clonidine, the maximum suppression occurring 2–4 h after administration of the drug. The plasma noradrenaline response to bladder stimulation, when measured 2 h after clonidine, was significantly lower than the response before clonidine. In two tetraplegic subjects with indwelling catheters the rise in intravesical pressure caused by bladder stimulation was unchanged by clonidine. 4. The pressor response to intravenous noradrenaline in two tetraplegic subjects and to intravenous phenylephrine in a further two tetraplegic subjects was unchanged by clonidine. 5. Clonidine may have additional antihypertensive effects which occur independently of actions in the brain. These effects may be exerted by an action either on sympathetic neurones in the spinal cord or on presynaptic α-adrenoreceptors in the periphery.

Plasma Concentrations of Catecholamines in Two Strains of Spontaneously Hypertensive Rats at Different Ages

1981 ◽  
Vol 61 (s7) ◽  
pp. 199s-202s ◽  
Author(s):  
P. Ferrari ◽  
G. B. Picotti ◽  
E. Minotti ◽  
G. P. Bondiolotti ◽  
A. M. Caravaggi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Concentrations ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Adult Rats ◽  
Plasma Adrenaline ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Normotensive Strain ◽  
Noradrenaline And Adrenaline

1. Blood pressure was measured and plasma levels of noradrenaline and adrenaline were determined radioenzymatically under basal conditions and after 10% blood volume reduction in blood drawn through catheters previously implanted in young and adult rats of two different genetically hypertensive strains: the Kyoto strain (SHR) and the Milan strain (MHS), and in their respective controls: Wistar—Kyoto strain (WKY) and Milan normotensive strain (MNS). 2. Under basal conditions no differences were observed between plasma noradrenaline and adrenaline levels in SHR and MHS rats and in the controls, at any age. Haemorrhage produced a greater fall in the blood pressure (P &lt; 0.01) of young and adult hypertensive strains (SHR-MHS) than in WKY and MNS rats, and a greater rise in plasma adrenaline (P &lt; 0.01). 3. These results suggest that: (a) there may be differences in involvement of the sympathetic nervous system in the pathogenesis of hypertension in SHR and MHS rats but not such as to cause differences in plasma catecholamine levels in either young or adult rats; (b) haemorrhage activates the sympatho—adrenal systems more in SHR and MHS rats, than in controls, and the greater percentage fall in blood pressure is probably due to a difference in reflex venoconstriction.

Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

1982 ◽  
Vol 242 (2) ◽  
pp. H185-H190 ◽  
Author(s):  
B. G. Wallin ◽  
D. L. Eckberg
Keyword(s):  
Sympathetic Activity ◽  
Chamber Pressure ◽  
Reduced Pressure ◽  
Cardiac Responses ◽  
Carotid Baroreceptor ◽  
Sympathetic Responses ◽  
Nerve Muscle ◽  
Neck Pressure ◽  
Pressure Changes ◽  
Neck Chamber

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.

Adrenomedullary pressor responses to stimulation of the rostral hypothalamus in the rat: influence of adrenaline-induced vasodilation and reflex cardioinhibition

1988 ◽  
Vol 66 (2) ◽  
pp. 213-221
Author(s):  
Pierre Gauthier
Keyword(s):  
Pressor Response ◽  
Primary Phase ◽  
Anterior Hypothalamus ◽  
Plasma Noradrenaline ◽  
Current Response ◽  
Adrenergic Blockade ◽  
Hypothalamic Region ◽  
Pressor Responses ◽  
Noradrenaline And Adrenaline ◽  
Stimulation Of

Electrical stimulation (100 Hz, 1 ms, 150 μA, 10 s) of the anterior hypothalamus in chloralose-anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in arterial pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response was accompanied by an increase in plasma noradrenaline and adrenaline levels. Peripheral sympathectomy with guanethidine selectively abolished the primary phase of the biphasic pressor response, while bilateral removal of the adrenal medulla eliminated only the secondary component. After α-adrenergic blockade with phentolamine, the primary phase of the stimulation-induced response was reduced while the secondary pressor component was blocked and replaced by a significant hypotension. The intravenous administration of sotalol enhanced the secondary pressor component without affecting the stimulation-induced plasma noradrenaline and adrenaline responses. After treatment with atropine, the secondary pressor effect was also potentiated, as the reflex bradycardia normally associated with the response was eliminated. A subsequent administration of sotalol in these rats further potentiated the secondary pressor component to stimulation. In rats treated with atropine and sotalol, the sympathetic vasomotor and the adrenomedullary pressor responses could be dissociated according to thresholds and stimulus frequency or current–response characteristics. The results suggest that in intact rats, adrenaline-induced vasodilation and reflex cardiac inhibition contribute to either reduce or mask the adrenomedullary component of the biphasic pressor response evoked by stimulation of the anterior hypothalamus. The study also raises the hypothesis of a dual regulation of both components of the sympathetic system in the anterior hypothalamic region.

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