Plasma Catecholamines, Plasma Renin Activity and Plasma Aldosterone in Tetraplegic Man, Horizontal and Tilted

1975 ◽  
Vol 49 (4) ◽  
pp. 291-299 ◽  
Author(s):  
C. J. Mathias ◽  
N. J. Christensen ◽  
J. L. Corbett ◽  
H. L. Frankel ◽  
T. J. Goodwins ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Cervical Spinal Cord ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Normal Male ◽  
Head Up Tilt ◽  
The Brain

1. Plasma catecholamines, plasma renin activity, plasma aldosterone and haematocrit were measured in four subjects with physiologically complete cervical spinal cord transections, before, during and after head-up tilt to 45° for 30 min. Plasma catecholamines were measured in five normal male volunteers in the supine position and after head-up tilt to 45° for 10 min. 2. After 10 min of head-up tilt, the plasma noradrenaline rose 14% in the tetraplegic patients and 115% in the control subjects. These findings indicate a failure of sympathetic activity in response to head-up tilt in the tetraplegic patients, probably caused by interruption of pathways by which the brain normally controls sympathetic outflow. 3. In the tetraplegic patients the resting plasma renin activities were above normal, and rose more quickly and greater on head-up tilt than in published studies of normal subjects. It is likely that the renal baroreceptors are important in the control of renin release. 4. In the tetraplegic patients, there was a late rise in plasma aldosterone which was probably due to the elevation in plasma renin activity.

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

1980 ◽  
Vol 59 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M. Epstein ◽  
M. D. Lifschitz ◽  
R. Re ◽  
E. Haber
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Normal Man

1. The relationship of the renin-angiotensin-aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 ± 7%) and plasma aldosterone concentration (55 ± 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin-aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

1981 ◽  
Vol 60 (4) ◽  
pp. 399-404 ◽  
Author(s):  
C. J. Mathias ◽  
H. L. Frankel ◽  
I. B. Davies ◽  
V. H. T. James ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Diastolic Blood Pressure ◽  
Pressor Response ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sympathetic Stimulation

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enhanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.

Changes in Plasma Renin Activity after Hypoglycaemia in Sympathectomized Man

1981 ◽  
Vol 61 (2) ◽  
pp. 245-247 ◽  
Author(s):  
B. M. Frier ◽  
R. J. M. Corrall ◽  
J. L. Pritchard ◽  
P. S. Sever
Keyword(s):  
Spinal Cord ◽  
Plasma Renin Activity ◽  
Cervical Spinal Cord ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Adrenal System ◽  
Glucose Plasma ◽  
Stimulation Of

1. The changes in blood glucose, plasma noradrenaline and plasma renin activity were measured in 11 normal subjects and in six tetraplegic subjects with a transection of the cervical spinal cord (preganglionic sympathectomy), in response to acute insulin-induced hypoglycaemia (0.15 unit/kg). 2. After hypoglycaemia, a pronounced rise in plasma noradrenaline was observed in the normal subjects but was absent in the tetraplegic group; plasma renin activity increased markedly in both groups. 3. It is concluded that the stimulation of renin release in response to hypoglycaemia can occur independently of any activation of the sympatho-adrenal system.

CARDIOVASCULAR HAEMODYNAMICS AND THE RESPONSE OF VASOPRESSIN, ALDOSTERONE, PLASMA RENIN ACTIVITY AND PLASMA CATECHOLAMINES TO HEAD-UP TILT IN YOUNG AND OLD HEALTHY SUBJECTS

1986 ◽  
Vol 15 (1) ◽  
pp. 17-28 ◽  
Author(s):  
ENRIQUE VARGAS ◽  
MICHAEL LYE ◽  
E. BRIAN FARAGHER ◽  
CHRISTOPHER GODDARD ◽  
BILL MOSER ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Healthy Subjects ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Renin Activity ◽  
Head Up Tilt

Effects of an acute calcium load on plasma ACTH, cortisol, aldosterone and renin activity in man

1984 ◽  
Vol 105 (2) ◽  
pp. 251-257 ◽  
Author(s):  
Roland Isaac ◽  
Jean-Paul Raymond ◽  
Muriel Rainfray ◽  
Raymond Ardaillou
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Aldosterone Secretion ◽  
Cortisol Responses ◽  
Calcium Load

Abstract. Plasma adrenocorticotrophin (ACTH), cortisol and aldosterone increased during and after iv administration of calcium gluconate in 4 normal subjects, one patient with hypoparathyroidism and one patient with hypothyroidism. On the other hand, there was a decrease in plasma renin activity but only in the normal subjects. Plasma ACTH and cortisol responses to calcium were abolished whereas plasma aldosterone response persisted in 2 normal subjects pre-treated with dexamethasone. The results observed after calcium administration were compared to those observed after infusion of the solvent only in 6 normal subjects and 4 thyroidectomized patients who were studied twice at 3 day intervals. Plasma ACTH, cortisol and aldosterone were higher when calcium was administered. Plasma renin activity was not statistically different whether or not calcium had been injected in the subjects studied twice. These results demonstrate a direct effect of calcium on ACTH and aldosterone secretion which is not mediated by calcitonin and parathyroid hormone. The stimulatory effect of calcium on cortisol secretion depends on the increase in plasma ACTH.

Lack of effect of Naloxone in a Moderate dosage on the Exercise-Induced Increase in Blood Pressure, Heart Rate, Plasma Catecholamines, Plasma Renin Activity and Plasma Aldosterone in Healthy Males

1985 ◽  
Vol 68 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Margareta Bramnert ◽  
Hökfelt Bernt
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Working Capacity ◽  
Exercise Induced ◽  
Maximal Working Capacity

1. There is evidence that opioid peptides influence blood pressure and heart rate in animals and man. In the present investigation the effect of naloxone on the exercise-induced increase in blood pressure, heart rate, plasma catecholamines, plasma renin activity (PRA) and plasma aldosterone was investigated in nine healthy men. A submaximal work test was performed on two occasions. The test consisted of ergometer bicycling for 10 min on 50% of maximal working capacity immediately followed by 10 min on 80% of maximal working capacity. Ten minutes before exercise the subjects received in a randomized manner a bolus dose of naloxone (10 μg/kg) or a corresponding volume of saline followed by a slow infusion (15 ml/h) of naloxone (5 μ h−1 kg−1) or saline, respectively. 2. After exercise systolic blood pressure, heart rate, plasma catecholamines, PRA and plasma aldosterone increased during both saline and naloxone infusion. The changes were similar in both studies. 3. Accordingly, opiate receptors sensitive to naloxone in a moderate dosage seem not to be involved in the cardiovascular response and the increase in plasma catecholamines, PRA and plasma aldosterone induced by exercise.

The Immediate Pressor Response to Saralasin in Man: Evidence against Sympathetic Activation and for Intrinsic Angiotensin II-Like Myotropism

1984 ◽  
Vol 66 (5) ◽  
pp. 517-524 ◽  
Author(s):  
C. J. Mathias ◽  
R. J. Unwin ◽  
F. A. Pike ◽  
H. L. Frankel ◽  
P. S. Sever ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Cervical Spinal Cord ◽  
Pressor Response ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Sympathetic Activation ◽  
Basal Plasma ◽  
Dose Dependent

1. The cardiovascular and hormonal effects of intravenous saralasin (0.5, 1 and 5 μg min−1 kg−1) were assessed in nine tetraplegic patients (with complete cervical spinal cord transaction above the sympathetic outflow) and in six normal subjects. 2. In the tetraplegic patients, saralasin caused an immediate transient pressor response which was not dose-dependent and substantially greater than the pressor response in normal subjects. The pressor response in the tetraplegic patients was not accompanied by a rise in levels of plasma noradrenaline. 3. In the tetraplegic patients, after α-adrenoceptor blockade with thymoxamine (1 mg kg−1 h−1), twice the dose of intravenous noradrenaline was needed to induce the same pressor response. The pressor response to saralasin (5 μg kg−1 min−1), however, was unaffected by thymoxamine. 4. Saralasin caused minimal changes in levels of plasma renin activity and plasma aldosterone in both groups. There was no relationship between basal plasma renin activity and the pressor response in either group. 5. We therefore conclude that the immediate transient pressor response to saralasin in man is not due to central sympathetic stimulation, is unlikely to be due to peripheral sympathetic activation and is probably the result of intrinsic angiotensin II-like myotropism.

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