Interrelations between age and plasma renin, aldosterone and cortisol, urinary catecholamines, and the body sodium/volume state in normal man

1977 ◽  
Vol 55 (15) ◽  
pp. 725-733 ◽  
Author(s):  
P. Weidmann ◽  
R. Chatel ◽  
Annamarie Schiffmann ◽  
Elfriede Bachmann ◽  
C. Beretta-Piccoli ◽  
...  
2018 ◽  
Vol 32 (1) ◽  
pp. 30-42 ◽  
Author(s):  
Claudia Traunmüller ◽  
Kerstin Gaisbachgrabner ◽  
Helmut Karl Lackner ◽  
Andreas R. Schwerdtfeger

Abstract. In the present paper we investigate whether patients with a clinical diagnosis of burnout show physiological signs of burden across multiple physiological systems referred to as allostatic load (AL). Measures of the sympathetic-adrenergic-medullary (SAM) axis and the hypothalamic-pituitary-adrenal (HPA) axis were assessed. We examined patients who had been diagnosed with burnout by their physicians (n = 32) and were also identified as burnout patients based on their score in the Maslach Burnout Inventory-General Survey (MBI-GS) and compared them with a nonclinical control group (n = 19) with regard to indicators of allostatic load (i.e., ambulatory ECG, nocturnal urinary catecholamines, salivary morning cortisol secretion, blood pressure, and waist-to-hip ratio [WHR]). Contrary to expectations, a higher AL index suggesting elevated load in several of the parameters of the HPA and SAM axes was found in the control group but not in the burnout group. The control group showed higher norepinephrine values, higher blood pressure, higher WHR, higher sympathovagal balance, and lower percentage of cortisol increase within the first hour after awakening as compared to the patient group. Burnout was not associated with AL. Results seem to indicate a discrepancy between self-reported burnout symptoms and psychobiological load.


1984 ◽  
Vol 6 ◽  
pp. S134 ◽  
Author(s):  
Carlo Beretta-Piccoli ◽  
Peter Weidmann ◽  
Jehoiada J. Brown ◽  
David L. Davies ◽  
Anthony F. Lever ◽  
...  

1994 ◽  
Vol 131 (1) ◽  
pp. 74-79 ◽  
Author(s):  
Noriyoshi Yamakita ◽  
Celso E Gomez-Sanchez ◽  
Tomoatsu Mune ◽  
Hiroyuki Morita ◽  
Hisashi Yoshida ◽  
...  

Yamakita N, Gomez-Sanchez CE, Mune T, Morita H, Yoshida H, Miyazaki S, Yasuda K. Simultaneous measurement of plasma 18-oxocortisol and 18-hydroxycortisol levels in normal man. Eur J Endocrinol 1994;131:74–9. ISSN 0804–4643 Plasma 18-oxocortisol (18-oxoF) and 18-hydroxycortisol (18-OH-F) were measured in 47 healthy subjects. Plasma 18-oxoF and 18-OH-F in the early morning were 0.827 ± 0.04 nmol/l and 3.29 ± 0.175 nmol/l, respectively. The plasma levels of both steroids correlated with each other and with cortisol, but not with aldosterone. Postural stimulation with or without furosemide administration increased 18-oxoF, 18-OH-F, aldosterone and plasma renin activity (PRA). Two hours after 2 mg of oral dexamethasone administration or after an overnight 2 mg of dexamethasone suppression cortisol, 18-oxoF and 18-OH-F decreased. Cortisol, aldosterone, 18-oxo-F and 18-OH-F increased after the intravenous administration of 250 μg of 1–24 ACTH. Changes in plasma 18-oxo-F and 18-OH-F levels correlated with PRA change during the posture studies and correlated with the change of ACTH during the dexamethasone studies. The ratios of post-/pre-test values of the postural stimulation and dexamethasone suppression in 18-oxoF and 18-OH-F were lower than that of aldosterone. Plasma 18-oxoF and 18-OH-F are more dependent on ACTH than on the reninangiotensin system. The ratio of 18-OH-F/18-oxoF, which is between 4 and 5, remains constant during the various stimulation or suppression maneuvers. Noriyoshi Yamakita, Department of Internal Medicine, Matsunami General Hospital, Kasamatsu, GifuPrefecture, 501-61 Japan


1992 ◽  
Vol 262 (5) ◽  
pp. R915-R920 ◽  
Author(s):  
S. Benlamlih ◽  
K. Dahlborn ◽  
R. Z. Filali ◽  
J. Hossaini-Hilali

When dehydrated camels are offered water they drink volumes of water exceeding their body water loss during the water deprivation period. The excess water is excreted during 2-4 days. To investigate the ability to retain fluid in the body, normohydrated camels were loaded with water or isotonic saline (0.1 l/kg body wt) by esophageal tube. After water loading plasma osmolality decreased and a water diuresis was seen, but it took 3 days until the body weight returned to prehydration level. Plasma aldosterone concentration (PAC) increased, but plasma renin activity (PRA) and plasma atrial natriuretic peptide (ANP) concentration did not change. After the saline loading plasma osmolality increased and total plasma proteins and hematocrit decreased. Renal Na excretion increased 4 h after the saline load, but the magnitude of the natriuresis was small, and the camels had not regained their body weight 6 days after the load. PAC and PRA decreased after saline loading, while plasma ANP concentration did not change. These data show that camels are able to retain excess water within the body and to tolerate blood hyposmolality for a relatively long time. With saline the retention of fluid lasts even longer despite an attenuation of PAC.


1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.


1994 ◽  
Vol 267 (5) ◽  
pp. E642-E647
Author(s):  
G. B. Pidgeon ◽  
A. M. Richards ◽  
M. G. Nicholls ◽  
R. R. Bailey ◽  
K. L. Lynn ◽  
...  

To assess the effects of ouabain on pressor and vasoactive hormone responsiveness, 10 healthy volunteers were pretreated with ouabain (0.5 mg i.v. 42 and 18 h before study) or placebo before pressor challenge with angiotensin II (ANG II; 2, 4, and 8 ng.kg-1.min-1 for 30 min/dose) and norepinephrine (NE; 5, 15, and 45 ng.kg-1.min-1 for 15 min/dose). There were no differences at baseline between the two study days regarding mean arterial pressure (MAP) or heart rate. Baseline pulse pressure, however, was significantly greater after ouabain (47 +/- 3 vs. 41 +/- 1 mmHg; P < 0.05). The mean maximum increments in MAP during ANG II and NE infusions were 17.5 +/- 1.1 and 10.5 +/- 1.3 (SE) mmHg, respectively, after ouabain and 19.2 +/- 1.3 and 10.4 +/- 1.5 mmHg after placebo (not significant). The mean heart rate was lower during both infusion periods on the ouabain study day compared with control (P < 0.05). Baseline plasma levels of ANG II, aldosterone, plasma renin activity, atrial and brain natriuretic peptide, guanosine 3',5'-cyclic monophosphate, NE, and epinephrine and achieved levels during the two infusions were similar on the two study days. We conclude that short-term ouabain administration does not alter pressor responsiveness or plasma levels of vasoactive hormones in healthy volunteers.


1972 ◽  
Vol 71 (2) ◽  
pp. 321-330 ◽  
Author(s):  
H. Hedeland ◽  
J.-F. Dymling ◽  
B. Hökfelt

ABSTRACT The present study was concerned with the relation of catecholamine production and plasma renin activity. The catecholamine production was measured as the urinary excretion of noradrenaline and adrenaline. Thirteen subjects were studied under basal conditions and also following insulin induced hypoglycaemia both before and during treatment with the imidazoline derivate clonidine. Before clonidine, hypoglycaemia produced a marked increase in catecholamine production and an elevation of plasma renin activity. These parameters were significantly correlated. Treatment with clonidine markedly suppressed noradrenaline production and plasma renin activity. Adrenaline production showed a minor decrease. During clonidine treatment insulin induced pronounced hypoglycaemia. In spite of this the increase in adrenaline production and plasma renin activity was less marked as compared to that before clonidine. There was no longer any significant correlation between catecholamine production and plasma renin activity. Our results indicate that sympathetic amines liberated from the adrenal medulla and/or the sympathetic nerve endings can stimulate renin production.


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