The Sympathetic Nervous System and the Renin-Angiotensin System in Borderline Hypertension

1981 ◽  
Vol 60 (1) ◽  
pp. 25-31 ◽  
Author(s):  
J. W. Henquet ◽  
T. Kho ◽  
M. Schols ◽  
H. Thijssen ◽  
K. H. Rahn

1. Plasma catecholamine levels as well as plasma renin activity and plasma renin concentration were compared in normotensive volunteers and in subjects with borderline hypertension. All subjects were studied at rest and during bicycle ergometry. 2. The two groups of volunteer subjects did not differ in the plasma concentrations of noradrenaline and adrenaline, both at rest and during physical activity. The same was true for plasma renin activity and plasma renin concentration. Furthermore, urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxymandelic acid was similar in both groups. 3. The results do not support the assumption that there is increased sympathetic activity in subjects with borderline hypertension.

1969 ◽  
Vol 44 (2) ◽  
pp. 231-NP ◽  
Author(s):  
I. A. REID ◽  
I. R. McDONALD

SUMMARY Using an enzyme kinetic technique, a substance with the properties of renin was assayed in extracts of kidney and peripheral blood from the Australian marsupial Trichosurus vulpecula. The renin concentration in peripheral venous plasma varied from 10 to 855 units/ml. and plasma renin activity from 1·0 to 3·6 ng. angiotensin/ml./hr. High plasma renin concentration and plasma renin activity was associated with an appetite for salt and were significantly reduced by ingestion of 0·9% NaCl solution. Animals with low renin levels did not have a salt appetite. Sodium deficiency caused by mercurial and non-mercurial diuretics increased plasma renin concentration and plasma renin activity, and induced an appetite for salt. Plasma renin concentration and plasma renin activity also increased after haemorrhage. Granulation of juxtaglomerular cells, demonstrated with Bowie's stain, increased considerably during sodium deficiency. It is concluded that T. vulpecula has the eutherian type of renin—angiotensin system.


1982 ◽  
Vol 101 (2) ◽  
pp. 242-247 ◽  
Author(s):  
Masanobu Uda ◽  
Noboru Sakamoto ◽  
Masayuki Tsuchiya ◽  
Keiichi Ito ◽  
Masao Ikeda ◽  
...  

Abstract. To investigate the roles of the sympatheticoadrenomedullary system and the renin-angiotensin system in the pathogenesis of essential hypertension, the levels of plasma catecholamine and plasma renin activity (PRA) after glucagon-stimulation were evaluated. In 9 patients with essential hypertension whose levels of PRA were either normal or high (NHREH), iv bolus injection of 1 mg glucagon caused a rapid and significant increase in plasma epinephrine concentration from the basal values of 170 ± 25 pg/ml, mean ± sem to 314 ± 30 pg/ml (P < 0.05) at 5 min after the injection, reaching the mean peak values of 358 ± 87 pg/ml (P < 0.05). Plasma norepinephrine also rose from the basal values of 357 ± 50 pg/ml to the peak values of 1065 ± 231 pg/ml (P < 0.02) while increase in PRA was detected in 4 of 9 patients. In 7 patients with low renin essential hypertension (LREH), plasma epinephrine failed to increase after glucagon stimulation whereas plasma norepinephrine increased significantly from the basal values of 391 ± 77 pg/ml, reaching 1212 ± 274 pg/ml at their peak values (P < 0.01). There was no discernible response of PRA to glucagon. These results suggest that both epinephrine secretion from adrenal medulla and renin release from juxtaglomerular (JG) cells after glucagon injection are impaired in LREH in contrast to their significant responses observed in NHREH. It also indicates that glucagon load may be useful for the simultaneous assessment of the reserve of both renin secretion and sympatheticoadrenomedullary function in essential hypertension.


1983 ◽  
Vol 64 (5) ◽  
pp. 463-470
Author(s):  
Y. Takata ◽  
A. E. Doyle ◽  
M. Veroni ◽  
S. G. Duffy

1. Blood pressure, the hypotensive effect of captopril, plasma renin activity, renal renin content and kidney weight were measured in the two-kidney—one-clip model, the one-kidney—one-clip model and the two-kidney—one-clip model with the ureter of the contralateral kidney ligated in rats. The ureteric ligation was performed to abolish urinary excretion from the contralateral kidney in the two-kidney—one-clip model. 2. The development of hypertension after renal artery constriction was earlier and greater in the one-kidney—one-clip model and the two-kidney—one-clip model with ureter of the contralateral kidney ligated than in the two-kidney—one-clip model. A single oral dose of captopril produced a greater fall in blood pressure in both the two-kidney models than in the one-kidney—one-clip group. 3. Plasma renin activity and renal renin content of the clipped kidney were higher in the two-kidney model rats, whether or not the ureter had been ligated, than in the one-kidney—one-clip model animals, although more than half the rats from the two-kidney model had normal values. There was a significant correlation between plasma renin activity and the response to captopril in all groups, whereas in none of the three groups was the correlation between plasma renin activity and blood pressure significant. 4. The clipped kidney had a higher renin content than did the contralateral kidney, and the weight of the ischaemic kidney was decreased compared with the contralateral kidney whether it was untouched or had its ureter ligated. The weight of the clipped kidney was in the order one-kidney—one-clip model > two-kidney—one-clip model with ureter of the contralateral kidney ligated > two-kidney—one-clip model. 5. It was concluded that the renin-angiotensin system was stimulated to the similar degree in some animals for the two-kidney—one-clip models, whether or not the ureter of the contralateral kidney had been ligated, compared with the one-kidney—one-clip animals. This finding suggests that the contralateral kidney can stimulate renin secretion and synthesis in the clipped kidney independently of Na+ excretion.


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.


1975 ◽  
Vol 80 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Helmut Armbruster ◽  
Wilhelm Vetter ◽  
Rainer Beckerhoff ◽  
Jürg Nussberger ◽  
Hans Vetter ◽  
...  

ABSTRACT In order to investigate the role of renin secretion and of ACTH on the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), plasma cortisol (PC) and PA were determined at short-time intervals in 10 normal supine men. Six subjects were studied under a normal sodium intake and 4 under sodium restriction. In 4 subjects the secretion of ACTH was suppressed by dexamethasone. Under normal sodium intake changes in PA seemed to be more in parallel with changes in PC than by those in PRA as indicated by a higher significant correlation between PA and PC than between PA and PRA in 3 of the 4 subjects. In 1 subject no correlation was observed between PA and PC despite visual synchronism between the plasma concentrations of both hormones. Under dexamethasone medication fluctuations in PA were followed by those in PRA while PC was less than 2 μg/100 ml. In the sodium restricted state, changes in PA were closely paralleled and significantly correlated to PRA while no correlation was seen between PA and PC. Under dexamethasone medication the significant correlation between PA and PRA persisted. Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake.


1980 ◽  
Vol 59 (s6) ◽  
pp. 101s-103s ◽  
Author(s):  
J. R. Sowers ◽  
M. L. Tuck ◽  
J. Barrett ◽  
M. P. Sambhi ◽  
M. S. Golub

1. In rats, intra-arterial metoclopramide, a dopamine antagonist, resulted in an elevation of plasma aldosterone at 5 min and plasma renin activity at 10 min and peak aldosterone and renin responses at 10 and 30 min respectively. 2. Pre-administration of l-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. 3. Pre-administration of angiotensin converting enzyme inhibitor, captopril (SQ 14 225) and the angiotensin II antagonist, saralasin, as well as bilateral nephrectomy did not significantly affect the aldosterone response to metoclopramide, Thus dopaminergic modulation of aldosterone secretion occurs independently of alterations in the renin-angiotensin system. 4. Modulating effects of dopamine on plasma aldosterone are probably mediated by direct effects as well as by interaction with other factors influencing aldosterone secretion at the adrenal zona glomerulosa.


1983 ◽  
Vol 65 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Michiko Handa ◽  
Kazuoki Kondo ◽  
Hiromichi Suzuki ◽  
Takao Saruta

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.


1979 ◽  
Vol 56 (3) ◽  
pp. 255-259 ◽  
Author(s):  
A. C. Burden ◽  
H. Thurston

1. The plasma renin activity (PRA) was measured in 76 diabetic patients who were attending an outpatients clinic. Of these patients 16 had untreated hypertension and 28 had diabetic complications, which ranged from microaneurysms to renal failure and blindness. 2. Compared with age- and sex-matched normotensive control subjects, both normotensive and hypertensive diabetic patients had significantly higher PRA (P < 0·001). 3. Hypertensive diabetic patients also showed a higher PRA than matched hypertensive control subjects (P < 0·005). There were no significant differences between diabetic patients with hypertension or complications compared with those without these features. 4. Although this elevation of PRA could be due to a change in another component of the renin—angiotensin system, hypersecretion of renin is the most likely explanation.


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