Noradrenaline Secretion by the Human Kidney

1978 ◽  
Vol 55 (s4) ◽  
pp. 85s-87s ◽  
Author(s):  
P. W. De Leeuw ◽  
H. E. Falke ◽  
R. Punt ◽  
W. H. Birkenhäger

1. In 20 subjects with uncomplicated essential hypertension, 10 of whom were on propranolol treatment, several blood samples were drawn simultaneously from the renal artery and vein after angiographic studies. In these samples we determined concentrations of noradrenaline, active renin, aldosterone and cortisol. 2. Renal blood flow was measured in all patients by Hippuran-clearance and xenon-washout. 3. Despite marked variations in the arteriovenous difference of noradrenaline, it was apparent in both groups that the kidney is able to release noradrenaline. 4. In the propranolol-treated group noradrenaline secretion by the kidney was enhanced when compared with untreated hypertensive patients.

1978 ◽  
Vol 55 (s4) ◽  
pp. 147s-149s
Author(s):  
W. H. Birkenhäger ◽  
P. W. De Leeuw ◽  
H. E. Falke ◽  
G. A. W. Van Soest

1. 20 subjects with uncomplicated essential hypertension were studied, 10 of whom were on propranolol treatment. Several blood samples for determination of total and active renin were drawn simultaneously from the renal artery and vein after angiographic studies. 2. In all patients renal blood flow was measured by Hippuran-clearance at the time of blood sampling. Intrarenal blood flow was assessed by xenon-washout. 3. The results indicate that under basal conditions renin is secreted mainly in the active form, although secretion of inactive renin does occur. During propranolol treatment there is a tendency for secretion of active renin to be reduced.


2009 ◽  
Vol 55 (5) ◽  
pp. 867-877 ◽  
Author(s):  
Duncan J Campbell ◽  
Juerg Nussberger ◽  
Michael Stowasser ◽  
A H Jan Danser ◽  
Alberto Morganti ◽  
...  

AbstractBackground: Measurement of plasma renin is important for the clinical assessment of hypertensive patients. The most common methods for measuring plasma renin are the plasma renin activity (PRA) assay and the renin immunoassay. The clinical application of renin inhibitor therapy has thrown into focus the differences in information provided by activity assays and immunoassays for renin and prorenin measurement and has drawn attention to the need for precautions to ensure their accurate measurement.Content: Renin activity assays and immunoassays provide related but different information. Whereas activity assays measure only active renin, immunoassays measure both active and inhibited renin. Particular care must be taken in the collection and processing of blood samples and in the performance of these assays to avoid errors in renin measurement. Both activity assays and immunoassays are susceptible to renin overestimation due to prorenin activation. In addition, activity assays performed with peptidase inhibitors may overestimate the degree of inhibition of PRA by renin inhibitor therapy. Moreover, immunoassays may overestimate the reactive increase in plasma renin concentration in response to renin inhibitor therapy, owing to the inhibitor promoting conversion of prorenin to an open conformation that is recognized by renin immunoassays.Conclusions: The successful application of renin assays to patient care requires that the clinician and the clinical chemist understand the information provided by these assays and of the precautions necessary to ensure their accuracy.


1975 ◽  
Vol 48 (5) ◽  
pp. 391-403 ◽  
Author(s):  
J. P. Grünfeld ◽  
D. Kleinknecht ◽  
J. F. Moreau ◽  
P. Kamoun ◽  
J. Sabto ◽  
...  

1. In forty-one patients who underwent renal homotransplantation the following measurements were made: (a) blood flow and its distribution in the transplanted kidney as measured by the 85Kr washout method; (b) renin release in the renal vein of the transplant; (c) arteriovenous difference in plasma renin activity (PRA) of the recipient's remaining left kidney. 2. Eleven transplanted patients were normotensive. Renal haemodynamic data were comparable with those obtained in potential kidney donors. 3. Three hypertensive patients had chronic rejection. The mean renal blood flow and the percentage of flow in the first component of the washout curve were reduced. Renin release from the transplant, however, was normal. 4. Ten hypertensive patients had transplant artery stenosis. In eight of them renin release from the graft as well as peripheral PRA were within normal range. This result is similar to experimental data obtained in Goldblatt renovascular hypertension. The two patients with the tightest artery stenosis had an elevated renin release from the transplant. 5. Thirteen hypertensive patients had elevated arteriovenous difference in PRA of the recipient's own left kidney. Peripheral PRA was significantly higher than in normotensive patients. Left nephrectomy relieved hypertension in ten of them; three have not so far undergone nephrectomy. 6. In four other cases hypertension was also relieved by removal of the patient's own kidney; however, the arteriovenous difference in PRA of that kidney fell within normal range.


1979 ◽  
Vol 56 (2) ◽  
pp. 115-120 ◽  
Author(s):  
F. H. M. Derkx ◽  
G. J. Wenting ◽  
A. J. Man In't Veld ◽  
R. P. Verhoeven ◽  
M. A. D. H. Schalekamp

1. In eight patients with essential hypertension (EHT) and six patients with renovascular hypertension (RVHT) peripheral venous enzymatically active and inactive renin values were followed after acute stimulation of renin release by the vasodilating agent diazoxide (300 mg intravenously). Active renin rose during the first hour after diazoxide and remained high during the following 15 h, but inactive renin fell during the first hour and rose thereafter. Peripheral venous active and inactive renin were not different from arterial values both before and after diazoxide. 2. Sixteen patients with EHT received propranolol, 80 mg, four times a day. Six of them had a first injection of diazoxide the day before propranolol was started and a second one after 10–14 days of propranolol treatment. Peripheral vein active renin was lowered by propranolol, but inactive renin was raised. Both the diazoxide-induced rapid rise of active renin and the fall of inactive renin observed in untreated patients were absent during treatment with propranolol. 3. In four patients with EHT and seven patients with RVHT renal vein sampling was performed before and 30 min after diazoxide. Increased release of active renin from kidneys that were not markedly contracted was associated with a fall of the renal vein to peripheral vein ratio of inactive renin to a value less than one. 4. It is concluded that under certain circumstances stimulated release of active renin is associated with removal of inactive renin from the circulation by the kidney. This may in fact be due to intrarenal transformation of circulating inactive renin into its active counterpart. The findings suggest that a β-adrenoreceptor might be involved in this activation process.


1980 ◽  
Vol 59 (s6) ◽  
pp. 477s-478s ◽  
Author(s):  
P. W. De Leeuw ◽  
R. Punt ◽  
W. H. Birkenhager

1. Fifty-five patients with uncomplicated essential hypertension were admitted to hospital, where 25 of them were treated with propranolol (average daily dose 240 mg) and 30 were left untreated. 2. In all of them renal arteriography was carried out, after which procedure renal plasma flow ([123I]hippuran clearance), cortical blood flow (xenon washout) and renal noradrenaline release were measured. 3. Compared with the untreated hypertensive patients, responders to propranolol (mean blood pressure ≤ 110 mmHg) during treatment showed enhanced cortical blood flow and reduced noradrenaline secretion. Non-responders had reduced cortical flow rates, but increased noradrenaline secretion. 4. Both in the untreated group and in the propranolol-treated group an inverse relationship between arterial noradrenaline concentration and cortical blood flow was found. 5. The results indicate that sympathetic activity may be an important determinant of renal blood flow in hypertension. The effectiveness of propranolol seems to depend upon a reduction in α-adrenergic tone.


2017 ◽  
Vol 6 (8) ◽  
pp. 5446
Author(s):  
Reddy I.J. ◽  
Ashish Mishra ◽  
Mondal S.

The objective of this study was to establish the effects of red spectrum of light (650nm, treated n=12) and normal spectrum of light (450nm control=12) on GnRH-I and GnIH mRNA expression, amplitude and frequency of luteinizing hormone (LH) and egg production from 42 to 52 weeks of age in white leghorn hens. Blood samples were collected at weekly interval from both the groups. At the 47th week of age blood samples from both the groups were collected at every 3 h for 36h to study the pulsatile secretion of LH surges. GnRH and GnIH mRNA expression pattern was studied between control and treated birds. Egg production and pause days were calculated between the two groups. LH concentration in the plasma was increased significantly (P<0.01) in hens exposed to red spectrum of light. Plasma LH concentration was higher (P<0.01) in treated birds with more number of LH surges. The amplitude and frequencies of LH were advanced in birds exposed to red spectrum of light during 36 h of sampling at 3h intervals. GnRH-I mRNA concentration was significantly (P<0.01) higher, whereas GnIH mRNA was significantly (P<0.01) lower in birds exposed to red spectrum of light compared to controls. It is hypothesized that exposure of birds to red spectrum of light enhanced (P<0.01) GnRH-I mRNA, along with LH required for ovulation and egg lay. During 77 days (42-52 weeks of age) of the experimental period, egg production was increased (p<0.01) with lower incidence of pause days in the treated group. It is concluded that low GnIH mRNA and higher levels of GnRH-I mRNA, LH, lower number of pause days enabled the birds to lay more eggs by stimulating GnRH through red spectrum of light.


1985 ◽  
Vol 185 (3) ◽  
pp. 207-215 ◽  
Author(s):  
C. Merkel ◽  
P. P. Cagol ◽  
P. P. Da Pian ◽  
M. Bolognesi ◽  
D. Sacerdoti ◽  
...  

1983 ◽  
Vol 396 (2) ◽  
pp. 182-183 ◽  
Author(s):  
Ulrik Abildgaard ◽  
O. Amtorp ◽  
S. Hans� ◽  
P. Rosenkilde ◽  
P. Sejrsen

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yedan Liu ◽  
Shaoxun Wang ◽  
Ya Guo ◽  
Huawei Zhang ◽  
Richard Roman ◽  
...  

Diabetes is the primary pathological factor attributed to Alzheimer’s disease and vascular cognitive impairment. Previous studies demonstrated that hyperglycemia promoted oxidative stress in the cerebral vasculature. Cerebrovascular pericytes contribute to maintaining blood-brain barrier (BBB) integrity and regulating cerebral blood flow (CBF). However, whether hyperglycemia diminishes the contractile capability of pericytes, impairs CBF autoregulation and increases BBB permeability are unclear. In the present study, we examined the role of pericytes in cerebrovascular function and cognition in diabetes using cell culture in vitro , isolated penetrating arterioles ex vivo and CBF autoregulation in vivo . Reactive oxygen species were elevated in high glucose (HG, 30 mM) treated vs. normal glucose (NG, 5.5 mM) treated pericytes. Further, mitochondrial superoxide production was increased in HG-treated vs. NG-treated group (13.24 ± 1.01 arbitrary unit (a.u.)/30min vs. 6.98 ± 0.36 a.u./30min). Mitochondrial respiration decreased in HG-treated vs. NG-treated pericytes (3718 ± 185.9 pmol/min/mg, n=10 vs. 4742 ± 284.5 pmol/min/mg, n=10) as measured by a Seahorse XFe24 analyzer. HG-treated pericytes displayed fragmented mitochondria in association with increased fission protein (DRP1) and decreased fusion protein (OPA1) expression. HG-treated pericytes displayed lower contractile capability than NG-treated cells (20.23 ± 7.15% vs. 29.46 ± 9.41%). The myogenic response was impaired in penetrating arterioles isolated from diabetic rats in comparison with non-diabetic rats. Autoregulation of CBF measured by a laser Doppler flowmeter was impaired in diabetic rats compared with non-diabetic rats. Diabetic rats exhibited greater BBB leakage than control rats. The cognitive function was examined using an eight-arm water maze. Diabetic rats took longer time to escape than the non-diabetic rats indicating learning and memory deficits. In conclusion, hyperglycemia induces pericyte dysfunction by altering mitochondrial dynamics and diminishing contractile capability, which promotes BBB leakage, decreases CBF autoregulation and contributes to diabetes-related dementia.


1977 ◽  
Vol 43 (2) ◽  
pp. 204-210 ◽  
Author(s):  
A. Capderou ◽  
J. Polianski ◽  
J. Mensch-Dechene ◽  
L. Drouet ◽  
G. Antezana ◽  
...  

An impairment of gluconeogenesis has been proposed to explain the low arterial blood glucose of highlanders. Therefore, we studied splanchnic blood flow, splanchnic uptake of oxygen and lactate, and output of glucose in nine normal and six anemic highlanders at an altitude of 3,750 m. Splanchnic blood flow, arteriovenous difference for oxygen, and oxygen consumption were comparable at rest in both groups and in lowlanders from the literature, whereas splanchnic output of glucose, and uptake of lactate were approximately twice those in lowlanders. After 10 min of mild exercise in 12 subjects (7 normals, 5 anemic), no significant changes in splanchnic hemodynamics and metabolism were found. During 29% oxygen breathing in 8 subjects (5 normals, 3 anemics), arterial lactate, splanchnic uptake of lactate and output of glucose fell to normal sea-level values. We concluded that splanchnic hemodynamics are similar in adapted highlanders and in lowlanders, and that there is no evidence of an impaired gluconeogenesis at the altitude of the present study.


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