PGE2 concentrations in renal venous plasma and renal lymph during basal and stimulated conditions in the dog

1989 ◽  
Vol 413 (6) ◽  
pp. 673-675 ◽  
Author(s):  
R. M. Hohenfellner ◽  
J. Rehbock ◽  
H. Brechtelsbauer ◽  
H. G. Klein ◽  
K. Thurau
Keyword(s):  
1992 ◽  
Vol 2 (7) ◽  
pp. 1241-1250 ◽  
Author(s):  
C S Wilcox ◽  
V J Dzau

The effects of captopril on the intrarenal renin-angiotensin system were assessed from measurements in arterial plasma, renal venous plasma, and renal lymph from salt-depleted dogs. In the basal state, immunoreactive angiotensin II (Ang II) in renal venous plasma averaged only 60 +/- 12% (P less than 0.01) of arterial plasma, although the concentration of Ang II in renal lymph was 2.0 +/- 0.4-fold (P less than 0.05) greater. The Ang II concentration of renal lymph incubated ex vivo at 37 degrees C doubled in 10 to 15 min, which was the time taken to collect renal lymph samples. Compared with arterial plasma, renal lymph contained lower concentrations (P less than 0.01) of renin substrate and angiotensin-converting enzyme but higher concentrations of active (5.3 +/- 2.1-fold) and inactive (8.9 +/- 3.2-fold) renin. Although captopril increased the secretion of active renin into renal venous plasma by six-fold, the secretion of total renin was unchanged because of a reciprocal fall in the secretion of inactive renin. The percent reduction in renal vascular resistance with captopril correlated with the percent fall in Ang II in renal lymph (r = 0.70). In conclusion: (1) all components of the renin-angiotensin system are represented in the renal interstitium, as reflected in lymph; (2) Ang II concentrations in renal lymph in vivo approximate arterial levels; (3) increased secretion of active renin into plasma during intrarenal infusion of captopril into denervated kidneys is due predominantly to renin activation; and (4) renal vascular resistance may depend on the concentration of Ang II in the renal interstitium.


1970 ◽  
Vol 38 (2) ◽  
pp. 157-174 ◽  
Author(s):  
K. F. Hosie ◽  
J. J. Brown ◽  
A. M. Harper ◽  
A. F. Lever ◽  
R. F. MacAdam ◽  
...  

1. In anaesthetized dogs the rate at which renin was released into the circulation of the right and left kidneys was estimated from renal blood flow, haematocrit, and the V-A renin concentration difference across the kidney. Renin was also measured in samples of renal lymph collected at the same time. 2. The effect on renin release of reducing blood flow in one kidney was studied. For all observations (control and experimental), renal venous plasma renin concentration (RVR) was directly related to arterial plasma renin concentration and to renin release; RVR was inversely related to renal plasma flow. 3. The concentration of renin in renal lymph was considerably higher than that in renal venous plasma taken at the same time. Arterial plasma renin concentration was directly related to the sum of the rates at which renin was released from the two kidneys. 4. Clamping the renal artery of one kidney for 1 hr led to a marked reduction of renal blood flow, to a marked increase in RVR and to a variable change in renin release. Removal of the clamp was followed by increased renin release and by reversal of a previously positive V-A renin difference in the control kidney. 5. On several other occasions negative V-A renin differences were observed. That is, more renin appeared to enter the kidney in arterial blood than left in the renal vein.


1982 ◽  
Vol 242 (3) ◽  
pp. F261-F266 ◽  
Author(s):  
R. K. Stephenson ◽  
M. J. Sole ◽  
A. D. Baines

Catecholamine production by innervated kidneys was examined by radioenzymatic assay of norepinephrine (NE), epinephrine (E), and dopamine (DA) in lymph, urine, arterial plasma, and renal venous plasma of hydropenic rats. Denervation reduced NE excretion in urine by 18% and both NE and DA efflux in renal venous plasma by 37 and 30%, respectively. The kidney's handling of E was unaltered by denervation. Renal nerves added 1.0 +/- 0.2 ng/min to the efflux of NE in urine and renal venous plasma. Denervation reduced this efflux to -0.1 +/- 0.2 ng/min. DA efflux from innervated kidneys was 1.4 +/- 0.2 ng/min but only half came from renal nerves, as denervated kidneys released 0.7 +/- 0.1 ng/min. Renal lymph from innervated kidneys contained slightly more NE but less DA than arterial plasma. We conclude that renal nerves release both NE and DA but that half of the renal contribution to urine and renal venous plasma DA efflux comes from extraneuronal tissue. Renal lymph NE and DA concentrations are similar to those in arterial plasma, suggesting that peritubular concentrations are low everywhere except within renal clefts.


1971 ◽  
Vol 50 (1) ◽  
pp. 119-126 ◽  
Author(s):  
Michael D. Bailie ◽  
Floyd C. Rector ◽  
Donald W. Seldin

1986 ◽  
Vol 250 (1) ◽  
pp. E55-E61 ◽  
Author(s):  
V. J. Dzau ◽  
C. S. Wilcox ◽  
K. Sands ◽  
P. Dunckel

It has been suggested that the dog is a useful model for studies of inactive renin (IR). However, the nature and origin of the trypsin-activated angiotensin-forming activity in dog plasma have not been fully defined. We characterized dog IR using renin-specific antibody, immunoaffinity, and Affigel blue chromatography. Activated IR resembles renal and plasma active renin in biochemical and immunological properties. IR was detected in renal lymph, arterial and venous plasma, as well as renal extracts. At basal state, there was a significant renal venous-arterial gradient of IR indicating secretion from the kidney. Furthermore, a sixfold higher concentration of IR was demonstrated in renal lymph than in plasma. Our data provides evidence for two possible routes of IR secretion from the kidney and supports the contention that the dog is a good model for studies of IR secretion and regulation.


2020 ◽  
Author(s):  
Keyword(s):  

Endocrinology ◽  
1967 ◽  
Vol 80 (2) ◽  
pp. 240-246 ◽  
Author(s):  
HIROSHI MASUDA ◽  
L. L. ANDERSON ◽  
D. M. HENRICKS
Keyword(s):  

1971 ◽  
Vol 41 (4) ◽  
pp. 289-299 ◽  
Author(s):  
D. R. Love ◽  
J. J. Brown ◽  
R. H. Chinn ◽  
R. H. Johnson ◽  
A. F. Lever ◽  
...  

1. The changes of peripheral venous plasma renin concentration (PRC) induced by head-up tilting were studied in four patients with orthostatic hypotension. 2. Two of the patients had the Holmes—Adie syndrome and tests of autonomic function suggested that they had an afferent block from baroreceptors with intact efferent pathways; the others had no evidence of the Holmes—Adie syndrome and investigations suggested that they had interruption of efferent sympathetic pathways. 3. In the two patients in whom lesions of the afferent side of baroreceptor reflexes were suspected, a marked increase in PRC occurred with upright tilting, whereas no change in PRC occurred in the two patients thought to have an efferent sympathetic block. 4. During repeated tilting, supine blood pressure and PRC increased progressively in the two patients with suspected afferent block, but not in the two patients with suspected efferent block. 5. It is suggested that an increase in plasma renin may contribute to the supine hypertension sometimes observed in patients with orthostatic hypotension. 6. It is also suggested that renin release does not require intact autonomic reflexes although certain components of efferent sympathetic pathways, not dependent on baroreceptor reflexes, may be important.


PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202082 ◽  
Author(s):  
Liusheng Huang ◽  
Norah Mwebaza ◽  
Richard Kajubi ◽  
Florence Marzan ◽  
Camilla Forsman ◽  
...  

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