Plasma renin activity and intrarenal blood flow distribution in a child with a pheochromocytoma

1976 ◽  
Vol 89 (6) ◽  
pp. 950-952 ◽  
Author(s):  
Linda B. Hiner ◽  
Alan B. Gruskin ◽  
H. Jorge Baluarte ◽  
Mary L. Cote ◽  
David W. Sapire ◽  
...  
1975 ◽  
Vol 229 (2) ◽  
pp. 370-375 ◽  
Author(s):  
W Flamenbaum ◽  
JG Kleinman ◽  
JS McNeil ◽  
RJ Hamburger ◽  
TA Kotchen

The effects of unilateral intrarenal arterial KCl infusion in dogs (12 mueq/kg per min) on bilateral renal function, renin secretory rates, and aldosterone excretion were studied. During KCl infusion, infused-side renal arterial plasma [K+] increased by 2.2 +/- 0.6 meq/liter. Systemic plasma [K+] simultaneously rose by 0.6 +/- 0.1 meq/liter. Plasma renin activity decreased 29 +/- 9%, and the decrease correlated with the increases in plasma [K+]. Renin secretory rate decreased bilaterally, the decrease being greater in each experiment on the infused side. Aldosterone excretion increased during KCl infusion by 72 +/- 17%, despite a decrease in plasma renin activity. With KCl infusion there was a bilateral increase in K+ excretion, and a positive correlation was observed between the net alterations in K+ and Na+ excretion. No significant alterations in systemic blood pressure, glomerular filtration rate, total renal blood flow, or intracortical renal blood flow distribution were observed. These studies suggest that K+ inhibits the release of renin by an intrarenal mechanism, which may be related to a K+-induced alteration in Na+ absorption.


1972 ◽  
Vol 50 (8) ◽  
pp. 774-783 ◽  
Author(s):  
Serge Carrière ◽  
Michel Desrosiers ◽  
Jacques Friborg ◽  
Michèle Gagnan Brunette

Furosemide (40 μg/min) was perfused directly into the renal artery of dogs in whom the femoral blood pressure was reduced (80 mm Hg) by aortic clamping above the renal arteries. This maneuver, which does not influence the intrarenal blood flow distribution, produced significant decreases of the urine volume, natriuresis, Ccreat, and CPAH, and prevented the marked diuresis normally produced by furosemide. Therefore the chances that systemic physiological changes occurred, secondary to large fluid movements, were minimized. In those conditions, however, furosemide produced a significant increase of the urine output and sodium excretion in the experimental kidney whereas Ccreat and CPAH were not affected. The outer cortical blood flow rate (ml/100 g-min) was modified neither by aortic constriction (562 ± 68 versus 569 ± 83) nor by the subsequent administration of furosemide (424 ± 70). The blood flow rate of the outer medulla in these three conditions remained unchanged (147 ± 52 versus 171 ± 44 versus 159 ± 54). The initial distribution of the radioactivity in each compartment remained comparable in the three conditions. In parallel with the results from the krypton-85 disappearance curves, the autoradiograms, silicone rubber casts, and EPAH did not suggest any change in the renal blood flow distribution secondary to furosemide administration.


1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.


1978 ◽  
pp. 41-74 ◽  
Author(s):  
Norbert H. Lameire ◽  
Elaine L. Chuang ◽  
Richard W. Osgood ◽  
Jay H. Stein

1970 ◽  
Vol 4 (5) ◽  
pp. 446-446
Author(s):  
Pedro A Jose ◽  
Alexander G Logan ◽  
Gilbert M Eisner ◽  
Lawrence M Slotkoff ◽  
Charles E Hollerman ◽  
...  

1983 ◽  
Vol 244 (6) ◽  
pp. R823-R831
Author(s):  
W. J. Ray ◽  
M. L. Zatzman

The effects of low doses of norepinephrine (NE) and furosemide and a volume load (nonhibernators only) on plasma renin activity (PRA), mean arterial pressure (MAP), heart rate (HR), left renal (RBF) and right iliac (IBF) blood flow, cardiac index (CI), and total peripheral resistance (TPR) were determined in euthermic and hibernating marmots. In nonhibernating marmots NE produced an increase in CI and TPR and a decrease in RBF. In hibernators this dose of NE caused an increase in MAP, HR, and renal resistance, whereas it decreased PRA and did not alter iliac resistance. Furosemide infusions led to an increase in PRA in both groups and an increase in TPR in nonhibernators. The volume load in nonhibernators produced only a decrease in PRA. A comparison of control data from the two groups indicated that the renal and iliac beds contribute only a small portion to the increase in TPR that occurs during hibernation.


1982 ◽  
Vol 5 (2) ◽  
pp. 57-67
Author(s):  
H.-H. Neumayer ◽  
K. Wagner ◽  
G. Schuhze ◽  
P. Laubner ◽  
M.K. Maiga ◽  
...  

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.


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