"REFLEX" ANURIA IN THE DOG

1956 ◽  
Vol 34 (2) ◽  
pp. 158-169 ◽  
Author(s):  
Sydney M. Friedman ◽  
Roland W. Radcliffe ◽  
J. E. H. Turpin ◽  
Constance L. Friedman
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Femoral Vein ◽  
Venous Catheter ◽  
Renal Vasoconstriction ◽  
Contralateral Kidney ◽  
Renal Pedicle ◽  
Ureteral Catheters ◽  
Surgical Manipulations ◽  
Reflex Anuria

The effects of various surgical manipulations on the function of the separate kidneys was studied in the dog. The application of a clamp to one renal artery produced vasoconstriction of varying severity in the contralateral kidney. The introduction of a venous catheter into the renal vein by passage upward from the femoral vein similarly caused renal vasoconstriction. The combination of manipulations involved in preparing the renal pedicle for later renal artery clamping with the passing of renal venous and ureteral catheters frequently produced oliguria or complete anuria. Since such nociceptive stimuli can cause renal vasoconstriction and, if sufficiently severe, antidiuresis, it is inferred that these mechanisms bear directly on the problem of traumatic anuria.

"REFLEX" ANURIA IN THE DOG

1956 ◽  
Vol 34 (1) ◽  
pp. 158-169
Author(s):  
Sydney M. Friedman ◽  
Roland W. Radcliffe ◽  
J. E. H. Turpin ◽  
Constance L. Friedman
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Femoral Vein ◽  
Venous Catheter ◽  
Renal Vasoconstriction ◽  
Contralateral Kidney ◽  
Renal Pedicle ◽  
Ureteral Catheters ◽  
Surgical Manipulations ◽  
Reflex Anuria

The effects of various surgical manipulations on the function of the separate kidneys was studied in the dog. The application of a clamp to one renal artery produced vasoconstriction of varying severity in the contralateral kidney. The introduction of a venous catheter into the renal vein by passage upward from the femoral vein similarly caused renal vasoconstriction. The combination of manipulations involved in preparing the renal pedicle for later renal artery clamping with the passing of renal venous and ureteral catheters frequently produced oliguria or complete anuria. Since such nociceptive stimuli can cause renal vasoconstriction and, if sufficiently severe, antidiuresis, it is inferred that these mechanisms bear directly on the problem of traumatic anuria.

scholarly journals Acute renal venous obstruction is more detrimental to the kidney than arterial occlusion: implication for murine models of acute kidney injury

2012 ◽  
Vol 302 (5) ◽  
pp. F519-F525 ◽  
Author(s):  
Xiang Li ◽  
Manchang Liu ◽  
Djahida Bedja ◽  
Christopher Thoburn ◽  
Kathleen Gabrielson ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Renal Artery ◽  
Renal Vein ◽  
Renal Tubule ◽  
Ischemia Reperfusion ◽  
Arterial Blood Flow ◽  
Whole Body ◽  
Renal Vasculature ◽  
Renal Pedicle ◽  
Arterial Blood

In this study, we compared the traditional murine model with renal pedicle clamp with models that clamped the renal artery or vein alone as well as to a whole body ischemia-reperfusion injury (WBIRI) model. Male C57BL/6J mice underwent either clamping of the renal artery, vein, or both (whole pedicle) for 30 or 45 min followed by reperfusion, or 10 min of cardiac arrest followed by resuscitation up to 24 h. After 30 min of ischemia, the mice with renal vein clamping showed the mostly increased serum creatinine and the most severe renal tubule injury. After 45 min of ischemia, all mice with renal vasculature clamping had a comparable increase in serum creatinine but the renal tubule injury was most severe in renal artery-clamped mice. Renal arterial blood flow was most decreased in mice with a renal vein clamp compared with a renal artery or pedicle clamp. A 30-or 45-min renal ischemia time led to a significant increase in the protein level of interleukin-6, keratinocyte-derived chemokine (KC), and granular colony-stimulating factor in the ischemic kidney, but the KC was the highest in the renal pedicle-clamped kidney and the lowest in the renal vein-clamped kidney. Of note, 10 min of WBIRI led to kidney dysfunction and structural injury, although less than longer time clamping of isolated renal vasculature. Our data demonstrate important differences in ischemic AKI models. Understanding these differences is important in designing future experimental studies in mice as well as clinical trials in humans.

scholarly journals Renal vein cytokine release as an index of renal parenchymal inflammation in chronic experimental renal artery stenosis

2013 ◽  
Vol 29 (2) ◽  
pp. 274-282 ◽  
Author(s):  
Alfonso Eirin ◽  
Xin Zhang ◽  
Xiang-Yang Zhu ◽  
Hui Tang ◽  
Kyra L. Jordan ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renal Vein ◽  
Artery Stenosis ◽  
Cytokine Release

RENOVASCULAR HYPERTENSION IN CHILDREN

PEDIATRICS ◽  
1970 ◽  
Vol 46 (3) ◽  
pp. 362-370
Author(s):  
Ernst P. Leumann ◽  
Robert P. Bauer ◽  
Paul E. Slaton ◽  
Edward G. Biglieri ◽  
Malcolm A. Holliday
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Pediatric Patient ◽  
Renal Vein ◽  
Diagnostic Problem ◽  
Bilateral Renal Artery Stenosis ◽  
Bilateral Renal Artery ◽  
Fibromuscular Hyperplasia ◽  
Hypertension In Children

Three children with renovascular hypertension are presented in order to demonstrate the wide clinical spectrum of this disease. Two patients had relatively minor symptoms, but one with neurofibromatosis showed frank hypokalemia, polyuria, and hyponatremia. Three different anatomical lesions were found: bilateral renal artery stenosis in the patient with neurofibromatosis, fibromuscular hyperplasia in the patient with stenosis of one renal artery, and an isolated malformation of one small intrarenal artery. The last of our patients presented a complicated diagnostic problem which required repeated arteriograms and renal vein catheterizations for differential renin assay. Renovascular hypertension should be excluded in any pediatric patient with otherwise unexplained hypertension.

Salt and water balance and renin activity in renal hypertension of rats

1975 ◽  
Vol 228 (6) ◽  
pp. 1847-1855 ◽  
Author(s):  
J Mohring ◽  
B Mohring ◽  
H-J Naumann ◽  
A Philippi ◽  
E Homsy ◽  
...  
Keyword(s):  
Water Balance ◽  
Renal Artery ◽  
Renal Hypertension ◽  
The Body ◽  
Renin Activity ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Contralateral Kidney ◽  
Salt And Water Balance ◽  
Renal Artery Constriction

In male Sprague-Dawley rats, renal artery constriction in the presence of an inact contralateral kidney induced sodium retention (for 2-3 wk), moderate potassium loss,elevation of blood volume (BV), and an increase in water turnover. It is suggestedthat renal artery constriction activates the renin-angiotensin-aldosterone system, resulting in disordered regulation of salt and water balance and in blood pressure (BP) elevation. Subsequently, sodium balance was reestablished in one group of hypertensive rats. The previously retained sodium was kept in the body, and BV and reninactivity remained elevated. In a second group of animals, a malignant course of hypertension developed: BP surpassed a critical level of about 180 mmHg; sodium, potassium, and water were lost; BV declined; renin activity was further stimulated; and in the contralateral kidney malignant nephrosclerosis occurred. It is assumed that pressure diuresis and natriuresis induce a vicious circle: the increasing renin activity may maintain or further increase BP level, therby inducing further salt and water loss, etc.; high BP levels and high renin activities induce vascular damage and deterioration of renal function.

scholarly journals Oxygen Saturation, Oxygen Tension, and pH of Renal Vein Blood in Experimental Unilateral Renal Artery Stenosis

1964 ◽  
Vol 28 (11) ◽  
pp. 878-882 ◽  
Author(s):  
CHI KONG LIU ◽  
ABRAHAM T.K.COCKETT ◽  
LONG TRUMAN ◽  
AKIO.J FURUSHO
Keyword(s):  
Renal Artery ◽  
Oxygen Saturation ◽  
Renal Artery Stenosis ◽  
Oxygen Tension ◽  
Renal Vein ◽  
Artery Stenosis

Experimental Renal Hypertension: Renin Content of Kidneys in Intact and Adrenalectomized Rats Given Cortexone

1958 ◽  
Vol 195 (3) ◽  
pp. 543-548 ◽  
Author(s):  
F. Gross ◽  
P. Lichtlen
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Normal Animal ◽  
Renal Ischemia ◽  
Characteristic Distribution ◽  
Contralateral Kidney ◽  
Moderate Reduction ◽  
Small Doses ◽  
Experimental Renal Hypertension ◽  
Renin Content

The effects were investigated in rats of unilateral renal ischemia, adrenalectomy and varying doses of cortexone on the development of hypertension and on the content of pressor substances in the kidney. Adrenalectomy prevented the hypertension which follows unilateral clamping of the renal artery when a life maintaining dose of 0.1 mg cortexone acetate was injected daily. However, administration of 75 mg cortexone in the form of implants restored but did not enhance the characteristic hypertensive response to renal ischemia. The characteristic distribution of renal pressor material, being normal in the clamped and diminished in the contralateral kidney, was no longer observed after adrenalectomy when only small doses of cortexone were given but was still evident when excess cortexone was given. Overdosage with cortexone without clamping a renal artery led only to a moderate reduction of pressor material in both kidneys while in animals with unilateral renal ischemia the pressor material (renin?) in the contralateral kidney disappeared completely. Clamping the renal artery prevented the diminution of pressor material in the ipsilateral kidney which otherwise occurs under overdosage with cortexone in the normal animal.

Tonic descending modulation of spinal neuronal responses to activation of renal receptors

1993 ◽  
Vol 265 (6) ◽  
pp. R1291-R1303
Author(s):  
A. Standish ◽  
M. A. Vizzard ◽  
W. S. Ammons
Keyword(s):  
Renal Artery ◽  
Renal Vein ◽  
Cell Activity ◽  
Neuronal Responses ◽  
Spinal Neurons ◽  
Descending Modulation ◽  
Spinal Circuitry ◽  
Renal Receptor ◽  
Somatic Input ◽  
The Brain

Experiments were conducted in anesthetized cats to determine if spinal neuronal responses to activation of renal receptors are tonically modulated by descending spinal pathways. Eighty-seven thoracolumbar spinal neurons with renal and somatic input were tested for responses to occlusion of the renal vein, renal artery, and ureter before, during, and after cooling the spinal cord rostral to the recording site. Cooling increased the number of neurons that responded as well as the magnitude of the responses to renal vein (RVO), renal artery (RAO), and ureteral occlusion (UO). RVO increased cell activity of 21 neurons from 12.5 +/- 2.7 to 31.7 +/- 6.0 spikes/s during cooling. UO increased cell activity of 24 neurons from 9.0 +/- 2.1 before cooling to 25.0 +/- 4.9 spikes/s during cooling. Cold block increased the magnitude of both types of responses to RAO that were due to mechanical deformation of the renal artery and prolonged renal ischemia. These data show that the majority of spinal neuronal responses to renal receptor stimulation are modulated by tonic inhibitory influences. Thus these results provide a mechanism by which the brain may control spinal circuitry that underlies reflexes of renal origin.

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