Effect of Mild Charge Modification of Albumin on Renal Excretion in the Rat

2015 ◽  
pp. 121-127 ◽  
Author(s):  
D. de Zeeuw ◽  
R. Tomasini ◽  
M. Haas ◽  
P. E. de Jong ◽  
J. J. Weening ◽  
...  
Keyword(s):  
Renal Excretion

Renal excretion of uric acid: Alterations during stressful underwater demolition team training.

1971 ◽  
Author(s):  
Leonard M. Zir ◽  
Robert T. Rubin ◽  
Richard H. Rahe ◽  
Ransom J. Arthur
Keyword(s):  
Uric Acid ◽  
Renal Excretion ◽  
Team Training

Renal Excretion of Gastrografin after Oral Administration: Clinical Significance in Gastric Resection Patients

1998 ◽  
Vol 39 (2) ◽  
pp. 373
Author(s):  
Kyung Myung Sohn ◽  
Oh Han Kwon ◽  
Sung Yong Lee ◽  
Jong Kwan Joo ◽  
Jae Hee Lee ◽  
...  
Keyword(s):  
Oral Administration ◽  
Clinical Significance ◽  
Gastric Resection ◽  
Renal Excretion

SOME EFFECTS OF PERCHLORATE ON THE DISTRIBUTION OF 131-IODIDE

1965 ◽  
Vol 50 (2) ◽  
pp. 195-201 ◽  
Author(s):  
E. Schönbaum ◽  
E. A. Sellers ◽  
M.J. Gill
Keyword(s):  
Urinary Excretion ◽  
Renal Excretion ◽  
Kidney Tissue ◽  
Intraperitoneal Dose ◽  
Blood Radioactivity ◽  
Radioactivity Levels

ABSTRACT The distribution of an intraperitoneal dose of 131-iodide was studied in rats receiving perchlorate. The accumulation of radioactivity in the stomach, which occurred soon after injection in controls, was inhibited by perchlorate. Concurrent with this, radioactivity in blood was higher in perchlorate treated rats than in controls. After perchlorate, more radioactivity in kidney tissue and an elevated urinary excretion of the tracer was noted. After 24 hours, plasma radioactivity was lower in perchlorate treated rats than in controls. Increased renal excretion of 131I after perchlorate is, at least in part, due to higher blood radioactivity levels, probably because of decreased iodide space due to the action of perchlorate.

scholarly journals Mammary and Renal Excretion of Sulphadoxine and Trimethoprim in Cows

1974 ◽  
Vol 15 (3) ◽  
pp. 340-355 ◽  
Author(s):  
Danis Davitiyananda ◽  
Folke Rasmussen
Keyword(s):  
Renal Excretion

scholarly journals Further evidence against the role renal medullary perfusion in short-term control of arterial pressure in normotensive and mildly or overtly hypertensive rats

2021 ◽  
Vol 473 (4) ◽  
pp. 623-631
Author(s):  
Bożena Bądzyńska ◽  
Iwona Baranowska ◽  
Janusz Sadowski
Keyword(s):  
Arterial Pressure ◽  
Renal Excretion ◽  
Sodium Concentration ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Critical Determinant ◽  
Human Hypertension ◽  
Pressure Elevation ◽  
Doppler Probe ◽  
Medullary Tissue

AbstractEarlier evidence from studies of rat hypertension models undermines the widespread view that the rate of renal medullary blood flow (MBF) is critical in control of arterial pressure (MAP). Here, we examined the role of MBF in rats that were normotensive, with modest short-lasting pressure elevation, or with overt established hypertension. The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. MBF was measured (laser-Doppler probe) and selectively increased using 4-h renal medullary infusion of bradykinin. MAP, renal excretion parameters and post-experiment medullary tissue osmolality and sodium concentration were determined. In the three experimental groups, baseline MAP was 117, 151 and 171 mmHg, respectively. Intramedullary bradykinin increased MBF by 45%, 65% and 70%, respectively, but this was not associated with a change in MAP. In normotensive rats a significant decrease in medullary tissue sodium was seen. The intramedullary bradykinin specifically increased renal excretion of water, sodium and total solutes in norepinephrine-treated rats but not in the two other groups. As previously shown in models of rat hypertension, in the normotensive rats and those with acute mild pressure elevation (resembling labile borderline human hypertension), 4-h renal medullary hyperperfusion failed to decrease MAP. Nor did it decrease in DOCA-salt model mimicking low-renin human hypertension. Evidently, within the 4-h observation, medullary perfusion was not a critical determinant of MAP in normotensive and hypertensive rats.

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