scholarly journals Direct evidence that thromboxane mimetic U44069 preferentially constricts the afferent arteriole.

1997 ◽  
Vol 8 (1) ◽  
pp. 25-31
Author(s):  
K Hayashi ◽  
R Loutzenhiser ◽  
M Epstein
Keyword(s):  
Calcium Antagonist ◽  
Direct Evidence ◽  
Rat Kidney ◽  
Afferent Arteriole ◽  
Filtration Fraction ◽  
Perfused Rat Kidney ◽  
Txa2 Receptor ◽  
Txa2 Receptor Antagonist ◽  
Vasodilator Action ◽  
Hydronephrotic Kidney

The thromboxane A2 (TXA2) mimetic U44069 has been demonstrated to reduce the GFR and filtration fraction of the normal isolated perfused rat kidney markedly, suggesting a predominant constriction of preglomerular vessels. To assess this possibility directly, effects of U44069 on the renal microvessels of the isolated perfused hydronephrotic kidney were examined. At 10(-6) mol/L, U44069 elicited a 27 +/- 2% decrease in afferent arteriolar (AA) diameter (from 18.8 +/- 0.3 to 13.7 +/- 0.3 micron, P < 0.001). In contrast, efferent arteriolar (EA) diameter decreased by only 9 +/- 1% (from 16.4 +/- 0.5 to 15.0 +/- 0.5 micron, P < 0.001). These effects on both AA and EA were completely reversed by the TXA2 receptor antagonist SQ29548. The calcium antagonist diltiazem reversed U44069-induced AA constriction by 83 +/- 5%. The U44069-induced EA constriction was insensitive to the vasodilator action of diltiazem at concentrations from 10(-8) to 10(-6) mol/L, but at 10(-5) mol/L, diltiazem increased the EA diameter significantly, albeit modestly. Nifedipine also reversed the U44069-induced AA constriction (81 +/- 7%), but failed to inhibit the EA constriction at concentrations from 10(-9) to 10(-6) mol/L. These findings constitute the first direct evidence that a TXA2 agonist preferentially constricts the afferent arteriole. Furthermore, the ability of both the calcium antagonist and SQ29548 to reverse the renal microvascular actions of TXA2 agonists suggests a potential utility of these agents in ameliorating TXA2-induced renal hemodynamic abnormalities.

Ca-dependent hemodynamic and natriuretic effects of atrial extract in isolated rat kidney

1984 ◽  
Vol 246 (4) ◽  
pp. F447-F456 ◽  
Author(s):  
M. J. Camargo ◽  
H. D. Kleinert ◽  
S. A. Atlas ◽  
J. E. Sealey ◽  
J. H. Laragh ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Electrolyte Excretion ◽  
Renal Vasculature ◽  
Filtration Fraction ◽  
Perfused Rat Kidney ◽  
Site Of Action ◽  
Initial Control ◽  
Renal Vascular

The effects of rat atrial tissue extract on renal hemodynamics and fluid and electrolyte excretion were investigated in the isolated perfused rat kidney (IK). IK were perfused at a constant effective perfusion pressure of about 90 mmHg. After control clearance periods (C), extracts of rat atria (AE) or ventricles (VE) were added to the perfusate and three 10-min experimental periods followed. AE, but not VE, significantly increased (P less than 0.001) renal vascular resistance (RVR) to 133 +/- 8% of C, GFR to 201 +/- 34%, filtration fraction to 245 +/- 41%, urine flow (V) to 675 +/- 131%, fractional excretion (FE) of H2O to 336 +/- 29%, absolute Na excretion (UNaV) to 1,259 +/- 290%, FENa to 642 +/- 129%, UKV to 2,226 +/- 1,237%, and FEK to 542 +/- 119%. Despite the marked natriuresis, since GFR doubled, Na reabsorption rose from 78.3 +/- 36.3 in C to 132 +/- 36.3 mueq/min after AE. The effects of AE were immediate and lasted to the end of the perfusion. The lower the initial control GFR, the larger was the AE-induced increase in GFR. Perfusion with low [Ca] (0.2 mM) or verapamil (10(-5) M) severely blunted the hemodynamic, diuretic, kaliuretic, and natriuretic effects of AE. AE decreased rather than increased the RVR when IK were perfused with vasoconstrictors such as angiotensin II, norepinephrine, or vasopressin. The results demonstrate that AE acts directly on the kidney, eliciting powerful Ca-dependent hemodynamic and natriuretic responses. The natriuresis induced by AE can be accounted for, at least in part, by its renal hemodynamic effects rather than by the presence of a putative tubular natriuretic factor. The hypothesis is advanced that AE contains a substance(s) which behaves as a functional agonist/antagonist of endogenous vasoconstrictors with a preferential site of action on the efferent arterioles of the renal vasculature.

Effect of exogenous and endogenous angiotensin II in the isolated perfused rat kidney

1978 ◽  
Vol 235 (6) ◽  
pp. F605-F610 ◽  
Author(s):  
M. Davalos ◽  
N. S. Frega ◽  
B. Saker ◽  
A. Leaf
Keyword(s):  
Angiotensin Ii ◽  
Driving Force ◽  
Constant Pressure ◽  
Enzyme Inhibitor ◽  
Rat Kidney ◽  
Filtration Fraction ◽  
Renin Substrate ◽  
Perfusate Flow ◽  
Perfused Rat Kidney ◽  
The Face

Rat kidneys were perfused with an artificial solution at constant pressure. The infusion of angiotensin II (AII) (1.5––6 ng min-1) reduced renal perfusate flow (RPF) from 36.6 +/- 2.4 to 19.3 +/- 1.4 ml min-1 (P less than 0.001) (n = 13); GFR rose from 0.48 +/- 0.06 to 0.63 +/- 0.04 ml min-1 (P less than 0.05), and filtration fraction (FF) rose accordingly from 0.015 +/- 0.002 to 0.033 +/- 0.003 (P greater than 0.01). The same results were obtained with purified renin substrate (synthetic tetradecapeptide, 100 ng min-1, n = 8); RPF fell from 31.5 +/- 2.9 to 17.2 +/- 2 ml min-1 (P less than 0.001), GFR rose from 0.36 +/- 0.05 to 0.51 +/- 0.04 ml min-1 (P less than 0.05), and FF increased from 0.021 +/- 0.002 to 0.034 +/- 0.006 (P less than 0.01). The effects of renin substrate were completely prevented by the converting enzyme inhibitor SQ 20,881 (3 X 10(-5) M). In another six experiments the effects of renin substrate at the same dose were fully reversed by addition of the analogue [Sar1,Ala8]AII. We interpret these findings to indicate that both exogenous and endogenous AII produce preferential vasoconstriction of the efferent arteriole, increasing the driving force for ultrafiltration and thereby maintaining or increasing GFR in the face of a reduced plasma flow.

Calcium antagonists preferentially dilate preglomerular vessels of hydronephrotic kidney

1987 ◽  
Vol 253 (6) ◽  
pp. F1157-F1163 ◽  
Author(s):  
J. T. Fleming ◽  
N. Parekh ◽  
M. Steinhausen
Keyword(s):  
Blood Pressure ◽  
Calcium Antagonist ◽  
Wistar Rats ◽  
Afferent Arteriole ◽  
Calcium Blockers ◽  
Efferent Arteriole ◽  
Female Wistar Rats ◽  
Afferent Arterioles ◽  
Arcuate Artery ◽  
Hydronephrotic Kidney

The hydronephrotic kidney of Inactin-anesthetized female Wistar rats was exteriorized in a controlled bath to directly observe preglomerular and postglomerular vessels via television microscopy. Nitrendipine, added to the bath in a concentration that did not alter blood pressure, induced a concentration-dependent dilation of preglomerular vessels. The arcuate artery maximally dilated by 29 +/- 4%, the interlobular artery by 24 +/- 5%, the afferent arteriole near the interlobular artery by 60 +/- 9%, and near the glomerulus by 28 +/- 13%. In contrast the efferent arteriole near the glomerulus dilated by only 11 +/- 6% and near the welling point by 7 +/- 9%. Similarly, diltiazem significantly dilated preglomerular vessels but not efferent arterioles. Acetylcholine significantly dilated all preglomerular vessels and dilated the afferent arterioles near the glomerulus (by 51 +/- 8%) to a greater extent than the calcium blockers. Acetylcholine also significantly dilated the efferent arterioles (near the glomerulus by 26 +/- 5% and near the welling point by 12 +/- 3%). These data suggest that the tone of the preglomerular vessels of the hydronephrotic kidney is more dependent on the entry of extracellular calcium through calcium antagonist-sensitive channels (i.e., potential dependent) than is the tone of the afferent arterioles near the glomerulus and the efferent arterioles.

The vasodilator action of parathyroid hormone fragments on isolated perfused rat kidney

1989 ◽  
Vol 340 (2) ◽  
Author(s):  
Marie-Jos� Musso ◽  
Mariette Barthehnebs ◽  
Jean-Louis Imbs ◽  
Martin Plante ◽  
Claude Bollack ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Rat Kidney ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Vasodilator Action ◽  
Parathyroid Hormone Fragments

Validation of a toxicity testing model by evaluating oxygen supply and energy state in the isolated perfused rat kidney

1991 ◽  
Vol 25 (3) ◽  
pp. 195-204 ◽  
Author(s):  
Takano Takehito ◽  
Nakata Kazuyo ◽  
Kawakami Tsuyoshi ◽  
Miyazaki Yoshifumi ◽  
Murakami Masataka ◽  
...  
Keyword(s):  
Oxygen Supply ◽  
Energy State ◽  
Rat Kidney ◽  
Toxicity Testing ◽  
Testing Model ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney

Aldosterone Effects on Renal Function in the Isolated Perfused Rat Kidney

1979 ◽  
Vol 2 (1) ◽  
pp. 1-11
Author(s):  
Richard Solomon ◽  
Patricio Silva ◽  
Franklin H. Epstein
Keyword(s):  
Renal Function ◽  
Rat Kidney ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney

Thromboxane and Prostacyclin Production by Irradiated and Perfused Rat Kidney

1987 ◽  
pp. 219-224 ◽  
Author(s):  
Z. Weshler ◽  
A. Raz ◽  
E. Rosenmann ◽  
S. Biran ◽  
Z. Fuks ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Perfused Rat Kidney ◽  
Prostacyclin Production

Expression of rat kidney anion exchanger 1 in type A intercalated cells in metabolic acidosis and alkalosis

1999 ◽  
Vol 277 (6) ◽  
pp. F841-F849 ◽  
Author(s):  
Saskia Huber ◽  
Esther Asan ◽  
Thomas Jöns ◽  
Christiane Kerscher ◽  
Bernd Püschel ◽  
...  
Keyword(s):  
Anion Exchanger ◽  
Direct Evidence ◽  
Rat Kidney ◽  
Enzyme Reaction ◽  
Type A ◽  
Mrna Levels ◽  
Intercalated Cells ◽  
Acid Base ◽  
Anion Exchanger 1 ◽  
Acid Base Status

By enzyme-linked in situ hybridization (ISH), direct evidence is provided that acid-secreting intercalated cells (type A IC) of both the cortical and medullary collecting ducts of the rat kidney selectively express the mRNA of the kidney splice variant of anion exchanger 1 (kAE1) and no detectable levels of the erythrocyte AE1 (eAE1) mRNA. Using single-cell quantification by microphotometry of ISH enzyme reaction, medullary type A IC were found to contain twofold higher kAE1 mRNA levels compared with cortical type A IC. These differences correspond to the higher intensity of immunostaining in medullary versus cortical type A IC. Chronic changes of acid-base status induced by addition of NH4Cl (acidosis) or NaHCO3 (alkalosis) to the drinking water resulted in up to 35% changes of kAE1 mRNA levels in both cortical and medullary type A IC. These experiments provide direct evidence at the cellular level of kAE1 expression in type A IC and show moderate capacity of type A IC to respond to changes of acid-base status by modulation of kAE1 mRNA levels.

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