Renal effects of prostaglandin inhibition during increases in renal venous pressure

1991 ◽  
Vol 260 (4) ◽  
pp. F525-F529 ◽  
Author(s):  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Venous Pressure ◽  
Interstitial Pressure ◽  
Pentobarbital Sodium ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Changes

The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.

Maintenance of renal autoregulation during infusion of aminophylline or adenosine

1985 ◽  
Vol 248 (3) ◽  
pp. F366-F373 ◽  
Author(s):  
A. J. Premen ◽  
J. E. Hall ◽  
H. L. Mizelle ◽  
J. E. Cornell
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Receptor Blockade ◽  
Renal Metabolism ◽  
Renal Autoregulation ◽  
Before And After ◽  
Anesthetized Dogs

Adenosine has been postulated to link control of glomerular filtration rate (GFR) and renal blood flow (RBF) with changes in renal metabolism. In the present study, we examined the role of adenosine in renal autoregulation by comparing the responses of normal anesthetized dogs to step decreases in renal artery pressure (RAP) to the response obtained after receptor blockade of adenosine with aminophylline or by flooding the kidney with exogenous adenosine. In six dogs at normal RAP, intrarenal infusion of aminophylline (10 mumol/min) did not alter renal hemodynamics. GFR and RBF were well autoregulated (greater than 90% of control) at RAP values equal to or greater than 85 mmHg before and after aminophylline. At RAP equal to 75 mmHg, GFR and RBF decreased by 27 +/- 10 and 20 +/- 8%, respectively, before aminophylline and by 25 +/- 7 and 13 +/- 6% after aminophylline. In a different group of six dogs, intrarenal infusion of adenosine (6 mumol/min) significantly increased RBF (32 +/- 9%) and decreased GFR (38 +/- 10%) at normal RAP. However, GFR and RBF were both well autoregulated (greater than 90% of control) at RAP values equal to or greater than 85 mmHg before and after adenosine. At RAP equal to 75 mmHg, GFR and RBF decreased by 10 +/- 5 and 7 +/- 3%, respectively, before adenosine and by 12 +/- 6 and 17 +/- 5% after adenosine. Neither aminophylline nor adenosine attenuated the elevations in plasma renin activity associated with reductions in RAP. These data fail to provide evidence that adenosine is an important factor in autoregulation of GFR and RBF during acute reductions in RAP within the autoregulatory range.

Renal interstitial pressure and sodium excretion during renal vein constriction

1980 ◽  
Vol 238 (4) ◽  
pp. F279-F282 ◽  
Author(s):  
J. C. Burnett ◽  
F. G. Knox
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Renal Vein ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Venous Pressure ◽  
Interstitial Pressure

Studies were performed on anesthetized dogs to determine the relationship of interstitial pressure to sodium excretion during renal vein constriction in the presence and absence of volume expansion. Renal interstitial pressure was measured from implanted capsules during basal renal venous pressure and increased pressures of 10, 20, 30, and 40 mmHg. A positive relationship between renal venous pressure and interstitial pressure was demonstrated in hydropenia and in volume expansion, with markedly higher interstitial pressures obtained in volume expansion. A positive correlation was demonstrated between fractional sodium excretion and renal interstitial pressure in hydropenia as compared to a significant negative correlation in volume expansion. Negative correlations were demonstrated in volume expansion between renal interstitial pressure and glomerular filtration rate and renal blood flow as compared to no significant change in these parameters in hydropenia. Accordingly, a positive correlation was demonstrated between renal interstitial pressure and sodium excretion in hydropenia but not in volume expansion. Volume expansion was characterized by higher interstitial pressure and decreased sodium excretion in association with decreased renal blood flow and glomerular filtration rate.

Renal interstitial pressure in mineralocorticoid escape

1985 ◽  
Vol 249 (3) ◽  
pp. F396-F399 ◽  
Author(s):  
J. C. Burnett ◽  
J. A. Haas ◽  
M. S. Larson
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Hydrostatic Pressure ◽  
Arterial Pressure ◽  
Filtration Rate ◽  
Interstitial Pressure ◽  
Peritubular Capillary ◽  
Renal Interstitium ◽  
Vasa Recta ◽  
Peritubular Capillaries

Studies were performed in normal and DOCA-treated rats to determine renal hydrostatic pressures within superficial peritubular capillaries, the vasa recta, and renal interstitium during mineralocorticoid escape to test the hypothesis that mineralocorticoid escape is associated with elevated renal interstitial hydrostatic pressure. Fractional sodium excretion was greater in the DOCA-treated rats (3.20 +/- 0.51%) compared with control rats (1.23 +/- 0.12%) with no difference in glomerular filtration rate and renal blood flow between the two groups. Superficial peritubular capillary hydrostatic pressure (13.4 +/- 0.6 vs. 8.3 +/- 0.3 mmHg), vasa recta hydrostatic pressure (13.8 +/- 0.5 vs. 9.0 +/- 0.4 mmHg), renal interstitial hydrostatic pressure (9.8 +/- 0.4 vs. 4.5 +/- 0.4 mmHg), and arterial pressure (145 +/- 6 vs. 120 +/- 7 mmHg) were greater in the DOCA-treated compared with the control rats. These studies establish that mineralocorticoid escape is characterized by high renal interstitial hydrostatic pressure.

Effects of adenosine on intrarenal oxygenation

1991 ◽  
Vol 261 (5) ◽  
pp. F787-F791 ◽  
Author(s):  
D. Dinour ◽  
M. Brezis
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Adenosine Receptor ◽  
Filtration Rate ◽  
Adenosine Receptor Antagonist ◽  
Renal Interstitium ◽  
Medullary Blood Flow ◽  
Tissue Po2 ◽  
Flow Effects

Although generally a vasodilator, adenosine vasoconstricts cortical vessels in the kidney, reduces glomerular filtration rate (GFR), and increases medullary blood flow, effects likely to improve the medullary O2 deficiency characteristic of mammalian kidneys. To evaluate a possible role of adenosine in medullary O2 balance, we investigated the effect of adenosine upon cortical and medullary tissue PO2. Adenosine was infused into renal interstitium through chronically implanted capsules. Cortical and medullary PO2 were measured using sensitive Clark-type O2 microelectrodes inserted into kidneys of anesthetized rats at the respective depths of 1.8 and 3.7 mm. Infusion of adenosine (0.1-0.5 mumol/min) increased medullary PO2 from 17 +/- 3 (SE) to 40 +/- 5 mmHG (P less than 0.001) and decreased cortical PO2 from 64 +/- 4 to 47 +/- 3 mmHg (P less than 0.001). After the infusion was stopped, PO2 returned to baseline at both sites. Coadministration of adenosine receptor antagonist 8-phenyltheophylline (0.01 mumol/min) prevented both cortical and medullary effects of adenosine. We concluded that adenosine could play an important protective and regulatory role in renal medullary O2 balance.

Transient response of glomerular filtration rate and renal blood flow to step changes in arterial pressure

1977 ◽  
Vol 233 (5) ◽  
pp. F396-F402 ◽  
Author(s):  
T. E. Jackson ◽  
A. C. Guyton ◽  
J. E. Hall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Steady State ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Hemodynamic Changes ◽  
Proximal Tubular ◽  
Anesthetized Dogs

Measurement of rapid renal hemodynamic changes were made for 90 s in pentobarbital-anesthetized dogs following step increases and decreases in renal arterial pressure between 80 and 120 mm Hg. Transient analysis was used to observe time characteristics of the autoregulatory relationships which are obscured in steadystate measurements. Temporal decoupling of blood flow and glomerular filtration rate (GFR) occurred with both step increases and decreases of arterial pressure. Steady-state autoregulation of blood flow was attained in about 30 s, whereas steady-state autoregulation of GFR was not demonstrably attained even 90 s after the arterial pressure maneuver. The temporal decoupling of renal blood flow and GRR supports the concept of transient involvement of proximal tubular dynamics and efferent resistance changes during acute autoregulation of GFR following step changes in arterial pressure.

Role of endothelium-derived nitric oxide in myocardial reactive hyperemia

1992 ◽  
Vol 263 (1) ◽  
pp. H8-H14 ◽  
Author(s):  
H. Yamabe ◽  
K. Okumura ◽  
H. Ishizaka ◽  
T. Tsuchiya ◽  
H. Yasue
Keyword(s):  
Nitric Oxide ◽  
Reactive Hyperemia ◽  
Suppressive Effect ◽  
Reactive Flow ◽  
Circumflex Coronary Artery ◽  
Pentobarbital Sodium ◽  
Before And After ◽  
Anesthetized Dogs ◽  
The Individual

In pentobarbital sodium-anesthetized dogs we investigated the role of the endothelium-derived nitric oxide and adenosine in the regulation of the coronary blood flow during myocardial reactive hyperemia. Repayments of flow debt after 10-, 20- and 60-s occlusion of the left circumflex coronary artery (LCX) were measured before and after infusion of NG-monomethyl-L-arginine (L-NMMA; n = 15), 8-phenyltheophylline (8-PT; n = 5), and both L-NMMA and 8-PT (n = 5) into the LCX. Infusion of L-NMMA (2 mumol/min, for 20 min) reduced repayments of flow debt after 10-, 20-, and 60-s LCX occlusion by 30 +/- 4 (P less than 0.01), 34 +/- 3 (P less than 0.01), and 14 +/- 3% (P less than 0.01), respectively. Infusion of 8-PT (0.75 mumol/min for 15 min) also reduced these repayments of flow debt by 31 +/- 7 (P less than 0.01), 30 +/- 7 (P less than 0.01), and 34 +/- 6% (P less than 0.01), respectively. Simultaneous infusion of L-NMMA and 8-PT significantly attenuated the peak reactive flow rate and reduced repayment of flow debt after 20-s LCX occlusion by 57 +/- 1% (P less than 0.001), and this reduction in repayment of flow debt was significantly greater than each of those by the individual administration of L-NMMA and 8-PT (both P less than 0.01). The suppressive effect of L-NMMA on repayment of flow debt after 20-s LCX occlusion was quickly reversed by the infusion of L-arginine (3 mg/min for 10 min; n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of histamine H1- and H2-receptors in postprandial intestinal hyperemia

1982 ◽  
Vol 243 (4) ◽  
pp. G248-G252 ◽  
Author(s):  
C. C. Chou ◽  
H. Siregar
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
H1 Receptor ◽  
H2 Receptor Antagonist ◽  
Arterial Infusion ◽  
H2 Receptors ◽  
Before And After ◽  
Anesthetized Dogs ◽  
H1 Receptor Antagonist

Studies were conducted in anesthetized dogs to assess whether histamine H1- and/or H2-receptors play a role in post-prandial intestinal hyperemia. The vascular and metabolic responses of jejunal segments to intra-arterial infusion of histamine and luminal placement of food before and after administration of tripelennamine, an H1-receptor antagonist, metiamide, an H2-receptor antagonist, and the combination of both antagonists were compared. Administration of the antagonists had no effect of jejunal blood flow and intestinal oxygen uptake (VO2). Tripelennamine or metiamide alone attenuated while the combination of both blocked the histamine-induced increases in blood flow and VO2. Metamide alone had no effect on the food-induced increases in flow and VO2. Tripelennamine significantly attenuated the food-induced increase in flow and blocked the increase in VO2. A 30% increase in flow was reduced to 15% after tripelennamine. The effects of tripelennamine plus metiamide were statistically the same as those of tripelennamine alone. It is concluded that endogenous histamines may play a role in postprandial intestinal hyperemia, and the effect is primarily mediated by the H1-receptors.

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