The effect of the inhibition of prostaglandin synthesis on renal blood flow in fetal sheep

1991 ◽  
Vol 165 (1) ◽  
pp. 185-190 ◽  
Author(s):  
Susan A. Arnold-Aldea ◽  
Ron A. Auslender ◽  
Julian T. Parer
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Prostaglandin Synthesis ◽  
Fetal Sheep ◽  
Inhibition Of Prostaglandin Synthesis

Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog

1979 ◽  
Vol 237 (3) ◽  
pp. F182-F187
Author(s):  
M. C. Blasingham ◽  
A. Nasjletti
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin Synthetase ◽  
Renal Functions ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Stimulation Of

To study the effects of stimulation of renal prostaglandin biosynthesis by bradykinin, we assessed the changes in renal functions induced by intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog anesthetized with pentobarbital before and during inhibition of prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of meclofenamate did not affect the bradykinin-induced increase in renal blood flow and urine volume, but suppressed the evoked output of "PGE" and reduced the associated natriuresis, i.e., sodium excretion increased by only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast, meclofenamate did not affect the natriuresis effected by an equidilator dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations suggest that a product of prostaglandin synthetase produced by the kidney during intrarenal infusion of bradykinin contributes to the natriuretic action of the peptide.

Exaggerated renal vascular reactivity to angiotensin and thromboxane in young genetically hypertensive rats

1990 ◽  
Vol 259 (2) ◽  
pp. F372-F382 ◽  
Author(s):  
C. Chatziantoniou ◽  
F. H. Daniels ◽  
W. J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Receptor Agonist ◽  
Vascular Reactivity ◽  
Prostaglandin Synthesis ◽  
Genetic Hypertension ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Renal Vascular

The objective of this study was to test the hypothesis that angiotensin II and thromboxane A2 (TxA2) contribute to the elevated renal vascular resistance observed during the development of genetic hypertension. In 6-wk-old anesthetized spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats, renal blood flow (electromagnetic flowmetry) and carotid arterial pressure were measured during bolus injections of different doses of angiotensin II and U46619 (stable receptor agonist of TxA2) into the renal artery before and during inhibition of prostaglandin synthesis by indomethacin. In all cases, arterial pressure remained unchanged at the pre-injection levels. Under control conditions, angiotensin II reduced renal blood flow in SHR almost twice as much as in WKY. This strain difference was abolished by inhibition of prostaglandin synthesis, suggesting that a deficiency in the action of endogenous vasodilator prostaglandins is responsible for the enhanced response to angiotensin II in SHR. Under control conditions, the TxA2-receptor agonist produced similar reductions of renal blood flow in SHR and WKY. However, after indomethacin, the agonist-induced vasoconstriction was twice as large in SHR as in WKY, suggesting that SHR kidneys have an increased vascular reactivity to TxA2, which is unmasked when indomethacin reduces elevated levels of endogenous TxA2. These findings indicate important strain differences between young SHR and WKY in the renal vascular response to angiotensin II and TxA2 that may contribute to the renal vasoconstriction observed during the development of genetic hypertension.

Effects of dopamine in the renal vascular bed of fetal, newborn, and adult sheep

1987 ◽  
Vol 252 (3) ◽  
pp. R490-R497 ◽  
Author(s):  
K. T. Nakamura ◽  
R. A. Felder ◽  
P. A. Jose ◽  
J. E. Robillard
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Renal Blood Flow ◽  
Blood Flow Velocity ◽  
Experimental Models ◽  
Dose Ratio ◽  
Fetal Sheep ◽  
Adult Sheep ◽  
Beta Adrenoceptor ◽  
Arterial Blood

The renal hemodynamic response to renal arterial dopamine infusions was compared in unanesthetized fetal (129-137 days gestation, full term 145 days), newborn, and adult sheep. Mean arterial blood pressure and heart rate remained unchanged during intrarenal dopamine infusions. Dopamine produced dose-related decreases in mean renal blood flow velocity in all three groups. When compared with adult sheep fetal sheep were slightly more sensitive to the vasoconstrictive effects of dopamine ED50 (mean effective dose ratio: fetus/ED50 adult = 0.368 +/- 0.047, P less than 0.05). Increases in mean renal blood flow velocity were not seen at any dose given (1-16 micrograms/kg body wt in fetuses, 2-32 micrograms/kg body wt in newborns and adults) until dopamine was infused during alpha- and beta-adrenoceptor blockade. The largest mean increase in renal flow velocity was 13 +/- 3, 16 +/- 3, and 17 +/- 4% in fetal, newborn, and adult sheep, respectively. cis-Flupentixol inhibited the vasodilation. This study demonstrates the presence of renal vasodilation following renal arterial dopamine infusions in fetal, newborn, and adult sheep when renal alpha- and beta-adrenoceptors are blocked. Vasodilator responses are similar in all three groups, and increases in renal blood flow velocity are small compared with that of other experimental models.

The Effect of Inhibition of Prostaglandin Synthesis on Microvascular Haemostatic Plug Formation in the Rabbit

1975 ◽  
Author(s):  
D. Bergqvist ◽  
E. Svensjö ◽  
K.-E. Arfors
Keyword(s):  
Blood Flow ◽  
Mesenteric Artery ◽  
Prostaglandin Synthesis ◽  
Formation Time ◽  
Initial Formation ◽  
Platelet Aggregability ◽  
Inhibition Of Prostaglandin Synthesis ◽  
The Difference ◽  
The Stability ◽  
Plug Formation

Bleeding induced by microvascular transection in the rabbit mesentery stops by the formation of a haemostatic plug. Normal platelets as well as the normal coagulation and fibrinolytic systems are essential for haemostatic plug formation, the initial formation being mainly ADP-dependent and the stability mainly an effect of fibrin formation. The difference in haemostasis between arterioles and venules was abolished by aspirin (Arfors et al. Scand. J. Haematol. 9, 322, 1972). In this study we have investigated the effect of indomethacin. As with aspirin, venular haemostatic plug formation time was shortened and plug stability increased. Local infusion of PGE1 into the cranial mesenteric artery significantly prolonged arteriolar and venular haemostatic plug formation time. Measuring blood flow velocity, vessel contraction and haemostatic plug volume makes it possible to determine the proportion of platelets participating in the formation of an effective plug in individual vessels. Platelet aggregability is significantly higher in plugs formed at injuries on the arteriolar side of the microcirculation than on the venular, but this difference is totally abolished after indomethacin. In conclusion the difference in haemostasis between arterioles and venules in this model can be explained by prostaglandin being formed in the mesenteric preparation.

Alteration of canine renal vascular response to hemorrhage by inhibitors of prostaglandin synthesis

1976 ◽  
Vol 230 (4) ◽  
pp. 940-945 ◽  
Author(s):  
JL Data ◽  
LC Chang ◽  
AS Nies
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Control Period ◽  
Prostaglandin Synthesis ◽  
Hemorrhagic Hypotension ◽  
Renal Cortical Blood Flow ◽  
Renal Vascular ◽  
Inner Cortex ◽  
Equal Thickness ◽  
Total Renal Blood Flow

The involvement of prostaglandins in the redistribution of renal cortical blood flow to inner cortical nephrons during hemorrhagic hypotension was studied in the pentobarbital-anesthetized dog. Total renal blood flow and distribution of renal cortical flow were determined with the radioactive microsphere technique by dividing the cortex into four zones of equal thickness, zone 1 being outermost and zone 4 being juxtamedullary. Two inhibitors of prostaglandin synthesis were used: indomethacin 8 mg/kg and aspirin 100 mg/kg. The inhibitor or the vehicle was given intravenously prior to a control period which was followed by a hemorrhage sufficient to decrease arterial pressure by about one-third. The distribution of cortical flow was determined before hemorrhage, during hemorrhagic hypotension, and after transfusion. In the vehicle-treated dogs, total renal blood flow was well maintained, but flow redistributed to favor the inner cortical nephrons. This vasodilation in the inner cortex was blocked by both inhibitors of prostaglandin synthesis resulting in a decrease in total renal blood flow and relative ischemia of the juxtamedullary nephrons. Salicylate levels required to accomplish blockage of inner cortical vasodilaton were less than 7 mg/100 ml. These studies indicate that prostaglandins are responsible for the decreased vascular resistance of the inner cortical nephrons which results in the redistribution of blood flow during hemorrhage, and when prostaglandin synthesis is blocked, the kidney vasculature constricts during hemorrhage.

Prostaglandin synthesis by isolated rat glomeruli: effect of angiotensin II

1980 ◽  
Vol 239 (5) ◽  
pp. F486-F495 ◽  
Author(s):  
D. Schlondorff ◽  
S. Roczniak ◽  
J. A. Satriano ◽  
V. W. Folkert
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Prostaglandin Synthesis ◽  
Breakdown Product ◽  
Isolated Glomeruli ◽  
Isolated Rat

Prostaglandins play a role in the regulation of renal blood flow and glomerular filtration. In the presence of [14C]arachidonate the pattern of prostaglandins produced by isolated glomeruli was PGF2 alpha > PGE2 > PGD2 = TXB2 = 6-keto-PGF1 alpha (a metabolite of prostacyclin). Glomeruli prelabeled with [14C]arachidonate showed an additional labeled prostaglandin that co-chromatographs with 6,15-diketo-13,13-dihydro-PGF1 alpha and may represent breakdown product of prostacyclin. Thus, prostacyclin, judged by its breakdown products, was the second most abundant prostaglandin produced. These results were confirmed by specific radioimmunoassays for PGF2 alpha, PGE2, and 6-keto-PGF1 alpha. Isolated glomeruli produced 1,740 pg x 10 min-1 x mg protein-1 of PGF2 alpha, 798 of 6-keto-PGF1 alpha, and 266 od PGE2. In prelabeled glomeruli angiotensin II causes a small but significant increase in 14C-labeled prostaglandins. Radioimmunoassay for 6-keto-PGF1 alpha showed that the angiotensin stimulation was specific for prostacyclin. Angiotensin II also affected the glomerular handling of [14C]arachidonate. It decreased the uptake of extracellular [14C]arachidonate and increased the incorporation of intracellular [14C]arachidonate into glomerular phospholipids. Based on these results, we propose that in the glomerulus angiotensin increases prostaglandin synthesis and stimulates deacylation and reacylation of phospholipids.

Prostaglandin E2 but not I2 restores furosemide response in indomethacin-treated rats

1986 ◽  
Vol 250 (6) ◽  
pp. F980-F985 ◽  
Author(s):  
K. A. Kirchner ◽  
C. J. Martin ◽  
J. D. Bower
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Prostaglandin E2 ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Synthesis Inhibition ◽  
Vasodilatory Effect ◽  
Sodium Load ◽  
Furosemide Administration

Indomethacin attenuates furosemide's natriuretic response. Although this has been attributed to cyclooxygenase inhibition, attempts to correlate prostaglandin (PG) production with furosemide's natriuresis have led some investigators to conclude that prostaglandins are not involved in this response. This study was designed to evaluate the effects of intraaortic administration of PGE2, PGI2 (100 ng X kg-1 X min-1), or the vasodilators secretin or bradykinin (75 microU X kg-1 X min-1) on the furosemide-indomethacin antagonism. Fractional sodium excretion (FENa) during furosemide administration was 4.59 +/- 0.50% in control rats but 1.84 +/- 0.33% in indomethacin-treated rats (Indo) (P less than 0.001). PGE2 prevented indomethacin from attenuating furosemide's response (FENa, 3.91 +/- 0.25%; P = NS vs. control; P less than 0.01 vs. Indo). PGI2, however, failed to prevent the furosemide-indomethacin antagonism (FeNa, 1.94 +/- 0.59%, P less than 0.001 vs. control; P = NS vs. Indo). Inulin clearance, arterial pressure, filtered sodium load, and renal blood flow were not different between groups. Neither secretin nor bradykinin prevented the indomethacin-furosemide antagonism. This study is consistent with the hypothesis that indomethacin antagonizes furosemide's natriuretic response by prostaglandin synthesis inhibition. Furthermore, PGE2 seems to restore furosemide's response through actions other than a vasodilatory effect.

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