Prostaglandin synthesis by isolated rat glomeruli: effect of angiotensin II

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.

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Dissociation Of renal blood flow (RBF) and glomerular filtration rate (GFR) by angiotensin II (A-II) in acute alterations of renal artery pressure (RAP)

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)62598-9 ◽

1984 ◽

Vol 36 ◽

pp. 196

Author(s):

Fumio Goto ◽

Edwin K. Jackson

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Angiotensin Ii ◽

Renal Artery ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Filtration Rate ◽

Artery Pressure

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Angiotensin II and renal prostaglandin release in the dog. Interactions in controlling renal blood flow and glomerular filtration rate

Acta Physiologica Scandinavica ◽

10.1111/j.1748-1716.1994.tb09708.x ◽

1994 ◽

Vol 150 (4) ◽

pp. 431-440 ◽

Cited By ~ 14

Author(s):

J. F. BUGGE ◽

E. S. STOKKE

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Angiotensin Ii ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Filtration Rate ◽

Prostaglandin Release

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

AJP Renal Physiology ◽

10.1152/ajprenal.1990.259.2.f372 ◽

1990 ◽

Vol 259 (2) ◽

pp. F372-F382 ◽

Cited By ~ 18

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.

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Characterization of the postocclusive response of renal blood flow in the cat

AJP Renal Physiology ◽

10.1152/ajprenal.1978.235.4.f286 ◽

1978 ◽

Vol 235 (4) ◽

pp. F286-F290 ◽

Cited By ~ 3

Author(s):

W. S. Spielman ◽

H. Osswald

Keyword(s):

Blood Flow ◽

Angiotensin Ii ◽

Renal Artery ◽

Renal Blood Flow ◽

Artery Occlusion ◽

Renal Nerves ◽

Vasoconstrictor Response ◽

Renal Artery Occlusion ◽

Chronic Denervation

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.

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Effect of chloride on renal blood flow in angiotensin II induced hypertension

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y91-076 ◽

1991 ◽

Vol 69 (4) ◽

pp. 507-511 ◽

Cited By ~ 5

Author(s):

John C. Passmore ◽

Agnes E. Jimenez

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Sodium Chloride ◽

Angiotensin Ii ◽

Renal Blood Flow ◽

Dietary Sodium ◽

Maximum Increase ◽

High Sodium ◽

Low Sodium ◽

Chloride Effect

The effect of selective dietary sodium and (or) chloride loading on blood pressure and renal blood flow (RBF) in the rat angiotensin II (AII) model of hypertension was determined. AII (200 ng/min) or saline was infused intraperitoneally. Diets were provided with either high or low concentrations of sodium, chloride or both ions for 22 days. The blood pressure of saline-treated animals was not increased by the high sodium chloride diet. Animals on a high sodium, high chloride diet had a significantly greater increase of blood pressure at 8, 15, 18, and 22 days of AII infusion compared with AII-treated animals on a low sodium, low chloride diet (p < 0.05). Selective dietary loading of either high sodium or chloride in AII-treated rats produced no greater elevation of blood pressure than AII with the low sodium, low chloride diet. Selective high dietary chloride was associated with a lower RBF in AII- and vehicle-treated rats compared with low dietary chloride. The chloride effect on RBF was greater in AII-treated animals. In conclusion, both sodium and chloride are necessary to produce the maximum increase of blood pressure in AII animals. AII enhances the decreased RBF induced by dietary chloride.Key words: angiotensin II, sodium chloride, blood pressure.

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