Work in progress: Angiotensin III - induced prostaglandin (PG) release

Blumberg, A L; Denny, Sue E.; Nishikawa, Kohei; Puré, Ellen; Marshall, Garland R.; Needleman, Philip

doi:10.1016/0090-6980(76)90184-2

Cited by 27 publications

(7 citation statements)

References 9 publications

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“…Angiotensin II (AII) has been shown to induce a release of prostaglandin E2 (PGE2)-like material from dog kidney [1], cat [2] and dog [3] spleen and isolated perfused rabbit mesenteric arterial vasculature [4]. Subsequent studies also demonstrated that AII caused the release of PGI2-1ike substances from dog kidney [5], dog lung [6] and isolated spontaneously beating cat right atria [7].…”

Section: Introductionmentioning

confidence: 97%

Modulation by endothelium of the vascular effects of angiotensin II

et al. 1987

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Modulation by vascular endothelium of the effects of AII was studied in the isolated rabbit aortic and superior mesenteric artery strips. The contractile effect of AII was enhanced in rubbed aortic strips. Similar enhancement was obtained in hydroquinone pretreated unrubbed strips. The relaxing effect of acetylcholine in AII--induced precontracted aortic strips was abolished after rubbing and hydroquinone pretreatment. However, no significant changes were observed in the contractile response to AII on aspirin and nicotine pretreated strips. In the isolated mesenteric artery strips AII produced a biphasic responses. The contractile effect of AII was enhanced in rubbed strips. Similar potentiation was also obtained in hydroquinone, aspirin and nicotine pretreated unrubbed strips. The relaxation phase of AII response was completely abolished in rubbed strips but partially inhibited in hydroquinone, aspirin and nicotine pretreated unrubbed strips. From these results it was concluded that EDRF is the main endothelial humoral factor which modulates the effect of AII in the rabbit aorta while both EDRF and PGI2 are involved for the modulation of the effects of octapeptide in the mesenteric artery.

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Section: Introductionmentioning

confidence: 97%

Modulation by endothelium of the vascular effects of angiotensin II

et al. 1987

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“…These peptides were found to release prostaglandin (PG)E from the perfused kidney and mesenteric arterial vasculature (3)(4)(5). The released prostaglandins were vasodilators and antagonized the vasoconstriction caused by the angiotensins.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of Angiotensin II- and III-induced Aldosterone Release by Prostaglandin Synthesis Inhibitors

Campbell¹,

Gómez-Sánchez²,

Adams³

et al. 1979

J. Clin. Invest.

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A B S T R A C T The effect of two prostaglandin synthesis inhibitors, indomethacin and meclofenamate, on angiotensin II (AII)-and III (AIII)-induced aldosterone release was studied in normal and sodiumdepleted conscious rats and in adrenal capsular cell suspensions obtained from normal rats. In normal rats, in vivo AII and AIII were equipotent in causing doserelated increases in serum aldosterone concentrations. Indomethacin decreased the basal serum aldosterone levels by 50% and serum renin levels by 43%. In addition, the steroidogenic effects of AII and AIII were reduced by 45 and 63% with 3 mg/kg of indomethacin and 63 and 73% with 10 mg/kg, respectively. In contrast, meclofenamate failed to alter basal serum levels of aldosterone or AII-stimulated aldosterone release but inhibited serum renin levels by 27% and the aldosterone-stimulating effect of AIII by 99%. Indomethacin (3 mg/kg) and meclofenamate (2 mg/kg) inhibited urinary prostaglandin (PG)E2 and PGF2G excretion by 63 1552 stimulated aldosterone release but inhibited that stimulated by AIII by 86%. The present findings suggest that prostaglandins modulate the effects of the renin-angiotensin system by stimulating the release of renin from the kidney and augmenting the steroidogenic effects of AII and AIII in the adrenal cortex.INTRODUCTION Recently, we have reported that both angiotensin II and III were equipotent in stimulating the release of aldosterone from the adrenal cortex; however, angiotensin III possessed only 30% of the pressor activity of angiotensin II (1, 2). These peptides were found to release prostaglandin (PG)E from the perfused kidney and mesenteric arterial vasculature (3-5). The released prostaglandins were vasodilators and antagonized the vasoconstriction caused by the angiotensins. Additionally, PGE stimulated the release of aldosterone from the adrenal, a property that was additive in effect with that of angiotensin II (6, 7). We, therefore, wondered if angiotensin II and III might simultaneously stimulate the release of aldosterone and PGE2 from the adrenal, and the released PGE2, acting as an intra-adrenal hormone, would also stimulate the release of aldosterone, thereby augmenting angiotensin-induced steroidogenesis. To test this hypothesis, the steroidogenic activity of angiotensin II and III were compared in conscious rats and adrenal cell suspensions in the presence and absence of the inhibitors of prostaglandin synthesis, indomethacin and meclofenamate (8).

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“…Cyclic AMP apparently does not act as the second messenger in this system (8,(13)(14)(15), and although potassium is required for steroidogenesis, there is no convincing evidence that this ion is the second messenger for angiotensin II (16)(17)(18)(19). Prostaglandins may augment or modulate effects of angiotensin II in the adrenal gland, but there is no direct proof that they are fundamentally responsible for its stimulation of steroidogenesis (20)(21)(22)(23)(24).…”

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confidence: 99%

Angiotensin alters 45Ca2+ fluxes in bovine adrenal glomerulosa cells.

Elliott¹,

Goodfriend²

1981

Proc. Natl. Acad. Sci. U.S.A.

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Angiotensin II stimulated 45Ca2" release from bovine adrenal glomerulosa cells. It also decreased the influx of ftCa2" into glomerulosa cells. The effects were observed within 2 min of hormone addition and were blocked by Saralasin, a competitive inhibitor of angiotensin. Des-Phe8-angiotensin II, a biologically inert analog, was inactive in this system. Angiotensin II also inhibited the influx of '33Ba2" and 54Mn2+, whereas 51Cr6+ and 57Co2+ were unaffected. Alterations in 45Ca2+ fluxes were seen with concentrations of angiotensin that stimulate aldosterone biosynthesis in bovine glomerulosa cell preparations. These results suggest that calcium plays a key role in angiotensin-stimulated aldosteronogenesis.Angiotensin II stimulates aldosterone synthesis both in vivo and in vitro (1)(2)(3)(4)(5)(6)(7)(8). It binds to specific receptors that are probably localized on the plasma membrane of adrenal glomerulosa cells (9, 10). Recent work has shown that angiotensin II increases the activity ofenzymes catalyzing side-chain cleavage ofcholesterol and 18-hydroxylation of corticosterone (11,12). However, the mechanism by which angiotensin II-receptor interaction leads to these effects is poorly understood. Cyclic AMP apparently does not act as the second messenger in this system (8,(13)(14)(15), and although potassium is required for steroidogenesis, there is no convincing evidence that this ion is the second messenger for angiotensin . Prostaglandins may augment or modulate effects of angiotensin II in the adrenal gland, but there is no direct proof that they are fundamentally responsible for its stimulation of steroidogenesis (20-24).Calcium apparently plays an important role in many of the actions of angiotensin II (13). Calcium in the medium is necessary for the hormone's effects on contraction ofrat descending colon (25), for its stimulation of hepatic gluconeogenesis from some substrates (26), and for aldosterone synthesis (8,14,27,28). Lanthanum and other calcium antagonists have been shown to inhibit angiotensin II-stimulated steroidogenesis (8,14,29 This buffer contained 115 mM NaCl/10 mM Na phosphate/i mM MgSO4/22 mM NaHCOJl.5 mM CaCl2/11 mM glucose (pH 7.4). In the laboratory, each adrenal was prepared by peeling off the capsule, bisecting the gland, and scraping away the medulla. Tissue was cut into squares 1 cm wide, and one 0.5-mm slice was cut from the outer surface of each square with a Stadie-Riggs microtome. All slices were cut into smaller pieces and placed into tubes (nitrocellulose, 3.8 x 10.2 cm) containing Krebs-Ringer buffer with 1% crystalline albumin, 7.4% (wt/ vol) collagenase, and 0.1% DNase. Of this enzyme solution, 40 ml were used for slices from eight adrenals. Tissue was incubated in a 37°C shaking water bath (60 cycles/min) under a stream of 95% 2/5% CO2 for 60 min, and the contents of each tube were mixed at 15-min intervals by pipetting up and down 25 times through a wide-mouth 10-ml pipette.At the end of60 min, the digested tissue was filtered through one layer of cheesecloth, ...

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Work in progress: Angiotensin III - induced prostaglandin (PG) release

Cited by 27 publications

References 9 publications

Modulation by endothelium of the vascular effects of angiotensin II

Modulation by endothelium of the vascular effects of angiotensin II

Attenuation of Angiotensin II- and III-induced Aldosterone Release by Prostaglandin Synthesis Inhibitors

Angiotensin alters 45Ca2+ fluxes in bovine adrenal glomerulosa cells.

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