Biosynthesis of prostaglandins in the renal medulla of rabbit

Hámberg, Mats

doi:10.1016/0014-5793(69)80312-1

Cited by 81 publications

(17 citation statements)

References 11 publications

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“…cAMP content of inner medullary slices exposed to a high atmospheric 02 resembled hormonally stimulated values seen in renal cortex and other tissues. Relative to cortex, the inner medulla is known to be an active site of prostaglandin synthesis (16)(17)(18)(19) and this process utilizes 02 as substrate (20). Furthermore, prostaglandins are recognized agonists of the adenylate cyclase-cAMP system in several tissues, including renal medulla (21).…”

Section: Resultsmentioning

confidence: 99%

Modulation of the cyclic AMP content of rat renal inner medulla by oxygen: possible role of local prostaglandins.

DeRubertis¹,

Zenser²,

Craven³

et al. 1976

J. Clin. Invest.

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A B S T R A C T The lower 02 tension and more active anerobic metabolism that pertain in the inner medulla (IM) of kidney relative to cortex (C) are well recognized, but there is no evidence that 02 availability constitutes a limitinig or regulatory factor in IM metabolism or function. In the present in vitro study, we examined the effects of 02 on adenosine 3',5'-monophosphate (cAMP) imietabolism in slices of rat renal C and IM. After a 20-min incubation of slices in Krebs Ringer bicarbonate buffer with 95% 02 + 5% C02 serving as the gas phase, the cAMP content of IM wZas 6-10-fold higher than that of C in either the presence or absence of 2 mM 1-methvl-3-isobutylxanthine in the incubation media. In slices of IM incubated for 20 min with 1-methyl-3-isobutvlxanthine, cAMP was 22.5±+SE 2.48 pmol/mg wet weight at 95% 02 and 4.37 without 02. Oxygenation of 02-deprived IM increased cAMP twtofold in 2 min, an effect fully expressed in 5 min (fivefold increase 17 August 1976. which had been incubated at 95% 02. In slices of IM previously exposed to indomethacin or meclofenamate at 95% 02, a maximally effective concentration of exogenous prostaglandin E, restored cAMP and adenylate cyclase activitv to levels which approximated those observed at 95% 02 in the absence of an inhibitor of prostaglandin synthesis. These results suggest that 02 enhancement of cAMP content in IM may be mediated at least in part by local prostaglandinis.

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Section: Resultsmentioning

confidence: 99%

Modulation of the cyclic AMP content of rat renal inner medulla by oxygen: possible role of local prostaglandins.

DeRubertis¹,

Zenser²,

Craven³

et al. 1976

J. Clin. Invest.

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“…1 Abbreviationis used in this paper: CPBA, competitive cating little direct excretory clearance of the primary prostaglandins from the circulation. The kidney itself, however, is a prime site of prostaglandin synthesis (3)(4)(5), and it was conceived that PG synthesized in the kidney might diffuse directly into the urine. Certainly some substances such as tryptamine (6) and cyclic AMP (7) appear in the urine totally or in part as a reflection of their intrarenal synthesis.…”

Section: Introductionmentioning

confidence: 99%

Urinary prostaglandins. Identification and origin.

Frölich¹,

Wilson²,

Sweetman³

et al. 1975

J. Clin. Invest.

497

136

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A BSTRA CT Human urine was analyzed by mass spectrometry for the presence of prostaglandins. Pros-taglandin E2 and F2. were detected in urine from females by selected ion monitoring of the prostaglandin E2-methylester-methoxime bis-acetate and the prostaglandin F2a-methyl ester-Tris-trimethylsilylether de-rivative. Additional evidence for the presence of prostaglandin F2. was obtained by isolating from female urine an amount of this prostaglandin sufficient to yield a complete mass spectrum. The methods utilized permitted quantitative analysis.The origin of urinary prostaglandin was determined by stimulating renal prostaglandin synthesis by arachidonic acid or angiotensin infusion. Arachidonic acid, the precursor of prostaglandin E2, when infused into one renal artery of a dog led to a significant increase in the excretion rate of this prostaglandin. Similarly, infusion of angiotensin II amide led to a significantly increased ipsilateral excretion rate of prostaglandin E2 and F2. in spite of a simultaneous decrease in the creatinine clearance. In man, i.v. infusion of angiotensin also led to an increased urinary elimination of prostaglandin E.These results show that urinary prostaglandins may originate from the kidney, indicating that renally synthesized prostaglandins diffuse or are excreted into the tubule. Thus, urinary prostaglandins are a reflection of renal prostaglandin synthesis and have potential as a tool to delineate renal prostaglandin physiology and pathology.

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“…The rabbit kidney has a high capacity for both synthesis (predominantly in the medulla) and degradation (in the renal cortex) of prostaglandins (Hamberg, 1969;Crowshaw, 1971;Larsson & Anggard, 1973). Prostaglandin E2 is the most abundant renal prostaglandin and is a potent vasodilator (Lee, Crowshaw, Takman, Attrep & Gougoutas, 1967;Daniels, Hinman, Leach & Muirhead, 1967).…”

Section: Introductionmentioning

confidence: 99%

Evidence for Prostaglandin Mediated Prejunctional Control of Renal Sympathetic Transmitter Release and Vascular Tone

Frame

Hedqvist

1975

British J Pharmacology

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I Prostaglandin E2 dose-dependently and reversibly inhibited the noradrenaline overflow resulting from nerve stimulation of the rabbit kidney. 2 The magnitude of this inhibition varied inversely with the frequency of stimulation employed. 3 The prostaglandin synthesis inhibitors, indomethacin and meclofenamic acid, both increased the transmitter overflow resulting from renal nerve stimulation, suggesting that endogenous prostaglandin has a role in the regulation of transmitter release. 4 In the presence of indomethacin, the inhibitory effect of exogenous prostaglandin E2 was enhanced. 5 The prostaglandin precursor, arachidonic acid, also caused a significant, dose-dependent and reversible inhibition of transmitter overflow. This inhibition became insignificant when arachidonic acid was applied in the presence of indomethacin, suggesting that the inhibition was mediated by newly formed prostaglandin rather than by arachidonic acid itself. 6 It is proposed that newly formed prostaglandin controls noradrenaline release primarily from inner cortical nerve endings, thereby maintaining juxtamedullary blood flow under periods of increased sympathetic nerve activity.

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Biosynthesis of prostaglandins in the renal medulla of rabbit

Cited by 81 publications

References 11 publications

Modulation of the cyclic AMP content of rat renal inner medulla by oxygen: possible role of local prostaglandins.

Modulation of the cyclic AMP content of rat renal inner medulla by oxygen: possible role of local prostaglandins.

Urinary prostaglandins. Identification and origin.

Evidence for Prostaglandin Mediated Prejunctional Control of Renal Sympathetic Transmitter Release and Vascular Tone

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