The Antihypertensive and Natriuretic Endocrine Function of the Kidney: Vascular and Metabolic Mechanisms of the Renal Prostaglandins

Lee, J. B.

doi:10.1007/978-1-4684-2844-5_21

Cited by 7 publications

(2 citation statements)

References 60 publications

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“…All these drugs cause alterations in stomach and kidney which, depending on the dose given, range from irritation and functional impariment [12] to vast necrosis of cellular components in these organs [17]. It has been argued that both effects might be due to inhibition of PG-synthesis in these organs because PG's appear to be physiological inhibitors o f secretion of hydrochloric acid in the stomach [18] and might also regulate electrolyte elimination and regional blood flow in the kidney [19]. But why do other inhibitors of PG-synthesis not cause these effects?…”

Section: Introductionmentioning

confidence: 99%

Inhibition of prostaglandin synthesis in vivo by nonsteroid anti-inflammatory drugs: Evidence for the importance of pharmacokinetics

Brune¹,

Gräf²,

Glatt³

1976

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A variety of acidic and non-acidic compounds are potent inhibitors of prostaglandin (PG) synthesis in vitro. However, only a few, namely the acidic nonsteroid anti-inflammatory drugs (NSAID) are useful anti-inflammatory analgesics in the clinic. Since inhibition of PG-synthesis is believed to be the main target of NSAID in inflammation this superiority of acidic compounds remains unexplained. We have considered that one explanation could be that only acidic NSAID appear in high concentrations in inflamed tissue to inhibit PG-synthesis sufficiently. To test this hypothesis the following experiments were carried out: (A) PG-synthesis and its inhibition by acidic and non-acidic NSAID was measured in vivo at the site of inflammation. It was found that in therapeutic doses only acidic NSAID were capable to reduce PG-synthesis significantly. (B) Measurement of drug concentration in inflamed tissue showed that only acidic NSAID were found in significantly higher concentrations in inflamed than in control tissue. From these observations it is concluded that a specific pharmacokinetic behaviour of acidic NSAID leading to high concentrations in inflamed tissue is a decisive aspect of their anti-inflammatory action.

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Section: Introductionmentioning

confidence: 99%

Inhibition of prostaglandin synthesis in vivo by nonsteroid anti-inflammatory drugs: Evidence for the importance of pharmacokinetics

Brune¹,

Gräf²,

Glatt³

1976

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“…Prostaglandins E and A have been shown to increase renal blood flow, urine volume, free water clearance, and sodium excretion when infused in dogs (10)(11)(12)(13)(14). Renal effects in hypertensive man are similar to those in dogs when PGA is infused at low concentrations, however at higher concentrations a vasodepressor effect predominates (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Chronic Sodium Loading and Sodium Restriction on Plasma Prostaglandin A, E and F Concentrations in Normal Humans

Rm¹,

Spector²,

Bv³

et al. 1973

J. Clin. Invest.

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A B S T R A C T It has been suggested that prostaglandins may be involved in the control of sodium homeostasis. Prostaglandin A and prostaglandin E have been shown to increase renal blood flow and urinary sodium excretion and prostaglandin A has been shown to stimulate aldosterone release. The purpose of this study was to determine the effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations.Seven normal human volunteers were placed on three sodium intake diets: (a) ad lib. sodium intake, (b) high sodium intake, and (c) low sodium intake. Plasma prostaglandin A, E, and F concentrations were measured by radioimmunoassay.Mean prostaglandin A levels on the ad lib. diet were 1.60 ng/ml. Prostaglandin A levels decreased 49% to 0.82 ng/ml on the high sodium intake and increased 34% to 2.14 ng/ml on the low sodium intake. Prostaglandin A levels increased 161% on the low sodium diet in comparison with levels on the high sodium diet. Plasma prostaglandin E and F concentrations did not change significantly during variation in sodium intake.These results show that dietary sodium content markedly effects plasma prostaglandin A levels and that prostaglandins may play a role in the physiologic mechanism of sodium homeostasis.

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Natriuretic “hormone” and the renal prostaglandins

Lee

1972

Prostaglandins

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The Antihypertensive and Natriuretic Endocrine Function of the Kidney: Vascular and Metabolic Mechanisms of the Renal Prostaglandins

Cited by 7 publications

References 60 publications

Inhibition of prostaglandin synthesis in vivo by nonsteroid anti-inflammatory drugs: Evidence for the importance of pharmacokinetics

Inhibition of prostaglandin synthesis in vivo by nonsteroid anti-inflammatory drugs: Evidence for the importance of pharmacokinetics

The Effect of Chronic Sodium Loading and Sodium Restriction on Plasma Prostaglandin A, E and F Concentrations in Normal Humans

Natriuretic “hormone” and the renal prostaglandins

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