Influence of prostaglandins on sodium transport of isolated medullary nephron segments

Fine, Leon G.; Trizna, Walter

doi:10.1152/ajprenal.1977.232.4.f383

Cited by 45 publications

(31 citation statements)

References 25 publications

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“…In the dog (Fulgraff &; Brandenbusch, 1974) and the rabbit (Fine &;Trizna, 1977) prostaglandin E2, the major renal prostaglandin (Daniels, Hinman, Leach &r Muirhead, 1967) exerts two prominent effects on renal function, i.e. vasodilatation and natriuresis.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin synthesis and renal function in man.

Haylor¹

1980

The Journal of Physiology

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SUMMARY1. Experiments were performed to determine the changes in renal function which occur following prostaglandin synthetase inhibition in healthy conscious humans. It was hoped that such experiments could provide information on the mechanism by which renal prostaglandin synthesis influences urinary excretion.2. In water-diuretic male subjects (receiving a slow saline infusion) the renal excretion of sodium and water was reduced following i.v. acetylsalicylic acid (1 g) administration, while the effective renal plasma flow (p-aminohippurate clearance), and glomerular filtration rate (inulin clearance) remained unaltered. 3. In normally hydrated female subjects on an unrestricted diet, the mean urinary prostaglandin E output was 8-5 ng/hr. The renal excretion of sodium, water and urinary prostaglandin E were significantly reduced (P < 0.05) following oral acetylsalicylic acid (1 -2 g) administration.4. In normally hydrated female subjects on an unrestricted diet the renal excretion of sodium and water was reduced following oral paracetamol (1-5 g) administration.5. It is concluded that following renal prostaglandin synthetase inhibition in conscious humans, the excretion of sodium and water can be reduced without measurable changes in the glomerular filtration rate or effective renal plasma flow. It is suggested that in conscious healthy humans, the kidney may continually synthesize prostaglandin which might help to maintain sodium and water excretion by a direct action on the renal tubule without influencing renal blood flow. The relevance of this hypothesis to the intrarenal location of prostaglandin synthetase is discussed.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin synthesis and renal function in man.

Haylor¹

1980

The Journal of Physiology

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“…However, although there is still some controversy concerning the effects of prostaglandins on the collecting tubule (e.g. Fine & Trizna, 1977;Stokes & Kokko, 1977), it should nevertheless be borne in mind that in transporting epithelia, potential difference is not an independent variable, since the potential difference across the tubule depends not only on sodium transport, but also on the conductance (ionic permeability) of the epithelium. Leyssac et al ( 1975) have pointed out that the collecting tubule is a 'high resistance' epithelium resembling frog skin and toad bladder, and in such epithelia, prostaglandins do not generally inhibit sodium transport.…”

Section: Dtscussionmentioning

confidence: 99%

“…Prostaglandins have both diuretic and natriuretic actions (Johnston, Herzog & Lauler, 1967;Fulgraff & Brandenbusch, 1974;Fine & Trizna, 1977), but the importance of endogenous prostaglandins in determining or regulating renal solute and water excretion remains uncertain. Following the in vivo administration of prostaglandin synthetase inhibitors, the renal excretion of sodium or water or both has been reported to be: (a) increased in conscious dogs (Kirschenbaum & Stein, 1976); (b) decreased in rats anaesthetized with Amytal (Leyssac, Christensen, Hill & Skinner, J. HAYLOR AND C. J. LOTE anaesthesia (Terragno, Terragno & McGiff, 1977) have all been shown to increase renal prostaglandin production.…”

Section: Introductionmentioning

confidence: 99%

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

Haylor¹,

Lote²

1980

The Journal of Physiology

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SuMMARY1. Conscious rats, with implanted carotid arterial cannulae, received a saline infusion (5.8 ml./hr) via a tail vein for a 6 hr period. The urinary excretion of water, sodium, potassium, urea and the osmolal output were monitored, together with the systemic blood pressure. Glomerular filtration rate (inulin clearance) and effective renal plasma flow (p-aminohippurate clearance) were also measured. Four hours after the start of the infusion, indomethacin (10 mg/kg body weight) in buffered saline, or buffered saline alone, was a inistered via the tail vein.2. Following indomethacin administration, urine flow, sodium output and osmolal output were markedly reduced (P < 0.01). However, there were no measurable changes in the systemic blood pressure, glomerular filtration rate, or effective renal plasma flow.3. It is concluded that the changes in urinary excretion observed after indomethacin are not dependent on changes in effective renal plasma flow or glomerular filtration, and it is suggested that indomethacin inhibits the synthesis of endogenous prostaglandins which directly influence renal tubular function.

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“…Prostacyclin (PGI2) mainly produced in the glomerulus, modulates cortical functions (maintenance or increase of renal blood flow, regulation of glomerular filtration rate, renin secretion) (Anderson et al, 1976;Weber et al, 1976;Dunn & Hood, 1977;Whorton et al, 1977;Terragno et al, 1978). Prostaglandin E2 (PGE2), synthesized primarily in the papilla, regulates medullary functions (water, sodium and chloride excretion) (Anderson et al, 1976;Fine & Trizna, 1977;Stokes, 1979;Sraer et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

Caussade¹,

Cloarec²

1993

British J Pharmacology

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1 The effects of tienoxolol, (ethyl 2-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-5-[(2-thienylcarbonyl) amino] benzoate, hydrochloride), a novel drug exhibiting both diuretic and Padrenoceptor blocking properties, were investigated on urinary 6-keto-prostaglandin Fl, (6-keto-PGFI,) and PGE2 excretion in the rat and compared to those of reference diuretic (furosemide) and Padrenoceptor antagonists (acebutolol, propranolol). Since tienoxolol was shown to bind to A, and A2 adenosine receptors, the action of theophylline was also evaluated.2 Tienoxolol (8-128mgkg-', p.o.) induced a dose-related increase of 6-keto-PGFI, excretion from 32 mg kg-' but a significant elevation of urinary PGE2 levels was only reached after administration of 128 mg kg-'. However, renal prostaglandin concentrations were not modified by tienoxolol.3 Furosemide (32 mg kg-') displayed a strong diuretic activity but did not enhance 6-keto-PGFI,, excretion. Likewise, the latter was unaffected by acebutolol and propranolol (128 mg kg-') and no significant diuresis was observed following administration of these two P-blocking agents. Theophylline (64 mg kg-1), like tienoxolol, was able to induce both diuresis and urinary prostaglandin excretion. Furthermore, they bound with similar affinities to A, and A2 adenosine receptors. This led to the suggestion that a relationship between P,-purinoceptors, prostaglandin release, diuresis and natriuresis could exist.4 Oral co-administration of NECA (0.2 mg kg-') with tienoxolol markedly reduced the urinary 6-keto-PGF,c, excretion observed when tienoxolol was administered alone. However, neither diuresis nor natriuresis were modified, demonstrating that the proposed relationship was untenable. 5 In conclusion, PGI2 probably does not participate in the diuretic and natriuretic activity of tienoxolol. The increase of urinary 6-keto-PGF,g excretion may result not only from the haemodynamic properties of the drug but also from the rise of the urinary flow induced by tienoxolol.

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Influence of prostaglandins on sodium transport of isolated medullary nephron segments

Cited by 45 publications

References 25 publications

Prostaglandin synthesis and renal function in man.

Prostaglandin synthesis and renal function in man.

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

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