Effect of glucocorticoids on vascular reactivity to vasoactive hormones in rat isolated kidney

lack of relationship to prostaglandins

Christy L. Cooper, Kafait Malik

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The relationship between the effects of glucocorticoids on renal vascular reactivity and prostaglandin synthesis elicited by noradrenaline (NA), angiotensin II (AII), arginine vasopressin (AVP) and bradykinin (Bk) was investigated in the isolated kidney of the rat perfused with Tyrode solution. Administration of NA 0.3–3.0 nmol, AII 0.028–0.28 nmol, AVP 0.027–0.27 nmol and Bk 0.28–2.8 nmol enhanced in a dose‐dependent manner the renal output of immunoreactive prostaglandin E2 (PGE2) and 6‐keto‐PGF1a. NA, AII and AVP, but not Bk, produced renal vasoconstriction and increased perfusion pressure. In the presence of dexamethasone (2.6 × 10−5m) or corticosterone (2.9 × 10−5m), the effects of NA and AII, in enhancing prostaglandin synthesis and producing renal vasconstriction, were reduced. In contrast, stimulation of prostaglandin synthesis by Bk and AVP and the renal vasoconstriction produced by AVP were not altered by the glucocorticoids. Dexamethasone or corticosterone did not alter the output of prostaglandins elicited by A‐23187 or arachidonic acid (AA). Addition of mepacrine (2.1 × 10−5m) to the perfusion fluid reduced the renal output of prostaglandins elicited by the vasoactive hormones and by A‐23187, but not by AA; the vasoconstrictor response to NA and AII, but not to AVP was reduced. In kidneys in which prostaglandin synthesis was inhibited by indomethacin (2.8 × 10−6m), administration of dexamethasone also reduced the renal vasoconstrictor effect of NA and AII. These data indicate that in Tyrode‐perfused rat kidney the glucocorticoids dexamethasone and corticosterone exert a differential effect on the renal vascular reactivity to vasoactive hormones, and that their inhibitory effect on NA and AII‐induced renal vasoconstriction appears to be unrelated to prostaglandin synthesis. 1984 British Pharmacological Society

Original languageEnglish (US)
Pages (from-to)679-688
Number of pages10
JournalBritish Journal of Pharmacology
Volume82
Issue number3
DOIs
StatePublished - Jan 1 1984

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Glucocorticoids
Prostaglandins
Blood Vessels
Hormones
Kidney
Arginine Vasopressin
Norepinephrine
Angiotensin II
Bradykinin
Dexamethasone
Corticosterone
Vasoconstriction
Calcimycin
Vasoconstrictor Agents
Arachidonic Acid
Perfusion
Quinacrine
Dinoprostone
Indomethacin
Pressure

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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title = "Effect of glucocorticoids on vascular reactivity to vasoactive hormones in rat isolated kidney: lack of relationship to prostaglandins",
abstract = "The relationship between the effects of glucocorticoids on renal vascular reactivity and prostaglandin synthesis elicited by noradrenaline (NA), angiotensin II (AII), arginine vasopressin (AVP) and bradykinin (Bk) was investigated in the isolated kidney of the rat perfused with Tyrode solution. Administration of NA 0.3–3.0 nmol, AII 0.028–0.28 nmol, AVP 0.027–0.27 nmol and Bk 0.28–2.8 nmol enhanced in a dose‐dependent manner the renal output of immunoreactive prostaglandin E2 (PGE2) and 6‐keto‐PGF1a. NA, AII and AVP, but not Bk, produced renal vasoconstriction and increased perfusion pressure. In the presence of dexamethasone (2.6 × 10−5m) or corticosterone (2.9 × 10−5m), the effects of NA and AII, in enhancing prostaglandin synthesis and producing renal vasconstriction, were reduced. In contrast, stimulation of prostaglandin synthesis by Bk and AVP and the renal vasoconstriction produced by AVP were not altered by the glucocorticoids. Dexamethasone or corticosterone did not alter the output of prostaglandins elicited by A‐23187 or arachidonic acid (AA). Addition of mepacrine (2.1 × 10−5m) to the perfusion fluid reduced the renal output of prostaglandins elicited by the vasoactive hormones and by A‐23187, but not by AA; the vasoconstrictor response to NA and AII, but not to AVP was reduced. In kidneys in which prostaglandin synthesis was inhibited by indomethacin (2.8 × 10−6m), administration of dexamethasone also reduced the renal vasoconstrictor effect of NA and AII. These data indicate that in Tyrode‐perfused rat kidney the glucocorticoids dexamethasone and corticosterone exert a differential effect on the renal vascular reactivity to vasoactive hormones, and that their inhibitory effect on NA and AII‐induced renal vasoconstriction appears to be unrelated to prostaglandin synthesis. 1984 British Pharmacological Society",
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N2 - The relationship between the effects of glucocorticoids on renal vascular reactivity and prostaglandin synthesis elicited by noradrenaline (NA), angiotensin II (AII), arginine vasopressin (AVP) and bradykinin (Bk) was investigated in the isolated kidney of the rat perfused with Tyrode solution. Administration of NA 0.3–3.0 nmol, AII 0.028–0.28 nmol, AVP 0.027–0.27 nmol and Bk 0.28–2.8 nmol enhanced in a dose‐dependent manner the renal output of immunoreactive prostaglandin E2 (PGE2) and 6‐keto‐PGF1a. NA, AII and AVP, but not Bk, produced renal vasoconstriction and increased perfusion pressure. In the presence of dexamethasone (2.6 × 10−5m) or corticosterone (2.9 × 10−5m), the effects of NA and AII, in enhancing prostaglandin synthesis and producing renal vasconstriction, were reduced. In contrast, stimulation of prostaglandin synthesis by Bk and AVP and the renal vasoconstriction produced by AVP were not altered by the glucocorticoids. Dexamethasone or corticosterone did not alter the output of prostaglandins elicited by A‐23187 or arachidonic acid (AA). Addition of mepacrine (2.1 × 10−5m) to the perfusion fluid reduced the renal output of prostaglandins elicited by the vasoactive hormones and by A‐23187, but not by AA; the vasoconstrictor response to NA and AII, but not to AVP was reduced. In kidneys in which prostaglandin synthesis was inhibited by indomethacin (2.8 × 10−6m), administration of dexamethasone also reduced the renal vasoconstrictor effect of NA and AII. These data indicate that in Tyrode‐perfused rat kidney the glucocorticoids dexamethasone and corticosterone exert a differential effect on the renal vascular reactivity to vasoactive hormones, and that their inhibitory effect on NA and AII‐induced renal vasoconstriction appears to be unrelated to prostaglandin synthesis. 1984 British Pharmacological Society

AB - The relationship between the effects of glucocorticoids on renal vascular reactivity and prostaglandin synthesis elicited by noradrenaline (NA), angiotensin II (AII), arginine vasopressin (AVP) and bradykinin (Bk) was investigated in the isolated kidney of the rat perfused with Tyrode solution. Administration of NA 0.3–3.0 nmol, AII 0.028–0.28 nmol, AVP 0.027–0.27 nmol and Bk 0.28–2.8 nmol enhanced in a dose‐dependent manner the renal output of immunoreactive prostaglandin E2 (PGE2) and 6‐keto‐PGF1a. NA, AII and AVP, but not Bk, produced renal vasoconstriction and increased perfusion pressure. In the presence of dexamethasone (2.6 × 10−5m) or corticosterone (2.9 × 10−5m), the effects of NA and AII, in enhancing prostaglandin synthesis and producing renal vasconstriction, were reduced. In contrast, stimulation of prostaglandin synthesis by Bk and AVP and the renal vasoconstriction produced by AVP were not altered by the glucocorticoids. Dexamethasone or corticosterone did not alter the output of prostaglandins elicited by A‐23187 or arachidonic acid (AA). Addition of mepacrine (2.1 × 10−5m) to the perfusion fluid reduced the renal output of prostaglandins elicited by the vasoactive hormones and by A‐23187, but not by AA; the vasoconstrictor response to NA and AII, but not to AVP was reduced. In kidneys in which prostaglandin synthesis was inhibited by indomethacin (2.8 × 10−6m), administration of dexamethasone also reduced the renal vasoconstrictor effect of NA and AII. These data indicate that in Tyrode‐perfused rat kidney the glucocorticoids dexamethasone and corticosterone exert a differential effect on the renal vascular reactivity to vasoactive hormones, and that their inhibitory effect on NA and AII‐induced renal vasoconstriction appears to be unrelated to prostaglandin synthesis. 1984 British Pharmacological Society

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