Antidiuretic hormone increases renal prostaglandin synthesis in vivo

Walker, L A; Whorton, A. R.; Smigel, Murray D.; FRANCE, RICHARD; Frölich, Jürgen C.

doi:10.1152/ajprenal.1978.235.3.f180

Cited by 55 publications

(30 citation statements)

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“…Vasopressin is another vasoconstrictor peptide that activates phospholipase A2 and releases AA (31). Previous studies have established that vasopressin stimulates the formation of PGE 2 in mesangial and tubular epithelial cells and increases the urinary excretion of PGE 2 (20,44,46). PGE 2 modulates both the tubular and vascular responses to vasopressin (9,15,38).…”

Section: Discussionmentioning

confidence: 99%

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

Sarkis¹,

Ito²,

Mori³

et al. 2005

American Journal of Physiology-Renal Physiology

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. Cytochrome P-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus. Am J Physiol Renal Physiol 289: F1333-F1340, 2005. First published July 12, 2005 doi:10.1152/ajprenal.00188.2005.-This study compared the renal metabolism of arachidonic acid in Brattleboro (BB) (vasopressin deficient) and Long-Evans (LE) control rats and the effects of a cytochrome P-450 (CYP) inhibitor 1-aminobenzotriazole (ABT) on renal function in these animals. The production of 20-hydroxyeicosatetraenoic acid (20-HETE) by renal cortical and outer medullary microsomes was significantly greater in BB than in LE rats (155 Ϯ 16 vs. 92 Ϯ 13 and 59 Ϯ 7 vs. 33 Ϯ 3 pmol ⅐ min Ϫ1 ⅐ mg protein Ϫ1 ). Renal cortical epoxygenase activity was not different in these strains. The expression of CYP4A proteins was 58 and 78% higher in the renal cortex and outer medulla of BB than in LE rats. Chronic treatment of BB rats with a vasopressin type 2 receptor agonist for 1 wk normalized the renal production of 20-HETE. Chronic blockade of the formation of 20-HETE and EETs with ABT had little effect on renal function in LE rats. However, urine flow increased by 54% and urine osmolarity decreased by 33% in BB rats treated with ABT. Plasma levels of oxytocin fell significantly from 7.2 Ϯ 1.3 to 3.9 Ϯ 1.0 pg/ml. The effects of ABT in BB rats were attenuated by chronic infusion of oxytocin (0.7 ng ⅐ min Ϫ1 ⅐ 100 g Ϫ1 ) to maintain fixed high plasma levels of this hormone. These results indicate that the expression of CYP4A protein and the renal formation of 20-HETE are elevated in the kidney of BB rats due to a lack of vasopressin and that chronic blockade of the formation of 20-HETE and EETs with ABT promotes water excretion in vasopressin-deficient BB rats by reducing the circulating levels of oxytocin, which is a weak vasopressin agonist. Brattleboro rats; 20-hydroxyeicosatetraenoic acid; cytochrome P-450; epoxyeicosatrienoic acid; renal hemodynamics ARACHIDONIC ACID (AA) is metabolized by cytochrome P-450 (CYP) enzymes in the kidney to produce epoxyeicosatrienoic acids (EETs), 20-hydroxyeicosatetraenoic acid (20-HETE), and dihydroxyeicosatrienoic acids (DiHETEs). These compounds have been reported to play an important role in the control of both renal tubular and vascular function (26). EETs are potent endothelial-derived vasodilators in the renal circulation (17, 47). They also inhibit sodium and water reabsorption in the collecting duct (40). In contrast, 20-HETE is produced by vascular smooth muscle cells and is a potent constrictor of renal arterioles (5,19,23). Inhibition of the synthesis of 20-HETE attenuates the vasoconstrictor response of renal arterioles to elevations in transmural pressure in vitro (16, 18) and autoregulation of renal blood flow and tubuloglomerular feedback responses in vivo (8,48). At the level of the renal tubules, 20-HETE inhibits sodium reabsorption in the proximal tubule and thick ascending limb of the loop of Henle (6,32,34,39).Previous studies indicated that the renal production of EETs an...

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Section: Discussionmentioning

confidence: 99%

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

Sarkis¹,

Ito²,

Mori³

et al. 2005

American Journal of Physiology-Renal Physiology

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“…It is suggested that DI rats present reduced in vivo synthesis of PGEj and PGF^. 16 Thus, probably the absence of hyperfiltration in remnant nephrons in DI rats was due to the lack of ADH, a diminished synthesis of PGs, or both. The present data suggest that reduction of renal mass associated with systemic hypertension enhances the adaptive mechanisms of the remnant nephron due to intrarenal vasodilation and an increase in K t that, ultimately, causes hyperfiltration.…”

Section: Discussionmentioning

confidence: 99%

Effects of systemic hypertension, antidiuretic hormone, and prostaglandins on remnant nephrons.

Boim

Santos

et al. 1990

Hypertension

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Renal function was evaluated in normal and after 30 days of % renal mass reduction (CRF) in Munich-Wistar (MW) rats, spontaneously hypertensive rats with superficial glomeruli (EPM), and in Brattleboro rats with congenital diabetes insipidus (DI). Mean arterial pressure was higher in EPM-Control and EPM-CRF rats as compared with MW and DI rats. MW and EPM rats with CRF showed increases of 120% and 196%, respectively, in single nephron glomerular filtration rate as compared with their controls. However, DI rats with CRF did not show any increase in single nephron glomerular filtration rate as compared with the control group. Therefore, the data suggest that the presence of hypertension enhances the adaptive mechanisms on remnant kidney's function. Conversely, in the absence of antidiuretic hormone, adaptive mechanisms of remnant nephrons did not occur. In addition, it was observed that rats with CRF submitted to prostaglandin blockade with indomethacin showed for MW rats a 55% and 20% reduction in ultrafiltration coefficient and in single nephron glomerular filtration rate, respectively. Decreases of 60% and 30% in ultrafiltration coefficient and single nephron glomerular filtration rate, respectively, were observed for EPM rats. Antidiuretic hormone (ADH) has been proposed to have a kidney trophic action, 4 and homozygous Brattleboro rats (DI), which lack ADH, do not show hyperfiltration after being fed a hyperproteic diet, 3 as is observed in other strains of rats. 2 Thus, the objectives of the present study were to evaluate the remnant kidney's function in hypertensive states and the role of ADH and PGs in this model by using spontaneously hypertensive rats with superficial glomeruli (EPM rats), DI rats, and indomethacin administration. MethodsStudies were performed in Munich-Wistar (MW) rats (Simonsen Laboratories, Gilroy, California), EPM rats, and DI rats. EPM rats are the first generation of spontaneously hypertensive rats (SHR) (National Institutes of Health [NIH], Bethesda, Maryland) mated with MW rats and, thus, present spontaneous hypertension and superficial glomeruli.5 DI rats (NIH) have hereditary hypothalamic diabetes insipidus. All studies were performed in 3-4-month-old male rats, and they all were bred in the Animal House of Escola Paulista de Medicina. Each of the three strains of rats were divided into a control group and a group submitted to Y6 renal mass ablation (chronic renal failure [CRF]), which was studied 30 days after. The subtotal 5 /6 nephrectomy was performed by ligation of two or three branches of the left renal artery and right nephrectomy at the same time. All rats were allowed free access to regular rat chow and tap water until the morning of the study. Inactin (Byk, Gulden, Konstanz, Germany) anesthetic was used, and replacement of surgical volume losses was

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“…Studies on the toad bladder by Zusman et al (23) (24,25). That DDAVP, a vasopressin analogue that lacks pressor activity, has the same effect strongly suggests that it is the antidiuretic property of vasopressin that is important in this respect (25).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Vasopressin Action by Prostaglandins

Kirschenbaum¹,

Lowe²,

Trizna³

et al. 1982

J. Clin. Invest.

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A B S T R A C T The present studies examined whether vasopressin increases prostaglandin biosynthesis in isolated rabbit cortical collecting tubules (CCT) and whether endogenous prostaglandin biosynthesis plays a role in modulating the response of this nephron segment to vasopressin. Three groups of studies were performed. In the first group, CCT and proximal straight tubules (PST) were incubated with [3H]arachidonic acid, and metabolites were separated and identified using silica gel thin-layer chromatography. CCT were capable of producing all of the major prostaglandins (PG)(PGE2> thromboxane B2 [TxB2]> PGF2,, > PGI2). PST produced significantly lesser quantities of these lipids. In the second group, radiolabeled arachidonic acid was incorporated into the phospholipid pool of both CCT and PST, vasopressin was added to the incubation medium, and metabolites were separated and identified as above. Vasopressin stimulated the release of all of the major prostaglandins in CCT but had no effect on PST. PGE release into the incubation medium, as assessed by a radioreceptor assay, increased 108%, and a vasopressin analogue, 1-desamino-8-D-arginine vasopressin, had a quantitatively similar effect. In the third group, a submaximal dose of vasopressin was administered to isolated, perfused CCT studied in the presence and absence of indomethacin to assess whether endogenous prostaglandins play a role in modulating the antidiuretic response to vasopressin. cess, basal prostaglandin synthesis was 63% lower, and vasopressin-stimulated prostaglandin synthesis 76% lower, than the synthesis observed in rabbits on a normal diet. Cyclooxygenase inhibition exposed a significant hydroosmotic response to a submaximal dose of vasopressin in CCT from DOCA-or KCI-loaded animals. With arachidonic acid in the bath, the same dose of vasopressin failed to elicit a hydroosmotic response in CCT from rabbits on a normal diet even in the presence of a cyclooxygenase inhibitor. However, removal of exogenous arachidonic acid, with a consequently lower rate of prostaglandin synthesis, allowed the cyclooxygenase inhibitor to enhance the hydroosmotic response to vasopressin in these tubules.We conclude from these studies that the rabbit CCT has the capacity to synthesize all of the major prostaglandins and that the rate of synthesis of these lipids is enhanced by vasopessin. Prostaglandin synthesis by the CCT is postulated to modulate the antidiuretic action of vasopressin via a closed feedback loop. The effectiveness of this feedback regulation is dependent upon the mineralocorticoid status of the animal, which determines the level of basal and vasopressin-stimulated prostaglandin synthesis by the CCT.

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Antidiuretic hormone increases renal prostaglandin synthesis in vivo

Cited by 55 publications

References 0 publications

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

CytochromeP-450-dependent metabolism of arachidonic acid in the kidney of rats with diabetes insipidus

Effects of systemic hypertension, antidiuretic hormone, and prostaglandins on remnant nephrons.

Regulation of Vasopressin Action by Prostaglandins

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