The Regulation of Prostaglandins by Vasoactive Hormones in Renal Tubular and Vascular Smooth Muscle Cells

Vallotton, Michel B.; Wüthrich, R.

doi:10.1007/978-3-0348-9299-5_2

Cited by 3 publications

(2 citation statements)

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“…Renal medullary interstitial cells are rich in COX-2. ANG II stimulates renal cortical tubular cells to produce PGE 2 Ͼ PGF 2␣ and no PGI 2 , while vascular smooth muscle cells produce PGI 2 (50). In terms of regional heterogeneity, it is interesting to note that the immediate contraction of isolated rabbit cortical afferent arterioles produced by ANG II is independent of TP receptor activation (52).…”

Section: Discussionmentioning

confidence: 99%

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA₂/isoprostane production

Vågnes¹,

Iversen²,

Arendshorst³

2007

American Journal of Physiology-Renal Physiology

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The relative contributions of vasoconstrictor and of dilator systems are balanced in health. The balance is reset in disease, often favoring a predominant role of vasoconstrictors, perhaps due to positive interactions between constrictor systems. For example, in hypertension, chronic high levels of angiotensin II (ANG II) stimulate the production of thromboxane (TxA 2/PGH2) and/or isoprostane that activate constrictor thromboxane prostanoid (TP) receptors in the vasculature. The present study evaluated a modest concentration of ANG II administered acutely into the renal artery on urinary excretion of TxB 2 and isoprostane and possible renal TP receptor activation that might amplify ANG IIinduced renal vasoconstriction. TP receptors were blocked with SQ29548 coinfused with ANG II. Results were compared with a time control group of continuous ANG II infusion (40 ng ⅐ min Ϫ1 ⅐ kg body wt Ϫ1 ) over 90 min. TP receptor antagonism during 30 -60 min had no effect on the reduction in renal blood flow (RBF) produced by ANG II (15.8 Ϯ 2.8 vs. 13.2 Ϯ 4.9%) (P Ͼ 0.6). Likewise, there was no difference between groups during ANG II-induced renal vasoconstriction between 60 -90 min in presence or absence of TP receptor antagonist (RBF Ϫ8.6 Ϯ 4.0 vs. Ϫ9.6 Ϯ 4.5%) (P Ͼ 0.8). Systemic arterial pressure was stable throughout, so RBF changes reflected localized changes in renal vascular resistance. Urinary excretion of TxB2 and isoprostane were nearly doubled by ANG II. The present data indicate that short-term intrarenal infusion of ANG II rapidly increases renal production of TxA2 but that the ANG II-induced renal vasoconstriction is independent of TP receptor activation during the initial 90 min of local challenge with ANG II. kidney; renal circulation; glomerular arterioles; renin-angiotensin system; prostanoids; oxidative stress; isoprostane RENAL HEMODYNAMIC REGULATORY mechanisms play an important role in maintaining glomerular function, salt and water balance, and arterial pressure (AP). Renal vascular resistance (RVR) is controlled by a balance of vasoconstrictor and dilatory stimuli in health, with the vasoconstrictor agents predominating in many disease states. For example, in genetic hypertension in the spontaneously hypertensive rat (SHR), exaggerated renal vasoconstriction is seen in response to ANG II, a response primarily due to defective buffering of vasodilator prostanoids (12,14,24,40). On the other hand, higher expression of a G protein-coupled receptor such as thromboxane prostanoid (TP) and vasopressin (V 1 ) receptors can account for the ability of thromboxane A 2 (TxA 2 ) and vasopressin, respectively, to produce more pronounced renal vasoconstriction in young SHR (11,13,18,48). In long-standing established hypertension, there are significant potentiating interactions among vasoconstrictor systems. In this regard, chronic increases in ANG II are known to stimulate production of TxA 2 /PGH 2 with subsequent constriction-mediated TP receptors as well as angiotensin AT 1 receptors. In ANG II-induced hypertension...

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Section: Discussionmentioning

confidence: 99%

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA₂/isoprostane production

Vågnes¹,

Iversen²,

Arendshorst³

2007

American Journal of Physiology-Renal Physiology

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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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Natriuretic hormone receptors and actions on bone endothelial cells.

et al. 1993

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[125I]Atrial natriuretic peptide (ANP) was used to identify ANP receptors on a clonal line of bovine bone endothelial (BBE) cells. Specific binding of [125I]ANP was saturable and of high affinity. Computer analysis of the equilibrium binding data indicated that the Scatchard plots are best fit by a straight line (Kd = 69.3 +/- 20.9 pM; binding capacity = 37.9 fmol/10(6) cells). The order of potency for competing with [125I]ANP binding was human ANP (hANP) > rat atriopeptin-1 (rAP-1) > porcine brain natriuretic peptide (pBNP) > porcine C-type natriuretic peptide. Affinity cross-linking studies indicated the presence of two major 130- and 70-kilodalton bands that specifically bound to hANP, rAP-1, pBNP, and porcine C-type natriuretic peptide. The binding of natriuretic peptides to BBE cells resulted in an increase in cGMP production and a significant decrease in Na+/K+/Cl- cotransport, without effects on cAMP intracellular accumulation. hANP, rAP-1, and pBNP at 100-nM concentrations, significantly inhibited PTH-induced cAMP production. Treatment with natriuretic hormones was also associated with an increase in 6-keto-prostaglandin F1 alpha levels in the culture medium of BBE cells and a higher cell growth rate. These studies demonstrate that bone endothelial cells bear receptors for natriuretic hormones associated with changes in PTH-induced cAMP production, prostaglandin production, and cell proliferation.

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The Regulation of Prostaglandins by Vasoactive Hormones in Renal Tubular and Vascular Smooth Muscle Cells

Cited by 3 publications

References 10 publications

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA₂/isoprostane production

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA₂/isoprostane production

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

Natriuretic hormone receptors and actions on bone endothelial cells.

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The Regulation of Prostaglandins by Vasoactive Hormones in Renal Tubular and Vascular Smooth Muscle Cells

Cited by 3 publications

References 10 publications

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA2/isoprostane production

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA2/isoprostane production

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

Natriuretic hormone receptors and actions on bone endothelial cells.

Contact Info

Product

Resources

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Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA₂/isoprostane production

Short-term ANG II produces renal vasoconstriction independent of TP receptor activation and TxA₂/isoprostane production