Adrenergic stimulation of renal prostanoids in the Lyon hypertensive rat.

Liu, Kiao Ling; Aïssa, A. Hadj; Laréal, M. C.; Benzoni, Daniel; Vincent, Madeleine; Sassard, J

doi:10.1161/01.hyp.17.3.296

Cited by 17 publications

(30 citation statements)

References 29 publications

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“…On the contrary, it significantly improved the pressure-induced increases in GFR and natriuresis in LH kidneys. This data confirms those of Liu et al, 13 who increased the perfusion pressure of LH kidneys by means of norepinephrine infusions. Interestingly, AH23848 significantly decreased the renin release by the kidneys of the three strains.…”

Section: Discussionsupporting

confidence: 92%

“…The composition of the perfusion medium has been described elsewhere. 13 Just before use, the perfusate was filtered through 2 millipore filters (1.2 jim and 0.8 jim, successively) and 0.5 g/1 polyfructosan was added (Inutest, Laevosan, Linz, Austria). This solution, maintained at 37°C, was continuously bubbled with a 95% 0^-5% CO 2 mixture and single pass perfused using a peristaltic pump (Minipuls 2, Gilson, Paris).…”

Section: Kidney Perfusionmentioning

confidence: 99%

“…At the end of the previous protocol, the kidneys were perfused with AH23848 (a gift from Glaxo, Greenford, England), a TXA 2 /PGH 2 antagonist, 15 at a final concentration of 4x10"* M according to Liu et al 13 After a 15-minute stabilization period (RPP, 90 mm Hg), RPP was stepwise changed from 170 to 60 mm Hg according to the protocol described above. Venous effluent and urine samples were obtained and processed similarly.…”

Section: Protocolsmentioning

confidence: 99%

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Pressure independence of renin release by isolated kidneys of Lyon hypertensive rats.

Medeiros¹,

Vincent²,

Benzoni³

et al. 1992

Hypertension

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In the present work the influence of perfuslon pressure on renal functions and renin release was studied before and after the blockade of thromboxane A 2 /prostaglandin H 2 (TXA 2 /PGH 2 ) receptors using isolated kidneys from 7-week-old genetically hypertensive (LH), nonnotensive (LN), and low blood pressure (LL) rats of the Lyon strain. Kidneys were single pass perfused with Krebs-Henseleit solution with a gelatine derivative (Polygeline) added as an oncotic agent A servocontrolled system stabilized the renal perfusion pressure (RPP) at any chosen (±1 mm Hg) level. In baseline conditions (RPP, 90 mm Hg), LH (n=7) kidneys differed from LN (n=6) and LL (n=8) controls by increased vascular resistance, decreased glomerular filtration rate, and natriuresis. The LH kidney responses to stepwise changes in RPP (between 60 and 170 mm Hg) differed from those of LN and LL rats by a significantly lower perfusion flow, glomerular filtration rate, and natriuresis. Above all, the reduction in RPP, which induced a marked and highly reproducible renin release in LN and LL kidneys, was devoid of effects in LH kidneys. The blockade of TXAJ/PGHJ receptors by AH23848 (4x 10~' M) did not change the baseline (RPP, 90 mm Hg) functions of kidneys of the three strains. During changes in RPP, the responses of LN and LL kidneys were not modified, whereas LH kidneys exhibited significant increases in both glomerular filtration rate and natriuresis. Finally, AH23848 significantly decreased the renin release by kidneys of the three strains. It is concluded that renin release of LH isolated kidneys is independent of the perfusion pressure and that renal TXA 2 /PGH 2 receptor activation participates in the renin release and in the altered functions exhibited by kidneys of LH rats. Several recent experiments using kidney transplantation 12 have emphasized the primary role played by the kidney in the pathogenesis of genetic hypertension. Obviously, among the pressor factors originating in the kidney, the most important is the renin-angiotensin system. In Lyon genetically hypertensive (LH) rats, the plasma renin activity is normal in young animals and low in adult ones. 3 Similar findings have been reported in Japanese spontaneously hypertensive rats (SHR). 4 Despite these low levels of plasma renin, both models are highly sensitive to the blockade of the renin-angiotensin system. 5 -6 This demonstrates that, in genetically hypertensive rats, the low renin levels remain inappropriate and actively contribute to blood pressure elevation.Such an inappropriate renin secretion may reflect a polymorphism of the renin gene, as found in Dahl saJt-sensitive rats, 7 or an abnormal control by its physiological regulators. Because the renin gene polymorphism in LH rats does not appear directly related to the blood pressure level, 8 we thought it of interest to assessFrom the Department of Physiology and Clinical Pharmacology,

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Section: Discussionsupporting

confidence: 92%

Section: Kidney Perfusionmentioning

confidence: 99%

Section: Protocolsmentioning

confidence: 99%

See 1 more Smart Citation

Pressure independence of renin release by isolated kidneys of Lyon hypertensive rats.

Medeiros¹,

Vincent²,

Benzoni³

et al. 1992

Hypertension

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“…increase in AP and a 40% reduction in RBF (36). Similar to our findings for ANG II in vivo, norepinephrine acutely increases prostanoid excretion (PGE 2 Ͼ TxB 2 Ͼ 6-keto-PGF 1␣ ), while the induced renal vasoconstriction of isolated perfused rat kidneys is unaffected by TP receptor blockade (30).…”

Section: Discussionsupporting

confidence: 84%

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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“…NO decreases renal vascular resistance and enhances glomerular filtration rate and natriuresis both in vitro (Mattson et al, 1992;Johnson & Freeman, 1992;Salazar et al, 1992;Majid & Gabriel Navar, 1992) and in isolated kidney preparations (Radermacher et al, 1990;Welch et al, 1991;Gardes et al, 1992). Concerning prostanoids, the vasoconstrictor effects of prostaglandin (PG)H2 and of thromboxane (Tx)A2 are well known and have been shown to participate in the control of renal vascular resistance in genetically hypertensive rats of the Japanese (Dai et al, 1992) and of the Lyon strains (Liu et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Eicosanoid‐dependence of responses of pre‐ but not postglomerular vessels to noradrenaline in rat isolated kidneys

Zhang¹,

Sassard²

1993

British J Pharmacology

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1 We investigated the role of nitric oxide (NO) and of vasoactive eicosanoids in the control of renal vascular resistance (RVR) and glomerular filtration rate (GFR) and of their responses to noradrenaline (NA). This study was conducted in single-pass perfused, isolated kidney preparations of the rat. 2 NA (63, 110 and 160 nM) dose-dependently increased RVR and to a lesser degree GFR.3 In baseline conditions, Nw-nitro-L-arginine methylester (L-NAME, 100 AM) increased GFR more than RVR, thus demonstrating a basal release of NO which predominates in postglomerular vessels. 4 In kidneys stimulated with NA, L-NAME potentiated the increases in RVR but not in GFR.Indomethacin (1.5, 150 nM and 15 gM) did not alter GFR but markedly and dose-dependently reduced the NA-induced increase in RVR. Similar results were obtained with GR 32191B (10 and 100I M), a prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist. 5 Indomethacin (15IM) suppressed the enhancing effects of L-NAME on RVR responses to NA but did not affect those on GFR. 6 It is concluded that the mechanisms of the response to NA differ among pre-and postglomerular vessels. In preglomerular vessels the vasoconstrictor action and the NO release depend upon the activation of PGH2/TxA2 receptors, while both are eicosanoid-independent in the postglomerular vessels.

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Adrenergic stimulation of renal prostanoids in the Lyon hypertensive rat.

Cited by 17 publications

References 29 publications

Pressure independence of renin release by isolated kidneys of Lyon hypertensive rats.

Pressure independence of renin release by isolated kidneys of Lyon hypertensive rats.

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

Eicosanoid‐dependence of responses of pre‐ but not postglomerular vessels to noradrenaline in rat isolated kidneys

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Adrenergic stimulation of renal prostanoids in the Lyon hypertensive rat.

Cited by 17 publications

References 29 publications

Pressure independence of renin release by isolated kidneys of Lyon hypertensive rats.

Pressure independence of renin release by isolated kidneys of Lyon hypertensive rats.

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

Eicosanoid‐dependence of responses of pre‐ but not postglomerular vessels to noradrenaline in rat isolated kidneys

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