Autoregulation and tubuloglomerular feedback in normotensive and hypertensive rats

Ploth, David W.; Schnermann, Jürgen; Dahlheim, H.; Hermle, M; Schmidmeier, Elfriede

doi:10.1038/ki.1977.110

Cited by 70 publications

(50 citation statements)

References 33 publications

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“…7910 This suggests that the role of EDNO in maintaining renal hemodynamics was greatly amplified compared with that seen in kidneys of normotensive rats, including those with chronically elevated Ang II. 10 We do not find evidence that a dysfunctional endothelium is a permissive characteristic of by guest on May 10, 2018 http://hyper.ahajournals.org/ Downloaded from hypertension, as has been suggested, 16 but rather that nitric oxide synthesis in vivo may be normal or even exaggerated in hypertension.…”

Section: Discussionmentioning

confidence: 51%

“…14 ' 15 In addition, various functional abnormalities have been reported in the contralateral, nonclipped kidney in 2K1C hypertension. Ploth et al 16 reported that the nonclipped kidney cannot autoregulate RBF and that pressure natriuresis is blunted. Also, contralateral RVR is increased as the result of an increase in both afferent and efferent arteriolar vasoconstriction.…”

Section: Renal Nitric Oxide and Angiotensin II Interaction In Renovasmentioning

confidence: 99%

See 1 more Smart Citation

Renal nitric oxide and angiotensin II interaction in renovascular hypertension.

Sigmon

Beierwaltes

1993

Hypertension

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In two-kidney, one clip (2K1C) renovascular hypertension, blood flow is reduced to the clipped but not to the nonclipped kidney, despite elevated angiotensin II. To determine possible interactions between endothelium-derived nitric oxide and angiotensin, we studied bilateral renal blood flow using radioactive microspheres in anesthetized 2K1C hypertensive rats 4 weeks after clipping. We studied the response to nitric oxide synthesis inhibition with 10 mg/kg body wt JV G -nitro-L-arginine-methyl ester (L-NAME) in hypertensive rats untreated (n=5) or treated (n=5) with 10 mg/kg body wt of the angiotensin II antagonist losartan. 2K1C rats had a blood pressure of 159±9 mm Hg, and renal blood flow to the clipped kidney was reduced 87% compared with the nonclipped kidney. L-NAME increased blood pressure 36±5 mm Hg and decreased renal blood flow in the nonclipped kidney 61% (4.9±0.5 to 1.9±0.4 mL/min per gram kidney weight, P<.00l). Renal vascular resistance increased 200% (33.4±2.2 to 100.7±15.0 resistance units [RU], / > <.005). Renal blood flow and resistance in the clipped kidney were unchanged by L-NAME. Treatment of 2K1C rats with losartan reduced blood pressure (154±8 to 116±11 mm Hg, P<.01), did not change blood flow in the nonclipped, but normalized it in the clipped kidney (4.8±0.8 mL/min per gram kidney weight). With losartan, L-NAME increased pressure by 38±10 mm Hg, decreased renal blood flow 10% (5.9±0.5 to 5.3±0.3 mL/min per gram kidney weight, P<.05), and increased renal resistance 49% (19.7±1.2 to 29.4±2.2 RU, P<.001) in the nonclipped kidney. Neither blood flow nor resistance was changed in the clipped kidney. Our results suggest that nitric oxide maintains renal perfusion of the nonclipped but not the clipped kidney in 2K1C rats. Nitric oxide counteracts elevated angiotensin to regulate perfusion in the nonclipped kidney, but angiotensin vasoconstriction predominates in the clipped kidney. Thus, nitric oxide vasodilation is a regulatory response to maintain contralateral renal perfusion despite elevated angiotensin after renal artery stenosis in 2K1C hypertension. In models including two-kidney, one clip (2K1C) Goldblatt, aortic coarctation, Dahl salt-sensitive, and deoxycorticosterone acetate-salt hypertension, as well as in spontaneously hypertensive rats, endothelium-dependent vasodilation is impaired 13 but may be restored by reversing the hypertension.1 Similar abnormalities have been reported in humans with essential hypertension. These reports suggest that endothelial dysfunction associated with hypertension may be due to insufficient endotheliumderived nitric oxide (EDNO). In normotensive subjects, EDNO has been found to be an important mediator of renal blood flow (RBF). intrinsic EDNO-mediated renal vasodilation, allowing endogenous vasoconstrictors, such as angiotensin II (Ang II), to predominate. The renal response occurs simultaneously with a rise in systemic pressure, suggesting that EDNO is important in maintaining both systemic and renal resistances.Using anesthetized rats, we have pr...

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Section: Discussionmentioning

confidence: 51%

Section: Renal Nitric Oxide and Angiotensin II Interaction In Renovasmentioning

confidence: 99%

Renal nitric oxide and angiotensin II interaction in renovascular hypertension.

Sigmon

Beierwaltes

1993

Hypertension

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“…This could occur due to greater vascular endothelin production or pressure per se. Angiotensin II, which is elevated in renovascular hypertension (Brunner et al, 1962;Fourcade et al, 1971;Ploth et al, 1977;Huang et al, 1981;Miyazaki et al, 1986), is known to stimulate the production of endothelin 6 5 4…”

Section: Discussionmentioning

confidence: 99%

“…Increased Miyauchi et al, 1989;Criscione et al, 1990), decreased (Dohi & Luscher, 1990b;Auch-Schwelk & Vanhoutte, 1989) and normal responses (Diederich et al, 1989;Criscione et al, 1990) to endothelin-1 have been reported in vessels from spontaneously hypertensive rats. The responsiveness of resistance arteries to endothelin-1 in renovascular hypertension would be of pathophysiological interest, since this type of hypertension is characterized by an increased activity of the renin-angiotensin system (Brunner et al, 1962;Fourcade et al, 1971;Ploth et al, 1977;Huang et al, 1981;Miyazaki et al, 1986;Wilson et al, 1989) and because angiotensin II stimulates the production of endothelin in cultured endothelial cells (Emori et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Renovascular hypertension impairs formation of endothelium‐derived relaxing factors and sensitivity to endothelin‐1 in resistance arteries

Dohi¹,

Criscione

Lüscher³

1991

British J Pharmacology

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1 Endothelium-dependent vascular regulation was investigated in mesenteric resistance arteries of Goldblatt two kidney-one clip (2K1C) renovascular hypertensive rats. 2 Third order branches of mesenteric arteries were dissected free and mounted on glass cannulae in an organ chamber. Changes in vascular diameter were measured in pressurized and perfused arteries with a video dimension analyzer. 3 Acetylcholine evoked endothelium-dependent relaxations that were much more pronounced with intraluminal than with extraluminal application. In 2K1C rats the relaxation induced by intraluminal, but not extraluminal acetylcholine was decreased compared to normotensive Wistar Kyoto rats (WKY). Increased duration of hypertension further decreased the response to intraluminal but not extraluminal acetylcholine. 4 Endothelin-1 and noradrenaline caused contractions which were augmented by removal of the endothelium. This augmentation was reduced in 2K1C rats compared to WKY; the difference was small with noradrenaline but more pronounced with endothelin-1. 5 In arteries without endothelium the sensitivity, but not the maximal contraction to endothelin-1 was lower in 2K1C rats, while the response to noradrenaline was not different in 2K1C rats and WKY. The sensitivity to the peptide was not further affected by increasing the duration of hypertension. 6 Thus, renovascular hypertension leads to an impaired intraluminal, but not extraluminal activation of the release of endothelium-derived relaxing factor and a decreased inhibitory effect of the endothelium against endothelin-1-and noradrenaline-induced contractions in mesenteric resistance arteries. Furthermore, the sensitivity, but not the maximal response of vascular smooth muscle to endothelin-1 was reduced.

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“…The reduced renin synthesizing ability of the nonclipped kidney is clearly reflected by the markedly reduced renin mRNA levels (41,42). Renin depletion and reduced renin mRNA levels in the non-clipped kidney have previously been considered as evidence that the activity of the intrarenal renin-angiotensin is greatly diminished in the non-clipped kidney (43,44). However, functional data have demonstrated that the non-clipped kidney is still highly responsive to pharmacological blockade of the renin-angiotensin system with ACE inhibitors or ANG II receptor antagonists (29,31,33,45,46).…”

Section: Responses To Unilateral Renal Arterial Stenosismentioning

confidence: 99%

Intrarenal Angiotensin II Augmentation in Angiotensin II Dependent Hypertension.

Navar

Harrison‐Bernard

2000

Hypertens Res

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In several models of angiotensin II (ANG II) dependent hypertension, intrarenal ANG II levels increase to a much greater extent than the circulating levels even though the renal renin levels are decreased. The 2-kidney-l-clip (2K1C) Goldblatt rat model is particularly intriguing because hypertension develops in the presence of an intact kidney which would be expected to maintain sodium balance and protect against hypertension.Although the non-clipped kidney becomes renin depleted, it exhibits enhanced microvascular reactivity and increased tubular fractional sodium reabsorption. content was due to accumulation of circulating ANG II in addition to continued production of endogenous ANG II. The renal accumulation of Va15-ANG II was markedly reduced by concomitant treatment with the AT, receptor blocker, losartan. In addition, we found an unchanged overall ANG II-AT, receptor protein which probably contributes to the maintained ANG II dependent influences. Collectively, the data support the concept that there is internalization of ANG II through an AT, receptor mediated process and that some of the internalized ANG II is protected from degradation. The augmented intrarenal ANG II coupled with sustained levels of AT, receptors contribute to the continued ANG II dependent suppression of renal function and sodium excretion thereby maintaining the hypertension. (Hypertens Res 2000; 23: 291-301)

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Autoregulation and tubuloglomerular feedback in normotensive and hypertensive rats

Cited by 70 publications

References 33 publications

Renal nitric oxide and angiotensin II interaction in renovascular hypertension.

Renal nitric oxide and angiotensin II interaction in renovascular hypertension.

Renovascular hypertension impairs formation of endothelium‐derived relaxing factors and sensitivity to endothelin‐1 in resistance arteries

Intrarenal Angiotensin II Augmentation in Angiotensin II Dependent Hypertension.

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