Changes in glomerular hemodynamic response to angiotensin II after subacute renal denervation in rats.

Tucker, B. J.; Mundy, C. A.; Maciejewski, Andrzej R.; Printz, Morton P.; Ziegler, Micah S.; Pelayo, Juan C.; Blantz, Roland C.

doi:10.1172/jci112627

Cited by 32 publications

(23 citation statements)

References 35 publications

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“…Before receiving All, volume-expanded animals treated with B-HT 933 tended toward lower blood pressures commensurate with the expected central sympatholytic effect of the a2 agonist. All caused BP to increase by an amount similar to that previously reported with this dose (5). After All infusion, the mean BP was similar between B-HT 933-treated and control groups but the incremental increase in BP after All administration was greater in animals pretreated with B-HT 933.…”

Section: Resultssupporting

confidence: 85%

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Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Thomson

Gabbai²,

Tucker³

et al. 1992

J. Clin. Invest.

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The hypothesis that renal a2 adrenoceptors influence nephron filtration rate (SNGFR) via interaction with angiotensin II (All) was tested by renal micropuncture. The physical determinants of SNGFR were assessed in adult male Munich Wistar rats 5-7 d after ipsilateral surgical renal denervation (DNX). DNX was performed to isolate inhibitory central and presynaptic a2 adrenoceptors from end-organ receptors within the kidney. Two experimental protocols were employed: one to test whether prior All receptor blockade with saralasin would alter the glomerular hemodynamic response to a2 adrenoceptor stimulation with the selective agonist B-HT 933 under euvolemic conditions, and the other to test whether B-HT 933 would alter the response to exogenous All under conditions of plasma volume expansion. In euvolemic rats, B-HT 933 caused SNGFR to decline as the result of a decrease in glomerular ultrafiltration coefficient (LpA), an effect that was blocked by saralasin. After plasma volume expansion, B-HT 933 showed no primary effect on LpA but heightened the response of arterial blood pressure, glomerular transcapillary pressure gradient, and LpA to All. The parallel results of these converse experiments suggest a complementary interaction between renal a2-adrenergic and All systems in the control of LpA. (J. Clin. Invest. 1992.

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Section: Resultssupporting

confidence: 85%

“…Renal denervation was carried out 5-7 d before micropuncture under sterile operating conditions according to protocols as previously described (2). We have previously demonstrated uniform success in achieving renal sympathetic denervation by these means as documented by a > 90% reduction in renal tissue norepinephrine (4,5).…”

Section: Introductionmentioning

confidence: 99%

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Thomson

Gabbai²,

Tucker³

et al. 1992

J. Clin. Invest.

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“…Renal denervation has been shown to increase ANG II receptors in the glomeruli of the denervated kidney (13). This is a potentially confounding factor if chronic denervation is a method used in studies involving ANG II.…”

Section: Discussionmentioning

confidence: 99%

Is the chronically denervated kidney supersensitive to catecholamines?

Ramchandra

Barrett

Guild

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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One method for discerning the role of the renal sympathetic nerves in the regulation of renal function has been to chronically denervate one kidney. One concern with this approach is that increased renal responsiveness to plasma levels of norepinephrine may develop over time. This may reduce the apparent magnitude of the effect of the renal nerves or indeed completely mask their effect. In the present experiment, we used the rabbit unilateral denervated kidney model to examine the acute renal blood flow responses to phenylephrine to determine if there were differences between the responses in chronically denervated kidneys compared with either intact or acutely denervated kidneys. In addition, we examined the responses in rabbits that had been made hypertensive using a continuous infusion of ANG II for 7 wk. We found that chronic denervation did not result in increased renal responsiveness to phenylephrine compared with either the intact or acutely denervated kidney, suggesting that differences in renal function between renal nerve-intact and -denervated kidneys observed in previous studies are unlikely to be confounded by supersensitivity. These results suggest that the unilateral denervated kidney model is a valid model to study the role of the renal nerves in the regulation of renal function.

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“…The aliquots were centrifuged at 3,000 RPM, 4 Њ C for 20 min. The pellet was extracted in 1 N NaOH and used for determination of protein content as previously described (25).…”

Section: Isolation and Incubation Of Glomerulimentioning

confidence: 99%

Inhibition of constitutive nitric oxide synthase (NOS) by nitric oxide generated by inducible NOS after lipopolysaccharide administration provokes renal dysfunction in rats.

Schwartz¹,

Mendonca²,

Schwartz³

et al. 1997

J. Clin. Invest.

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242

169

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Excess NO generation plays a major role in the hypotension and systemic vasodilatation characteristic of sepsis. Yet the kidney response to sepsis is characterized by vasoconstriction resulting in renal dysfunction. We have examined the roles of inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) on the renal effects of lipopolysaccharide administration by comparing the effects of specific iNOS inhibition, L -N 6 -(1-iminoethyl)lysine (L-NIL), and 2,4-diamino-6-hydroxy-pyrimidine vs. nonspecific NOS inhibitors (nitro-L -arginine-methylester). cGMP responses to carbamylcholine (CCh) (stimulated, basal) and sodium nitroprusside in isolated glomeruli were used as indices of eNOS and guanylate cyclase (GC) activity, respectively. LPS significantly decreased blood pressure and GFR (112 Ϯ 4 vs. 83 Ϯ 4 mmHg; 2.66 Ϯ 0.29 vs. 0.96 Ϯ 0.22 ml/min, P Ͻ 0.05) and inhibited the cGMP response to CCh. GC activity was reciprocally increased. L-NIL and 2,4-diamino-6-hydroxy-pyrimidine administration prevented the decrease in GFR (2.71 Ϯ 0.28 and 3.16 Ϯ 0.18 ml/min, respectively), restored the normal response to CCh, and GC activity was normalized. In vitro application of L-NIL also restored CCh responses in LPS glomeruli. Neuronal NOS inhibitors verified that CCh responses reflected eNOS activity. L-NAME, a nonspecific inhibitor, worsened GFR (0.41 Ϯ 0.15 ml/min), a reduction that was functional and not related to glomerular thrombosis, and eliminated the CCh response. No differences were observed in eNOS mRNA expression among the experimental groups. Selective iNOS inhibition prevents reductions in GFR, whereas nonselective inhibition of NOS further decreases GFR. These findings suggest that the decrease in GFR after LPS is due to local inhibition of eNOS by iNOS, possibly via NO autoinhibition. ( J. Clin. Invest. 1997. 100:439-448.)

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Changes in glomerular hemodynamic response to angiotensin II after subacute renal denervation in rats.

Cited by 32 publications

References 35 publications

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Is the chronically denervated kidney supersensitive to catecholamines?

Inhibition of constitutive nitric oxide synthase (NOS) by nitric oxide generated by inducible NOS after lipopolysaccharide administration provokes renal dysfunction in rats.

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