Abstract 9839: Beta Blockers Improve Renal Tissue Oxygenation in Hypertensive Patients Suspected of Renal Artery Stenosis

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Michael E Hall ◽  
Michael V Rocco ◽  
Timothy M Morgan ◽  
Craig A Hamilton ◽  
Jennifer H Jordan ◽  
...  

Background: Chronic renal hypoxia influences the progression of chronic kidney disease (CKD). Blood oxygen level dependent (BOLD) magnetic resonance (MR) is a noninvasive tool for assessment of renal tissue oxygenation. Beta blockers reduce cardiovascular mortality in patients with CKD and systolic heart failure, however the mechanisms of this benefit remain unclear. We sought to determine the association between beta blocker use, renal cortical and medullary oxygenation, and renal blood flow in hypertensive patients suspected of renal artery stenosis. Hypothesis: Chronic receipt of beta blockers will be associated with improved renal tissue oxygenation as assessed by BOLD MR. Methods: We measured renal cortical and medullary oxygenation using BOLD MR and renal artery blood flow using MR phase contrast techniques in 38 participants suspected of renal artery stenosis. Results: Chronic beta blocker therapy was associated with improved renal cortical (p=0.0007) and medullary (p=0.03) oxygenation (Figure). Receipt of angiotensin converting enzyme inhibitors or angiotensin receptor blockers was associated with reduced medullary oxygenation (p=0.01). In a multivariable model including gender, hemoglobin, diabetes, loop diuretic use, and mineralocorticoid use, chronic receipt of beta blockers was the only significant predictor of renal tissue oxygenation (β= 8.4, p=0.008). Conclusions: Beta blocker therapy was associated with improved renal oxygenation independent of renal blood flow suggesting may these findings may be related to reduced renal oxygen consumption. In addition to their known benefits to reduce cardiovascular mortality in patients with renal disease, beta blockers may reduce or prevent progression of renal dysfunction in patients with hypertension, diabetes, and renovascular disease. These observations may have important implications for treatment of patients with CKD.

2016 ◽  
Vol 6 (4) ◽  
pp. 261-268 ◽  
Author(s):  
Michael E. Hall ◽  
Michael V. Rocco ◽  
Timothy M. Morgan ◽  
Craig A. Hamilton ◽  
Jennifer H. Jordan ◽  
...  

Background: Chronic renal hypoxia influences the progression of chronic kidney disease (CKD). Blood oxygen level-dependent (BOLD) magnetic resonance (MR) is a noninvasive tool for the assessment of renal oxygenation. The impact of beta-blockers on renal hemodynamics and oxygenation is not completely understood. We sought to determine the association between beta-blocker use, renal cortical and medullary oxygenation, and renal blood flow in patients suspected of renal artery stenosis. Methods: We measured renal cortical and medullary oxygenation using BOLD MR and renal artery blood flow using MR phase contrast techniques in 38 participants suspected of renal artery stenosis. Results: Chronic beta-blocker therapy was associated with improved renal cortical (p < 0.001) and medullary (p = 0.03) oxygenation, while the use of calcium channel blockers or diuretics showed no association with either cortical or medullary oxygenation. Receipt of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with reduced medullary oxygenation (p = 0.01). In a multivariable model, chronic receipt of beta-blockers was the only significant predictor of renal tissue oxygenation (β = 8.4, p = 0.008). Beta-blocker therapy was not associated with significant changes in renal artery blood flow, suggesting that improved renal oxygenation may be related to reduced renal oxygen consumption. Conclusions: In addition to known benefits to reduce cardiovascular mortality in patients with renal disease, beta-blockers may reduce or prevent the progression of renal dysfunction in patients with hypertension, diabetes, and renovascular disease, partly by reducing renal oxygen consumption. These observations may have important implications for the treatment of patients with CKD.


Circulation ◽  
1975 ◽  
Vol 51 (6) ◽  
pp. 1114-1119 ◽  
Author(s):  
F H Messerli ◽  
J Genest ◽  
W Nowaczynski ◽  
O Kuchel ◽  
M Honda ◽  
...  

2001 ◽  
Vol 12 (9) ◽  
pp. 1836-1843
Author(s):  
THOMAS K. A. WIEREMA ◽  
ALPHONS J. H. M. HOUBEN ◽  
ABRAHAM A. KROON ◽  
DERK KOSTER ◽  
KIM VAN DER ZANDER ◽  
...  

Abstract. In ischemia, nitric oxide (NO) production is increased, possibly to preserve flow. The role of NO was investigated in hypertensive patients with or without renal artery stenosis (RAS). Fifty-five hypertensive patients scheduled to undergo diagnostic renal angiography underwent mean renal blood flow (MRBF) measurements before and after an intrarenal injection of the NO synthase blocker Ng-monomethyl-L-arginine (L-NMMA) at 0.03 μg/kg, before angiography. A dose-response study indicated that this dose of L-NMMA significantly blocked NO synthesis. MRBF was measured at baseline and 1, 5, 10, and 20 min after L-NMMA treatment. On the basis of the angiographic results, patients were divided into three diagnostic categories, i.e., essential hypertension (n = 26), unilateral RAS (n = 16), or bilateral RAS (n = 8). In essential hypertension, MRBF was decreased by 18 ± 4% at 20 min. In unilateral RAS, L-NMMA did not affect MRBF in the stenotic kidney but reduced MRBF in the nonstenotic kidney by 40 ± 9% at 20 min. In bilateral RAS, L-NMMA reduced flow by 32 ± 14% at 20 min. In the nonstenotic kidney in unilateral RAS, a positive correlation was observed between the effect of NO blockade on MRBF and arterial renin levels (P = 0.009). In the stenotic kidney, in contrast, this correlation was inverse (P = 0.007). In conclusion, MRBF depends on NO in hypertensive patients, except in the stenotic kidney in unilateral RAS. In the nonstenotic kidney in unilateral RAS, NO bioavailability is increased. It is suggested that a compensatory mechanism, regulated by NO and possibly angiotensin II, may preserve renal function.


2004 ◽  
Vol 65 (1) ◽  
pp. 245-250 ◽  
Author(s):  
Claire Mounier-Vehier ◽  
Benjamin Cocheteux ◽  
Stephan Haulon ◽  
Patrick Devos ◽  
Christophe Lions ◽  
...  

Hypertension ◽  
2010 ◽  
Vol 55 (4) ◽  
pp. 961-966 ◽  
Author(s):  
Monika L. Gloviczki ◽  
James F. Glockner ◽  
Lilach O. Lerman ◽  
Michael A. McKusick ◽  
Sanjay Misra ◽  
...  

2009 ◽  
Vol 32 (11) ◽  
pp. 1009-1014 ◽  
Author(s):  
Samad Ghaffari ◽  
Bahram Sohrabi ◽  
Reza Beheshti Siahdasht ◽  
Leili Pourafkari

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