scholarly journals Peristenotic Collateral Circulation in Atherosclerotic Renovascular Disease

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 497-505
Author(s):  
Mohsen Afarideh ◽  
Xin Zhang ◽  
Christopher M. Ferguson ◽  
James F. Glockner ◽  
Amir Lerman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Kidney Function ◽  
Medical Therapy ◽  
Collateral Circulation ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Kidney Volume ◽  
Renovascular Disease ◽  
Atherosclerotic Renovascular Disease

The significance of peristenotic collateral circulation (PCC) development around a stenotic renal artery is unknown. We tested the hypothesis that PCC is linked to loss of kidney function and recovery potential in patients with atherosclerotic renovascular disease (ARVD). Thirty-four patients with ARVD were assigned to medical-therapy with or without revascularization based on clinical indications. The PCC was visualized using multidetector computed tomography and defined relative to segmental arteries in patients with essential hypertension. PCC number before and 3 months after treatment was correlated with various renal parameters. Thirty-four stenotic kidneys from 30 patients were analyzed. PCC number correlated inversely with kidney volume. ARVD–stenotic kidneys with baseline PCC (collateral ARVD [C-ARVD], n=13) associated with elevated 24-hour urine protein and stenotic kidney vein level of tumor necrosis factor-α, lower single-kidney volume and blood flow, and greater hypoxia than in stenotic kidneys with no PCC (no collateral ARVD [NC-ARVD], n=17). Revascularization (but not medical-therapy alone) improved stenotic kidney function and reduced inflammation in both NC-ARVD and C-ARVD. In C-ARVD, revascularization also increased stenotic kidney volume, blood flow, and oxygenation to levels comparable to NC-ARVD, and induced PCC regression. However, revascularization improved systolic blood pressure, plasma renin activity, and filtration fraction only in NC-ARVD. Therefore, patients with C-ARVD have greater kidney dysfunction, atrophy, hypoxia, and inflammation compared with patients with NC-ARVD, suggesting that PCC does not effectively protect the stenotic kidney in ARVD. Renal artery revascularization improved in C-ARVD stenotic kidney function, but not hypertension or renin-angiotensin system activation. These observations may help direct management of patients with ARVD.

Plasma renin activity and forearm blood flow in paraplegic humans

1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Forearm Blood Flow ◽  
Control Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Body ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.

Oestrogen-induced changes in renal haemodynamics in the rat: Influence of plasma and intrarenal renin

1986 ◽  
Vol 71 (5) ◽  
pp. 613-619 ◽  
Author(s):  
Mr J. K. Evans ◽  
P. F. Naish ◽  
G. M. Aber
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renal Haemodynamics ◽  
Renin Activity ◽  
Female Rats

1. The effect of oestrone acetate (in total doses of 5 and 10 mg) on systemic and renal haemodynamics and the renin-angiotensin system has been studied in adult female rats. 2. The administration of 10 mg of oestrogen resulted in a significant fall in renal blood flow associated with significant rises in both renal vascular resistance and mean arterial pressure. No changes were noted in cardiac output or total peripheral resistance at either dose. 3. Whilst the higher dose of oestrogen induced a significant increase in plasma renin activity, no change was noted in animals receiving 5 mg of oestrogen. Both regimens caused significant reductions in plasma and intrarenal renin concentrations. 4. Although renal blood flow correlated with plasma renin activity in animals with a normal renal blood flow, no such correlation was noted in animals with oestrogen-induced reductions in renal blood flow. 5. The present study demonstrates that oestrogen-induced reductions in renal blood flow result from a rise in intrarenal vascular resistance which cannot be accounted for by simultaneous changes in either plasma renin activity or renal renin concentration.

Ischaemic nephropathy

2015 ◽  
Author(s):  
Helen Alderson ◽  
Constantina Chrysochou ◽  
James Ritchie ◽  
Philip A. Kalra
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Filtration Rate ◽  
Blood Pressure Reduction ◽  
Western World ◽  
Pressure Reduction ◽  
Renovascular Disease ◽  
Angiotensin Blockade ◽  
Atherosclerotic Renovascular Disease ◽  
Common Manifestation

Ischaemic nephropathy describes loss of renal function or renal parenchyma due to stenosis or occlusion of the renal artery or its branches. In the Western world, this is usually the result of atherosclerotic renovascular disease, but other aetiologies include arteritis, embolic disease, dissection, and fibromuscular disease.Chronic kidney disease is the most common manifestation of ischaemic nephropathy, but hypertension, flash pulmonary oedema, sensitivity to angiotensin blockade, and sensitivity of glomerular filtration rate to blood pressure reduction are all possible manifestations of occlusive diseases of the renal artery or its branches. Proteinuria may also occur.This chapter describes these clinical features and the outcomes of ischaemic nephropathy. It goes on to discuss the haemodynamics and mechanisms and what we understand of the pathophysiology of the condition.

Local control of mesenteric blood flow by the renin-angiotensin system

1988 ◽  
Vol 255 (3) ◽  
pp. G267-G274
Author(s):  
A. Suvannapura ◽  
N. R. Levens
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Mesenteric Artery ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Ang Ii ◽  
Volume Depletion ◽  
Mesenteric Blood Flow ◽  
Direct Role ◽  
Mesenteric Circulation

The purpose of this study is to determine whether locally acting angiotensin II (ANG II) plays a direct role in the control of mesenteric blood flow after volume depletion in the anesthetized dog. Infusion of the ANG II receptor antagonist saralasin into the mesenteric artery at doses between 0.05 and 0.1 microgram.kg-1.min-1 attenuated the reduction in renal blood flow produced by intrarenal injection of ANG II. In contrast, infusion of saralasin at 0.01 microgram.kg-1.min-1 did not affect the change in renal blood flow produced by ANG II, indicating that at this dosage the antagonist did not leave the mesenteric circulation in pharmacologically significant quantities. ANG II produced a dose-dependent decrease in splanchnic blood flow when injected into the mesenteric artery. Simultaneous infusion of 0.01 microgram.kg-1.min-1 saralasin into the mesenteric artery blocked the action of up to 1 ng ANG II by 80%. Infusion of saralasin at 0.01 microgram.kg-1.min-1 into the mesenteric artery of hemorrhaged animals increased mesenteric blood flow without significantly affecting renal blood flow, blood pressure, or plasma renin activity. These data demonstrate that saralasin can be localized to the mesenteric circulation at a dose capable of inhibiting angiotensin action and that endogenous ANG II plays a direct, physiologically important local role in controlling splanchnic resistance after volume depletion.

Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Vascular Beds ◽  
Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

Abstract P345: Plasma Insulin Like Growth Factor Binding Protein-7 and Tissue Inhibitor of Metalloproteinase-2 are Associated with Reduced Renal Blood Flow and Change in Kidney Function After Revascularization in Human Atherosclerotic Renovascular Disease RVD

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Ahmed Saad ◽  
Sandra Herrmann ◽  
Hui Tang ◽  
John Woollard ◽  
Michael McKusick ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Blood Flow ◽  
Growth Factor ◽  
Renal Artery ◽  
Cell Cycle Arrest ◽  
Renal Blood Flow ◽  
Kidney Function ◽  
Renal Vein ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Cycle Arrest

Background: Insulin-like growth factor binding protein7 (IGFBP-7) and tissue inhibitor of metalloproteinase-2 (TIMP-2) reflect G1-cell cycle arrest and are used as biomarkers for AKI. Recent studies show that these biomarkers rise in ischemic conditions and suggest that they actually may limit the severity of AKI. We tested the hypothesis that renal vein [IGFBP-7]*[TIMP-2] correlate with reductions in renal blood flow (RBF) and post-stent single kidney (SK)-GFR changes in patients with RVD undergoing contrast-based imaging and stent revascularization Methods: Inpatient studies were performed during 150 mEq Na+ intake and ACE/ARB Rx in patients with hemodynamically severe RVD (n=29, Doppler velocity = 318 ± 100cm/sec, and eGFR= 34.7 ± 11.7 mL/ min) scheduled for renal artery stenting, and compared to essential hypertensive (EH) healthy controls (n=32). Cortical and medullary RBFs (by multidetector CT) and renal vein levels of IGFBP-7 and TIMP-2 were measured before renal artery stenting and 3 months later Results: Pre-stenting IGFBP-7 and TIMP-2 levels were elevated in RVD compared to EH (18.5±2. vs 15.7±1.5 and 97.4±23.1vs 62.7±9.2 ng/mL respectively, P <0.0001). Baseline renal vein levels of IGFBP-7 * TIMP-2 correlated inversely with pre-stent RBF (r= - 0.53, P=0.01) and directly with the change (%) in SK-GFR observed 3 months after stenting Conclusion: IGFBP-7 and TIMP-2 levels are elevated in patients with chronic RVD as a function of the baseline reduction in RBF, and associate with subsequent improvement in SK-GFR 3 months after revascularization. These data are consistent with renovascular occlusion inducing cell-cycle arrest that serves to protect kidney function.

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