Stenosis-dependent role of nitric oxide and prostaglandins in chronic renal ischemia

2002 ◽  
Vol 282 (5) ◽  
pp. F859-F865 ◽  
Author(s):  
Hirobumi Tokuyama ◽  
Koichi Hayashi ◽  
Hiroto Matsuda ◽  
Eiji Kubota ◽  
Masanori Honda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Renal Ischemia ◽  
Artery Stenosis ◽  
Left Renal Artery ◽  
Severe Stenosis

The role of nitric oxide (NO) and prostaglandins (PG) in modifying renal hemodynamics was examined in clipped and nonclipped kidneys of unilateral renal artery stenosis. Chronic unilateral renal ischemia was established by 4-wk-clipping the left renal artery of canine kidneys, and renal interstitial nitrate+nitrite and PGE2 contents were evaluated by the microdialysis technique. Unilateral renal artery stenosis caused 45 ± 1 and 73 ± 1% decrements in renal plasma flow (RPF) in moderately and severely clipped kidneys and 21 ± 3% decrements in nonclipped kidneys with severe stenosis. Renal nitrate+nitrite decreased in moderately (−31 ± 1%) and severely clipped kidneys (−63 ± 4%). N ω-nitro-l-arginine methyl ester reduced RPF (−56 ± 3%) and glomerular filtration rate (GFR; −54 ± 3%) in moderately clipped kidneys, whereas this inhibitory effect was abolished in severely clipped kidneys. In contrast, renal PGE2 contents increased modestly in moderate clipping and were markedly elevated in severely clipped kidneys (from 111 ± 7 to 377 ± 22 pg/ml); sulpyrine impaired renal hemodynamics only in severely clipped kidneys. In contralateral nonclipped kidneys, although renal PGE2 was not increased, sulpyrine reduced RPF (−32 ± 1%) and GFR (−33 ± 3%) in severe stenosis. Collectively, NO plays a substantial role in maintaining renal hemodynamics both under basal condition and in moderate renal artery stenosis, whereas the contributory role shifts from NO to PG as renal artery stenosis progresses. Furthermore, because intrarenal angiotensin II is reported to increase in nonclipped kidneys, unilateral severe ischemia may render the nonclipped kidney susceptible to PG inhibition.

Traumatic Left Renal Artery Stenosis Managed with Splenorenal Bypass

1990 ◽  
Vol 30 (12) ◽  
pp. 1594-1596 ◽  
Author(s):  
GARY W. BARONE ◽  
MARK B. KAHN ◽  
JAMES M. COOK ◽  
BERNARD W. THOMPSON ◽  
ROBERT W. BARNES ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Left Renal Artery

scholarly journals Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II.

1978 ◽  
Vol 43 (3) ◽  
pp. 437-446 ◽  
Author(s):  
S Ichikawa ◽  
J A Johnson ◽  
W L Fowler ◽  
C G Payne ◽  
K Kurz ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Pressor Responses

Renal actions of angiotensin II in renovascular hypertension

1987 ◽  
Vol 65 (8) ◽  
pp. 1559-1565 ◽  
Author(s):  
W. P. Anderson ◽  
R. L. Woods ◽  
K. M. Denton ◽  
D. Alcorn
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
Filtration Fraction ◽  
Severe Stenosis ◽  
Glomerular Ultrafiltration

In renal artery stenosis severe enough to cause hypertension, angiotensin II maintains glomerular filtration rate (GFR) both in the initial high renin phase of hypertension and later when plasma levels are normal. Angiotensin II also maintains GFR in less severe stenosis, which does not cause hypertension. This homeostatic action of angiotensin II to maintain GFR has minimal effects on blood flow. In renal-wrap hypertension, plasma renin levels are elevated for longer than after renal artery stenosis, but in other respects this initial phase of the hypertension is similar to that after renal artery stenosis. GFR is reduced, the rate of development of hypertension is accelerated by angiotensin II, and angiotensin II maintains the glomerular filtration fraction. Renal resistance is markedly increased owing to both compression of the kidney by the hypertrophying renal capsule and to angiotensin II. Thus angiotensin II apparently plays a primarily homeostatic role in renovascular hypertension to maintain glomerular ultrafiltration. It is suggested that the angiotensin II may be formed intrarenally and may act on sites other than resistance blood vessels.

scholarly journals Renal artery stenosis of atherosclerotic etiology – the single kidney surgical recurrence 12 years after nephrectomy

2016 ◽  
Vol 63 (3) ◽  
pp. 251-254
Author(s):  
Maria Daniela Tănăsescu ◽  
◽  
Marcel Pălămar ◽  
Mihai Ovidiu Comşa ◽  
Alexandru Mincă ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Left Kidney ◽  
Secondary Hypertension ◽  
Artery Stenosis ◽  
The Other ◽  
Left Renal Artery ◽  
Arterial Blood ◽  
The Moment ◽  
The Right

Objectives. Renal artery stenosis, as main cause of renovascular secondary hypertension, is mainly caused by atherosclerosis of large vessels and is clinically characterized by resistant or malignant hypertension, impacting the kidney function to various degrees. The present article brings into attention the case of a patient which developed renal artery stenosis on the left kidney, the same condition occurring 12 years later on the right kidney. Material and method. Our patient was initially diagnosed at the age of 48 with complete occlusion of the left renal artery, for which left nephrectomy was performed, while the right artery was normal. Twelve years later she presents with renal artery stenosis on the right kidney, which is treat by stent-angioplasty. Results. After surgery, the patient’s evolution was positive, with amelioration of the laboratory values, in parallel to the arterial blood pressure. Discussions. The probability that, in the moment of diagnosis of renal artery stenosis with progressive evolution to occlusion caused by atherosclerosis, the other artery would be normal, both seen by ultrasonography and angiography, while years later to develop stenosis, is minimal. Up to present, the literature holds little evidence of such similar cases. Conclusions. In the particular case of patients that were diagnosed with severe renal artery stenosis of atherosclerotic origin and had only one of the arteries affected, it is necessary to keep a permanent monitoring, justified by the risk of development of the same pathology to the other artery

scholarly journals Refractory hypertension secondary to renal artery stenosis with a honeycomb-like structure

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Cheng Chen ◽  
Ying Zhang ◽  
Da Yin ◽  
Yan Liu ◽  
Yunpeng Cheng ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Fibrous Tissue ◽  
Honeycomb Structure ◽  
Artery Stenosis ◽  
Proximal Segment ◽  
Left Renal Artery ◽  
Renal Infarction ◽  
Refractory Hypertension ◽  
Spider Web

Abstract Background A honeycomb-like structure (HLS) is a rare abnormality characterized by a braid-like appearance. Angiograph and intravascular examination, including coherence tomography and intravascular ultrasound (IVUS), can further confirm the multiple intraluminal channels or honeycomb structure, which can also be described as looking like ‘swiss cheese’, a ‘spider web’ or a ‘lotus root’. Previous studies have mostly reported this abnormality in coronary arteries, with a few cases in renal arteries. More information about the characteristics and development of HLS is needed. Case presentation A 69-year-old Han man with resistant hypertension received abdominal enhanced computerised tomography and was revealed to have left renal artery stenosis with the possibility of left renal infarction. Renal artery angiography confirmed a 95% stenosis located in the proximal segment of the left renal artery, and the middle segment was blurred with multi-channel-like blood flow. Further IVUS was performed and identified multiple channels surrounded by fibrous tissue. It was a rare case of HLS in the renal artery secondary to the thrombus, with organisation and recanalisation. Balloon dilatation and stent implantation at the proximal segment of the left renal artery were performed successfully. Blood pressure was well controlled after the procedure. Conclusions The IVUS findings are helpful for forming interventional therapeutic strategies for HLS lesions in the renal artery.

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