The Goldblatt memorial lecture. Part I: Experimental renovascular hyptertension.

Barger, A. C.

doi:10.1161/01.hyp.1.5.447

Cited by 35 publications

(10 citation statements)

References 36 publications

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“…The (V-A)/A ratio showed the best sensitivity and predictive value of all parameters used, but again specificity was only slightly improved. Various explanations for the finding of negative tests in patients with renovascular hyperten sion proved by successful revascularisation have been given: technical errors, a two-stage course of renovascu lar hypertension and the syndrome of nonrenin-mediated renovascular hypertension [7,14,[28][29][30]. Technical errors as the only explanation seem unlikely, since exclu sion criteria for uninterpretable renin data reduced but did not exclude false-negative tests.…”

Section: Judson and Helmermentioning

confidence: 99%

Renal Venous Renin Determinations in Renovascular Hypertension

Lüscher¹,

Greminger²,

Kuhlmann

et al. 1986

Nephron

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To assess the diagnostic and prognostic value of renal venous renin levels in renovascular hypertension, 95 patients with severe unilateral renal artery stenosis were studied. Surgery (n = 52) or percutaneous transluminal dilation (n = 43) were done irrespective of renal venous renin levels. Lateralization of renin secretion as assessed by the PRA ratio and the renin secretion index was found in the majority of patients (66% and 88%, respectively). Patients with fibromuscular hyperplasia had more frequently PRA ratios < 1.5 than those with arteriosclerotic stenosis (p < 0.05). The renin secretion index proved to have a higher sensitivity (92%) and predictive value (92%) for a successful outcome of both surgery and PTA than the PRA ratio (69% and 89%, respectively), while the specificity was the same with both parameters (42% and 43%, respectively). The contralateral suppression index was most specific in predicting an unfavorable outcome. However, with all ratios used, a considerable number of false-negative and false-positive tests were observed both with surgery and PTA, a finding limiting the value of the method in selecting patients for these interventions. Other factors, such as age of the patient, kidney function and the underlying arterial disease turned out to be equally important prognostic factors. Thus, although cure after both surgery and PTA is more likely in the presence of lateralized renin secretion and contralateral suppression, the method does not allow to exclude patients with severe renal artery stenosis, hypertension and negative renal venous renin tests from these interventions. Therapeutic decisions in renovascular hypertension therefore should not depend on a single test, but rather on various clinical, radiological and laboratory findings together.

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Section: Judson and Helmermentioning

confidence: 99%

Renal Venous Renin Determinations in Renovascular Hypertension

Lüscher¹,

Greminger²,

Kuhlmann

et al. 1986

Nephron

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“…1). Acute administration of angioten sin II antagonist or converting enzyme inhibitor does not significantly affect blood pressure or renal blood flow at this stage [3,5]. The time course for the development of the chronic phase differs between species and models.…”

Section: Pathogenesis and Pathophysiologymentioning

confidence: 90%

“…The causal relationship between the increase in hormonal levels and the increased blood pressure has been demonstrated by normalization of blood pressure by administration of angiotensin II antagonist, angioten sin-converting enzyme inhibitor or renin-specific anti body in this phase. Moreover, the acute hypertension can be prevented by pretreatment with pharmacologic block ade of the renin-angiotensin system [3,4], During this phase, angiotensin also induces changes in intrarenal hemodynamics (decreases glomerular filtration rate and blood flow) and stimulates aldosterone secretion. The combination of hemodynamic and direct hormone ef fects on tubular function result in increased sodium reab sorption.…”

Section: Pathogenesis and Pathophysiologymentioning

confidence: 99%

“…Furthermore, Barger and coworkers have shown that renovascular hypertension can be induced without volume expansion in IK-1C dogs maintained continuously on a low sodium intake. In this preparation, the renin-angiotensin system remained activated in the chronic phase and was pathogenic in all phases of the hypertension [3], Experimental data suggest that increased vascular reactivity [10][11][12][13] In summary, there are two basic models of Goldblatt renovascular hypertension. The pathogenesis of both models produces a spectrum of plasma renin and angio tensin levels from high to normal that is inversely related to sodium balance.…”

Section: Pathogenesis and Pathophysiologymentioning

confidence: 99%

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Renovascular Hypertension: An Update on Pathophysiology, Diagnosis and Treatment

Dzau¹,

Gibbons²,

Levin³

1983

Am J Nephrol

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“…It is well established that renal hypoperfusion accompanied by low mean arterial pressure is ultimately associated with the classical signs of pre-renal AKI, often referred to as ''acute tubular necrosis'' (ATN) [5][6][7][8][9][10]. In contrast, the model applied in the present study resembles the one-kidney Goldblatt model used to study renal (arterial) hypertension [13]. And indeed, the authors clearly demonstrate that reduced renal blood flow resulted in increased systemic mean arterial pressure (MAP), something rarely encountered in a systemic hypoperfusion state.…”

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confidence: 99%