Sequential renal hemodynamics in experimental benign and malignant hypertension.

Dzau, Victor J.; Siwek, Leland; Rosen, S. M.; Farhi, E R; Mizoguchi, Hiroaki; Barger, A. C.

doi:10.1161/01.hyp.3.3_pt_2.i63

Cited by 22 publications

(8 citation statements)

References 14 publications

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“…Natriuresis and weight loss 18 and muscle ischaemia 19 may accompany the transition to the malignant phase. In addition, many of those with MHT had advanced renal failure and this may have contributed to the weight loss.…”

Section: Discussionmentioning

confidence: 99%

Factors influencing the development of malignant hypertension in Nigeria

2000

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Hypertension prevalence rates remain comparatively low in Nigeria, although the associated morbidity and mortality including that due to malignant hypertension (MHT) is considerable. To determine the factors that may be associated with the development of MHT we compared 74 patients with essential MHT (age 48 ؎ 9 years, 59 male, blood pressure (BP) 234 ؎ 31/140 ؎ 17 mm Hg) with 74, age, gender and BP-matched patients with essential benign hypertension (BHT) (49 ؎ 8 years, 60 male, 227 ؎ 26/136 ؎ 15 mm Hg). Body mass index was higher in the MHT group by 1.3 (95% Cl: 0.5 to 2.1, P Ͻ 0.01). In the subset (25 MHT, 43 BHT) in whom hypertension had been diagnosed before presentation, duration of hypertension was shorter (P Ͻ 0.05) in the Keywords: malignant hypertension; risk factors; black Nigerians IntroductionMalignant hypertension (MHT) remains a common condition in some populations, 1,2 and although its prognosis may be improving, it is still associated with considerable morbidity.1 Very high blood pressure (BP) is required for the development of MHT, but since the BP alone does not distinguish non-malignant, benign hypertension (BHT) from MHT and both conditions may exist at similar BP, other factors are clearly in operation.3-5 Some of these may relate to the kidney or vasculature, 3 the immune system 4 and to external or environmental differences.5 It may be possible to manipulate these external variables and prevent the transition to the malignant phase. Prevention of the transition to the malignant phase would reduce the morbidity and mortality attributable to hypertension, since the prognosis is worse in MHT. 6,7 This study aims at identifying these external factors in black Nigerian hypertensives, a group that is arguably underserved. Patients and methodsA record has been kept of the cases of MHT seen in over 10 years. MHT was diagnosed on the basis of severe hypertension with bilateral retinal exudates and haemorrhages with or without papilloedema. 8,9 A detailed account of the clinical presentation of some of the patients has been published elsewhere. 10Patients with secondary causes of hypertension were excluded. Secondary hypertension was excluded on the basis of history, physical examination, urine examination, serum electrolytes, renal ultrasound and renal arteriography as presented in the earlier study. 10 The presence of primary renal disease was suggested by the presence of urinary red cells, red and white cell casts, granular casts and proteinuria up to 1.5 g/24 h. 11 Where there was some doubt as to the cause of the hypertension, such patients were excluded. Accordingly, 74 patients were considered to have primary MHT. These patients were compared with 74 age, gender and BPmatched controls with benign essential hypertension newly presenting at the hypertension clinic. They necessarily had repeatedly high BP readings and grade 3 hypertension. 12Age, gender, body mass index (BMI), socio-economic group, BP, serum creatinine, history of smoking and alcohol use, perception of stress, known duration o...

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Section: Discussionmentioning

confidence: 99%

Factors influencing the development of malignant hypertension in Nigeria

2000

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“…14 " 16 The present data do not allow a distinction to be made between these possibilities, since intravenous saralasin blocks All receptors at both central' 2 and peripheral 16 sites of interaction of All with the sympathetic nervous system, and since ganglionic blockade interrupts all neurogenic vascular tone resulting from either existing nerve traffic or alterations in transmitter release. In recent unpublished studies however, we have demonstrated that removal of the central pressor actions of All through surgical ablation of a pathway in the anterior hypothalamus which mediates these effects 33 significantly attenuates the development of hypertension following acute RSt.…”

Section: Figure 5 Effect Of Peripheral Sympathectomy (6-hydroxydopammentioning

confidence: 62%

Neural contribution to renal hypertension following acute renal artery stenosis in conscious rats.

Faber

Brody

1983

Hypertension

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SUMMARY To assess the hemodynamic changes during acute renal artery stenosis (RSt) and their dependence on alterations in the renin-angiotensin and sympathetic nervous systems, we studied conscious rats chronically instrumented with miniaturized pulsed-Doppler flow probes. Probes were implanted on the superior mesenteric and both renal arteries, and on the lower abdominal aorta for measurement of mesenteric (MR), renal (RR), and hindquarters (HQR) vascular resistance. Unilateral RSt, with a pneumatic cuff occluder that reduced flow by approximately 50%, increased mean arterial pressure (MAP) by 32%, reduced heart rate, and increased MR, nonstenotic (contralateral) RR and HQR. The hypertension was renin-dependent since plasma renin activity increased 6-fold and the angiotensin II (All) antagonist, saralasin, significantly reduced MAP and regional resistances. The acute hypertension was also associated with increased neurogenic vasoconstrictor tone since hexamethonium markedly reduced MAP, MR, HQR and non-stenotic RR. Hexamethonium similarly decreased MAP during hypertension induced by AH infusion, whereas hypertension produced by the "pure" peripheral vasoconstrictor, phenylephrine, was unaffected by ganglionic blockade. In animals with peripheral sympathectomy produced by 6-hydroxydopamine, acute RSt produced hemodynamic changes similar in magnitude to intact animals; however, PRA increased 3-fold more than in intact rats. We conclude that hypertension induced by acute RSt in conscious rats is not only renindependent, but is also associated with inappropriately high neurogenic vasoconstrictor tone, presumably activated by indirect neural actions of AH. has received intensive study, knowledge concerning both the mechanisms that maintain hypertension and produce the initial disturbances remains incomplete. There is, however, growing interest in the possibility that significant interactions may exist between the renin-angiotensin system (RAS) and sympathetic nervous system. It is clear from studies on plasma renin activity (PRA) and the effects of angiotensin (All) blockade that the RAS is activated at the onset of renal hypertension.'" 1 On the other hand, during the chronic phase of renal hypertension PRA is normal or only slightly elevated and All antibodies and receptor antagonists do not substantially reduce blood pressure.

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“…Further occlusion again reduces perfusion to the renal circulation and triggers a repeat cycle of elevation of systemic pressures. Unless interrupted, this sequence ultimately produces malignant-phase hypertension (23).…”

Section: Pathophysiology Of "Critical" Ras and "Ischemic Nephropathy"mentioning

confidence: 99%

Ischemic Nephropathy

Textor

2004

Journal of the American Society of Nephrology

148

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Abstract. Identification and reversing the loss of kidney function beyond occlusive disease of the renal arteries poses a major clinical challenge. Recent studies indicate that atherosclerotic renal artery stenosis develops as a function of age and is commonly associated with other microvascular disease, including nephrosclerosis and diabetic nephropathy. The risks of renal artery stenosis are related both to declining kidney function and to accelerated cardiovascular disease, with increased morbidity and mortality. Newer drugs, including agents that block the renin-angiotensin system, have improved the level of BP control for renovascular hypertension. Progressive renovascular disease during medical therapy can produce refractory hypertension, congestive heart failure, and renal failure with tubulointerstitial fibrosis. Recent studies indicate a complex interplay of oxidative stress, endothelial dysfunction, and activation of fibrogenic cytokines as a result of experimental atherosclerosis and renal hypoperfusion. Advances in imaging and interventional devices offer major new opportunities to prevent progressive loss of kidney function. Recent series indicate that although 25 to 30% of patients with impaired renal function can recover glomerular filtration after revascularization, many have no apparent change in kidney function and 19 to 25% experience a significant loss of kidney function, in some cases as a result of atheroemboli. To select patients who are most likely to benefit from vascular intervention, clinicians should understand the pathophysiology of developing ischemic nephropathy and the potential hazards of revascularization in the setting of diffuse atherosclerotic disease. Further research should be directed toward identification of critical disease, regulation of fibrogenesis, and the interaction with other atherosclerotic processes.

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Sequential renal hemodynamics in experimental benign and malignant hypertension.

Cited by 22 publications

References 14 publications

Factors influencing the development of malignant hypertension in Nigeria

Factors influencing the development of malignant hypertension in Nigeria

Neural contribution to renal hypertension following acute renal artery stenosis in conscious rats.

Ischemic Nephropathy

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