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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.
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PMID:Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats. 736 76

Nonsteroidal anti-inflammatory drugs predispose to acute renal failure in conditions associated with decreased RBF. Such conditions include advanced age, hypertension, chronic renal insufficiency, diuretic use, and any condition decreasing effective circulating volume. Strenuous exercise also causes marked reductions in RBF. The patient discussed developed severe acute renal failure after strenuous exercise and therapeutic doses of ibuprofen and hydrochlorothiazide-triamterene. Urinalysis showed a nephritic sediment with red blood cell casts. Renal biopsy showed acute tubular necrosis and arteriolar nephrosclerosis. Although exercise-associated acute renal failure is uncommon, susceptible patients with exercise-induced renal ischemia and prostaglandin inhibition may develop this complication.
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PMID:Exercise-induced acute renal failure associated with ibuprofen, hydrochlorothiazide, and triamterene. 757 49

Renal ischaemia, both unilateral or bilateral, is the cause of renin dependent hypertension but only at the beginning of kidney hypoperfusion. Long lasting renovascular hypertension is progressively becoming more and more independent from the renal renin-angiotensin (RA) system and finally mostly dependent from extrarenal hypertensinogenic factors. This is the reason, why assessment of the individual components of the renal RA system and anatomical or physiological methods of kidney imaging are becoming progressively less sensitive and less specific in the diagnosis of renovascular hypertension of long-term duration.
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PMID:[Renovascular hypertension--a persistently difficult diagnostic problem]. 767 27

Renovascular hypertension is one of the more common causes of secondary hypertension. The true prevalence of this condition is not known, because only a selected few with hypertension are considered for thorough diagnostic work-up. The higher incidence figures come from centers with a special interest in this disease. The ability of a clinician to detect renovascular hypertension has improved substantially, thanks to the advances in radiology. The predominant mechanism of blood pressure elevation from renal ischemia is activation of the renin-angiotensin system. Clinically, the pathological lesions that cause renal artery stenosis are atherosclerosis and fibromuscular dysplasia; the former is typically seen in older men, and the latter is typically found in young women. Suspicion of the presence of renovascular disease should prompt the physician to obtain appropriate screening and confirmatory tests. Once diagnosed, the management of patients with renovascular hypertension requires a carefully planned multidisciplinary approach to offer the patient a best possible therapeutic option, with surgical revascularization or balloon angioplasty, or chronic medical therapy. However, these options are not mutually exclusive. The best long-term results are obtained with surgical therapy. Although balloon angioplasty is being increasingly used perhaps as the preferred initial therapeutic procedure for many patients with renal artery stenosis, long-term results comparable with surgery are not yet available. The ideal rational therapy for patients with renal artery stenosis is reperfusion of the ischemic kidney either by surgical correction or by balloon dilation. The aim is not only to improve the blood pressure control, but also to prevent and at times to reverse renal failure. Although effective antihypertensive drugs have become available, the role of medical management of renovascular hypertension is shrinking and should be limited to patients who have contraindications to or unwilling to undergo corrective procedures to relieve renal ischemia.
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PMID:Renovascular hypertension. 777 25

In the present review, the possibilities of ergometric and pharmacological "intervention" with a view to improving the validity of scintirenography are reported. Exercise renography at present does not have a defined role in clinical routine. This procedure, however, gives additional information in hypertensive patients with respect to renal ischemia. Captopril scintirenography can be recommended as a screening test for renovascular hypertension. Furosemide-"intervention" differentiates between obstructive uropathy and dilatation of renal collecting system without obstruction. This is true especially in newborns with congenital abnormalities of the upper urinary tract, in order to stratify these young patients for surgical or conservative treatment.
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PMID:[Intervention in nuclear medicine kidney diagnosis]. 784 1

More than 40,000 new patients begin treatment for end-stage renal disease in the United States each year. The most frequent causes are diabetes and hypertension. The incidence rates for blacks and Native Americans are six- to sevenfold in excess of those for whites. Studies are seeking to determine the roles of atherosclerotic vascular disease, renal ischemia, and the amount of renal mass on the rate of progressive renal disease. Other studies seek to identify the factors that predict the development of nephropathy in patients with diabetes mellitus. Treatment of hypertension slows the rate of progressive renal disease by 40% to 50%. Meta-analysis of several European studies suggests that dietary protein restriction appears to delay the onset of end-stage renal disease.
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PMID:Epidemiology and prevention of renal disease. 792 79

The effect of chronic hypobaric hypoxia (CHH) on the development of 2k-2c Goldblatt renovascular hypertension has been analyzed in rats of both sexes. Results have shown lower values of blood pressure (BP) in all the animals exposed to CHH compared with their normoxic control (P < 0.001). Haematocrit was increased by adaptation to CHH (P < 0.001), and was larger in male than in female hypoxic rats, both normotensive (P < 0.05) and hypertensive (P < 0.01). Plasma renin activity was higher in normoxic and hypoxic hypertensive female rats than in their normotensive controls (P < 0.05). Plasma angiotensinogen concentration was higher in normoxic control male rats than in all the other groups. This difference disappeared after adaptation to CHH or development of hypertension. Plasma aldosterone concentration was lowest in normoxic control male rats and the difference also disappeared after CHH or renal ischemia. Present data indicate that CHH blunts the hypertensive response to bilateral renal ischemia in male and female rats. Sexual differences related to the mechanisms that could be involved in hypertension development have been observed. The renin-angiotensin-aldosterone system might be modulated by gonadal hormones during the development of hypertension.
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PMID:Changes in the renin-angiotensin-aldosterone system in 2 kidney -2 clip Goldblatt hypertensive rats of both sexes submitted to chronic hypobaric hypoxia. 800 44

The experimental discovery of the pathophysiological relationship between renal artery stenosis and arterial hypertension was historically reported (1934) before the clinical description of the disease in human patients (1950). The experimental model explains the relation between renal ischemia, renal endocrine activation, and morphological alterations of the homo and contralateral kidneys. In particular, the experimental model improves the understanding of the evolution of renovascular disease. In human patients, renal artery stenosis does not always lead to clinical disease. Because of the frequency of arterial hypertension, there is not always a clear relationship between hypertension and renal insufficiency or renal artery stenosis. Therefore a complete diagnosis of renal endocrine and exocrine function is needed to understand this relation before deciding on the therapeutic approach. This diagnosis is made by exploration of the renal renin-angiotensin axis, its pharmacological blockade and the response of the excretory function. This approach corresponds to the clinical description of the evolution of the disease; the peripheral and renal vein renin assays; the pressure and scintigraphic response to converting enzyme inhibition and renal morphological definition by echography and CT scan. This pathological approach permits a rational choice of the therapeutic indication: non-intervention, specific medical treatment, endovascular or surgical revascularization or nephrectomy.
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PMID:[Is in depth diagnosis important in renal artery stenosis?]. 815 92

We report a case of hyponatremia, polyuria-polydipsia, hypokalemia, nephrotic syndrome, and hypertension caused by unilateral renal ischemia, and the resolution after nephrectomy of the ischemic kidney. The renin-angiotensin-aldosterone axis seems to play an essential role in the pathogenesis of these features. Mechanisms by which angiotensin II, hypokalemia, and proteinuria can affect salt and water balances, and the role of angiotensin II as a cause of heavy proteinuria are discussed. Renovascular hypertension should be considered in the differential diagnosis of hyponatremia, hypokalemia, and polyuria-polydipsia.
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PMID:Multiple manifestations of renovascular hypertension. 820 70

Typical causes of renovascular hypertension include intramural atherosclerotic lesions of the main renal arteries or their branches and fibromuscular dysplasia of the renal arterial wall with luminal narrowing. We report a patient with new-onset, accelerated hypertension (blood pressure 220/140 mm Hg, status epilepticus, retinal hemorrhages) secondary to a dissection of the anterior division of the right renal artery that was accompanied by hyperreninemia, hyperaldosteronism, and hypokalemia. At presentation in the untreated state, unstimulated plasma renin activity and the serum aldosterone level were markedly elevated. Following right nephrectomy, blood pressure levels normalized without antihypertensive therapy, and plasma renin activity, serum aldosterone and potassium levels normalized. Histologic study of the right renal artery showed an isolated dissection of the anterior branch of the vessel between the muscularis and adventitia that created marked reduction in luminal diameter and renal ischemia. There was no evidence of any other vascular abnormalities, atherosclerosis, or fibromuscular dysplasia. These findings demonstrate that an isolated dissection of a branch of the renal artery may induce profound hyperreninemia and represents a rare, reversible etiology for accelerated hypertension associated with acute encephalopathy.
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PMID:Accelerated hypertension with encephalopathy due to an isolated dissection of a renal artery branch vessel. 820 71


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