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

Multiunit and single-unit recordings of afferent renal nerve activity (ARNA) were obtained in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats between 35 and 150 days of age. Intrapelvic backflow of urine at 20 mmHg excited ARNA at all ages in SHR (152 +/- 18% above control) and WKY rats (262 +/- 24%). In SHR, complete renal ischemia was more excitatory in rats older than 120 days (1,233 +/- 103%, n = 8) than in younger SHR (317 +/- 28%, n = 42). Single-unit recordings showed that this was related to the appearance of R1 chemoreceptors in older SHR and coincided with a decline in the proportion of R2 chemoreceptors in the renal nerves. Other chemoreceptive responses were identified in single units that did not show complete R1 or R2 characteristics, some of which showed responses consistent with a transformation process from R2 to R1 receptor type. R1 chemoreceptors were not present in WKY rats studied up to 150 days of age and, unlike SHR, the proportion of R2 chemoreceptors did not decline with age. Accordingly, complete renal ischemia in WKY rats caused a comparable excitation in multiunit ARNA at all ages (285 +/- 33%, n = 43). Oral enalapril from weaning to 100 days of age prevented hypertension in SHR but did not impair the responsiveness of ARNA to any stimulus. In WKY rats, enalapril treatment for the same period resulted in exaggerated ARNA response to renal ischemia (1,250 +/- 377% above control).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-dependent changes in afferent renal nerve activity in genetically hypertensive rats. 159 Apr 77

alpha 2-Adrenoceptors were characterized on neural and vascular membranes from 2-kidney-1-clip renal hypertensive (RHT) and normotensive (NT) rats. Rats were sacrificed 6 weeks after induction of renal ischemia, and the specific binding of 3H-clonidine to smooth muscle membranes form tail arteries and neural membranes from various brain regions was examined. Additionally, isometric contractions of helically cut tail artery strips produced by various alpha-adrenoceptor agonists were measured. Scatchard analysis indicated an increased number of high-affinity binding sites on the smooth muscle membranes from RHT rats (Bmax = 43.5 +/- 1.4 fmol/mg protein) compared to that from the NT rats (25.4 +/- 3.8 fmol/mg protein). An increased contractile sensitivity to clonidine was also observed in tail artery strips from RHT rats (EC50 for RHT = 3.04 x 10(-8) M; NT = 1.52 x 10(-7) M). In neural tissue, the number of alpha 2-adrenoceptor-binding sites was significantly increased in the locus coeruleus from RHT rats, but not in the amygdala, hypothalamus, parietal cortex, hippocampus or lower brain stem. These results demonstrate that renal ischemia produces changes in both peripheral and neural alpha 2-adrenoceptor density. The increase in smooth muscle alpha 2-adrenoceptors might also provide a partial explanation for the supersensitivity to adrenergic agonists in this model of hypertension.
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PMID:Changes in alpha 2-adrenoceptors on vascular smooth muscle and neural membranes following hypertension induced by renal ischemia. 168 46

The aneurysms of the abdominal aorta requiring suprarenal clamping are rare. Suprarenal clamping was required for only 43 of 544 aneurysms operated electively from 1981 to 1989. Twenty-five patients had a juxtarenal aneurysm, without any normal aortic segment under the renal arteries, and suprarenal clamping was therefore necessary while the upper anastomosis was being established (group I). Eighteen patients had an aneurysm enclosing the root of at least one renal artery (group II). Several prognostic factors have been assessed: patient's age, presence of preoperative renal insufficiency, of arterial hypertension or of coronary insufficiency, and revascularization method. Five patients died. Four of them belonged to group II and were over 75 years old. All presented with a preoperative renal insufficiency. Two of these deaths were caused by mesenteric infarction. Four cases of regressive postoperative renal insufficiency were observed in patients for whom renal clamping had lasted longer than 45 minutes. This study allowed outlining three prognostic factors: the patient's age, preoperative renal insufficiency, a period of renal ischemia exceeding 40 minutes. On the other hand, the severity of hypertension had no predictive value. Coronary insufficiency requires a strict hemodynamic surveillance, but is not a contraindication for revascularization.
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PMID:[Early prognostic factors of the surgery of aneurysms of the abdominal aorta with renal artery clamping]. 176 86

Although the role of angiotensin II (Ang II) in the pathogenesis and progression of the failing heart is uncertain, previous reports have suggested that myocyte injury may be a component in this process. In this study, we investigated this possibility in more detail. Cardiotoxic effects of nonacutely hypertensive doses of Ang II were examined in 90 rats, including those receiving an angiotensin infusion (200 ng/min i.p.) and those with renovascular hypertension, where endogenous stimulation of Ang II occurred. Myocyte injury and wound healing resulting from these treatments were evaluated by 1) immunofluorescence after in vivo monoclonal antibody labeling of myosin to detect abnormal sarcolemmal permeability, 2) [3H]thymidine incorporation into DNA, to detect fibroblast proliferation, and 3) light microscopic evidence of myocytolysis and subsequent scar formation. We found that exogenous Ang II produced multifocal antimyosin labeling of cardiac myocytes and myocytolysis, which were maximal on days 1-2 of the infusion. Subsequently, DNA synthesis rates were increased, with fibroblast proliferation reaching peak levels on day 2 (Ang II-treated rats, 90.0 +/- 18.6 cpm/micrograms DNA; control rats, 11.4 +/- 2.3 cpm/micrograms DNA; p less than 0.05); microscopic scarring was found on day 14 and represented 0.12 +/- 0.02% of the myocardium. Concurrent treatment with both propranolol (30 mg/kg/day s.c.) and phenoxybenzamine (5 mg/kg/day i.m.) did not attenuate Ang II-induced antimyosin labeling. Increased endogenous Ang II, resulting from renal ischemia after abdominal aortic constriction, produced both antimyosin labeling and increased rates of DNA synthesis like that observed with Ang II infusion. Both myocyte injury and fibroplasia were prevented with captopril (65 mg/day p.o.), but this protective effect was not seen with reserpine pretreatment. Infrarenal aortic banding without renal ischemia, on the other hand, produced hypertension without necrosis. We conclude that pathophysiological levels of endogenous as well as low-dose exogenous Ang II were associated with altered sarcolemmal permeability and myocytolysis with subsequent fibroblast proliferation and scar formation. Myocyte injury was unrelated to the hypertensive or enhanced adrenergic effects of Ang II or to hypertension per se. Captopril was effective in preventing myocyte injury in renovascular hypertension. The mechanism(s) responsible for Ang II-induced necrosis will require further study.
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PMID:Cardiac myocyte necrosis induced by angiotensin II. 183 62

After the development of blood pressure measurements in humans, the association of high blood pressure with renal disease was established. Injection of extracts of various organs in an attempt to replace their secretions was common in the 19th century, and it was therefore natural for Tigerstedt and Bergman to investigate the effects of renal extracts. In this way, they discovered renin. This paper covers the methods by which its mode of action was uncovered, as well as its relation to renal ischemia and hypertension.
Hypertension 1991 Nov
PMID:Evolution of renin. 184 50

Several interventions are used to induce hypertension in the experimental animal. The three most used interventions are renal ischemia, mineralocorticoid excess, and genetic manipulation. The sequence of events leading from these initiating manipulations to the elevated arterial pressure is being explored to define the mechanism responsible for hypertension. The following mechanisms are currently extensively evaluated: Pressor and depressor factors of renal origin, neurogenic regulation, circulating humoral factors, vessel wall hypertrophy, and membrane transport abnormality. The experimental models of hypertension hold great promise in providing an understanding of the mechanisms and developing effective treatment in clinical hypertension.
Hypertension 1991 Jan
PMID:Experimental hypertension. 184 23

Spontaneous renal artery dissection is an uncommon cause of renovascular hypertension, usually associated with fibromuscular dysplasia. Among reported nonautopsy cases (N = 80), arterial reconstruction has seldom been attempted (N = 21) and the outcome has frequently been poor (48% clinical failure rate). This is attributed in part to the frequent involvement of renal artery branches by the dissection. Furthermore, the report of spontaneous reversion to normotension among patients treated medically has also clouded the role of surgery in this disease. Since progress in the technique of renal artery repair now allows successful treatment of anatomically complex lesions, we reviewed our experience with arterial reconstruction in the management of spontaneous renal artery dissection to determine the frequency of and factors correlating with cure after operative repair. Ten patients (eight men, two women; mean age, 39.3 +/- 5.9 years) were admitted with severe hypertension (10/10), often associated with neurologic symptoms, hematuria, or flank pain (8/10). Serum creatinine was elevated in only two patients. Angiography demonstrated changes consistent with fibromuscular dysplasia in 7 of 10 patients and evidence of dissection in 6 of 10. Bilateral disease was present in three patients. Only five patients had a single renal artery on the involved side. The dissection extended into the primary branches in 8 of 10 patients and involved both renal arteries in four of the five patients with two arteries. Histologic study confirmed fibromuscular dysplasia in six and intramural dissection in all operative specimens. Five patients underwent revascularization (in one case requiring the ex vivo technique), with use of hypogastric artery as a conduit in four of five or resection and primary reanastomosis in one of five. Three patients became normotensive, and two returned to their previous level of blood pressure control. Follow-up averaged 14.5 years. Two patients underwent nephrectomy after exploration demonstrated nonreconstructible vessels, and two underwent nephrectomy when intraoperative assessment of the kidney showed that revascularization had failed to adequately reverse extensive renal ischemia. After a mean follow-up of 14.6 years these patients remain normotensive, although two require antihypertensive medications. One patient was treated medically and is currently hypertensive off all medications. Nine of 10 patients have maintained a normal serum creatinine during follow-up. We conclude that renal revascularization is frequently successful in spontaneous renal artery dissection (five of seven, 71.4%) and results in sustained relief of hypertension with maximal conservation of renal tissue. This is important because of the young age at onset and the not infrequent occurrence of bilateral fibromuscular dysplasia, and even of dissection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of arterial reconstruction in spontaneous renal artery dissection. 192 Jun 44

The study included 15 patients with nephrogenic hypertension of various genesis. 13 of them had unilateral disease, 2 bilateral one. The diagnosis was established from the data provided by a single captopril test, radionuclide and angiographic examinations. The blood for renin and prostaglandin quantitation was obtained from the renal veins and infrarenal portion of the vena cava inferior. The results show that in unilateral renal lesions prostaglandin E secretion on the affected side was significantly lower than on the contralateral side (p less than 0.05). Plasma renin activity in 3 patients with a contracted kidney was significantly lower on the affected side (p less than 0.05), though the rest 10 patients were reported to exhibit opposite results. No significant relationships occurred in the levels of prostaglandins I2, F2 alpha, thromboxane A2. It is suggested that renal ischemia may inhibit synthesis of depressor prostaglandin E2 in renal medullary interstice. A separate analysis is presented of plasma renin and prostaglandin activity in 2 cases of nephrogenic hypertension as a result of bilateral renal affection.
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PMID:[The diagnostic importance of determining prostaglandins in patients with nephrogenic arterial hypertension]. 194 11

Page kidney is caused by the accumulation of blood in the perinephric or subcapsular space, resulting in compression of the involved kidney, renal ischemia, and high renin hypertension. Most patients are young hypertensives with a remote history of blunt trauma to the abdomen or back. We describe a case of acute Page kidney following a renal biopsy in a patient with underlying IgA nephropathy. In addition to the new-onset hypertension, this patient developed a significant decline in renal function due to the inability of the contralateral diseased kidney to compensate. Magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound were valuable in making this diagnosis. Medical and surgical therapeutic options were considered. This report also reviews all previously described cases of Page kidney.
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PMID:Page kidney: case report and review of the literature. 195 41

Renovascular hypertension is caused by two distinct conditions with different causes, fibromuscular dysplasia and atheroma. Diagnosis of the former is both simpler and more rewarding, whereas atheromatous lesions of the renal artery may be secondary to essential hypertension. It is therefore important to establish existence of functional renal ischemia as well as an anatomical lesion. Universal screening of all hypertensive patients is not recommended because of the relatively low prevalence of the disease and insufficient accuracy of available screening tests. When renovascular hypertension is clinically suspected, an oral captopril test is the most reliable office screening test. After this, digital subtraction angiography with renal vein renins or captopril renography are appropriate steps. However, the latter procedure, while promising, requires further evaluation. Duplex scanning of the renal arteries also comes into this category. Arteriography is done last, so that if renal ischemia is indicated, angioplasty can be attempted at the same time as arteriography.
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PMID:Diagnosis and evaluation of renovascular hypertension. Indications for therapy. 199 96


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