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

Traditionally the initial evaluation of a patient with high blood pressure has focused on exluding secondary correctable causes of hypertension. Such all-inclusive evaluations are expensive, time-consuming, and expose the patient to some risk. A complete history, physical examination, and relatively simple laboratory procedures such as CBC, urinalysis, SMA-6 and 12, and ECG yield sufficient information to detect damage to target organs caused by elevated blood pressure and to exclude the presence of secondary causes fairly adequately. In that small number of patients in whom clues for correctable causes of hypertension are uncovered, or if patients fail to respond to appropriate treatment for essential hypertension, a more extensive evaluation can be undertaken.
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PMID:Initial evaluation of patients with hypertension: an office procedure. 63 18

Accumulated experience with triple contrast percutaneous nephrocystography (water-soluble contrast, iophendylate [Pantopaque], and air) in 42 patients with avascular lesions is presented. Diagnostic studies were accomplished in 40 with surgical correlation in 11. Of the 35 patients with intracystic iophendylate, progressive cyst shrinkage was observed in the 29 with adequate x-ray follow up. The reduction in cyst size was attributed to a marked reactive inflammatory proliferative response with fibrosis of the cyst wall which was found in 6 patients after introduction of iophendylate when compared with a control group of 13 others with surgically proved cysts. Intracystic iophendylate may be especially therapeutic in the nonsurgical management of renal cysts associated with pain, calyceal obstruction, and hypertension. The cyst aspirate was analyzed for appearance, culture, cytology, fat content, and multichannel chemistries (SMA). The index accuracy of these combined tests is high although instances of false positives and negatives for tumor are stressed. The nonsurgical diagnosis of renal cystic lesions is incomplete without percutaneous cyst puncture, contrast study, and analysis of cyst aspirate.
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PMID:Triple contrast percutaneous nephrocystography and analysis of cyst aspirate. 70 32

This summary of management of pill patients covers contraindications, individualizing pill formulations for normal women, and for diabetics, hypertensives, hyperlipidemics and those with personal or familial history of thrombophebitic or vascular disorders. The estrogen or progestagen balance of a pill can be selected to suit the individual. All patients beginning oral contraception should have pelvic exam, breast exam, cervical smear, fasting blood glucose, hematology and SMA-12, repeated in 3 months and yearly thereafter. Normally the pill causes transitory deterioration in glucose tolerance, increased growth hormone, a permanent change in insulin response, effects that are irreversible in 20% of users. Prediabetics should be given sequentials; diabetics should be followed weekly or monthly during oral contraception. Severe hypertension occurs in about 1% of pill users, but the risk is 4 times higher in women who had hypertension in pregnancy. Patients with increased personal or familial risk should be checked every 3 months and pills stopped immediately if blood pressure exceeds 150/100. In pill users cholesterol and free fatty acids remain normal, but lipoproteins, lecithins and triglycerides increase after 6 weeks to a plateau by 6-18 months, in proportion to estrogen dose. Since patients normally only discover hyperlipidemia after a clinical event such as xanthoma or vascular accident, those with related familial or personal history should have blood lipid studies every 3 months, and be given a progestagen only pill. Adolescents who are at high risk of pregnancy should receive progestagen or sequential pills, if their growth, bone age, hypothalamic function and reproductive organs are mature. The risk of idiopathic or posttraumatic thromboembolism is 3-9 times higher in pill users than in the normal population, but the only way of testing for risk in an individual is to do a detailed series of coagulation tests. Those predisposed should be given progestagen only or low dose pills.
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PMID:[Program of surveillance of patients under oral contraceptives]. 122 Jan 2

The purpose of this study was to investigate whether local mechanisms of blood flow autoregulation mediate vasoconstriction during the early development of renal hypertension. Anesthetized rats were instrumented with Doppler flow probes on the celiac (CA), superior mesenteric (SMA), and renal arteries to measure flow velocity in these vessels. Acute two-kidney, one clip renal hypertension was produced by inflating a pneumatic occluder on the left renal artery to reduce flow velocity by 50%. Two hours after renal artery stenosis (RAS), femoral artery pressure (AP) was increased by 35%, CA resistance by 45%, and SMA resistance by 57%. No increases were observed in AP or in CA and SMA resistances for sham-operated, control rats. To determine if autoregulation contributed to the increase in SMA resistance, we protected the SMA vasculature from the increased arterial pressure by servocontrolled inflation of a pneumatic cuff implanted around the SMA. Although normalizing SMA pressure with the protective cuff significantly reduced (p less than 0.05) the increase in SMA resistance that occurred after RAS, SMA resistance remained elevated above control levels. These results suggest that (1) reduced intensity of SMA constriction produced by protection of the SMA is due to inhibition of a local autoregulatory mechanism that is contributing to the increase in SMA resistance during the acute development of renal hypertension, and (2) maintenance of elevated SMA resistance during protection from increased AP is the result of pressure-independent mechanisms that are activated subsequent to renal artery stenosis.
Hypertension
PMID:Autoregulation and vasoconstriction in the intestine during acute renal hypertension. 399 21

To elucidate the critical role of superoxide dismutase (SOD) and nitric oxide in brain injury and systemic circulation during brain ischemia, we performed bilateral carotid artery ligation (BCAL) on rats and evaluated the effects of NG-monomethyl-L-arginine (L-NMMA) and a long-acting SOD derivative (SMA-SOD). After administration of L-NMMA, specific inhibitor against nitric oxide synthase (NOS), most of BCAL rats died within 6 h while no BCAL rats without L-NMMA died at all. Administration of SMA-SOD exhibited no effect on the life span of BCAL rats. Magnetic resonance imaging (MRI) and microscopic analysis for the ischemic brain revealed that, although administration of L-NMMA showed no significant effect on the ischemic brain of BCAL rats, SMA-SOD effectively prevented the ischemic changes based on permeability edema in the frontal lobe. Measurement of changes in the blood flow of the ischemic brain revealed that administration of L-NMMA decreased the blood flow in the BCAL rats while no remarkable changes were seen after administration of SMA-SOD. Urinary secretion of NO2-/NO3-, the metabolites of nitric oxide, was increased by challenging BCAL, and the presence of L-NMMA or SMA-SOD diminished this elevation. Blood pressure was increased by performing BCAL to rats, and administration of L-NMMA showed further elevation of the blood pressure. On the contrary, administration of SMA-SOD decreased post-ischemic hypertension. These results suggest that SOD may play a protective role for brain ischemia by suppressing increased vascular permeability, while nitric oxide showed beneficial effect on the ischemic brain by increasing the blood flow in the ischemic brain.
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PMID:Role of superoxide dismutase and nitric oxide on the interaction between brain and systemic circulation during brain ischemia. 752 76

The classical presentation of primary hyperparathyroidism, "moans, bones, groans," is no longer commonly seen since the diagnosis of hypercalcemia is now made much earlier with the routine use of the SMA 12. In the past 8 1/2 years, 85 patients underwent cervical exploration in our institution for primary hyperparathyroidism. There were 34 male and 51 female patients, ranging in age from 18-84 years. The specific symptoms included hypertension in 40 patients, generalized weakness in 25, renal stones in 14, psychiatric problems in 2, and bone changes on X-ray in 4. Forty-one patients were totally asymptomatic. The diagnosis was made mainly on the basis of history, serum calcium and phosphorous levels, parathormone assay, and 24-hour urinary calcium studies. Preoperative localization studies were performed in 38 patients. Thallium technetium subtraction scans, when positive, were very helpful. The surgical approach involved stepwise exploration of both sides of the neck with identification of all four parathyroid glands. In patients with uniglandular pathology (87%), the adenoma was removed with biopsy of at least one normal gland. In multiglandular disease, the abnormal glands were removed. Frozen section was routinely performed to confirm the presence of parathyroid tissue and no attempt was made to pathologically distinguish adenoma from hyperplasia. Two patients had parathyroid carcinoma. In three patients, serum calcium levels did not fall, resulting in an operative success rate of 96%. One patient treated by subtotal parathyroidectomy developed permanent hypoparathyroidism and one other patient developed temporary hypocalcemia. Only a single patient developed vocal cord palsy. Early exploration in patients with primary hyperparathyroidism is indicated. The basic diagnostic workup is sufficient for initial exploration. It is important to distinguish uniglandular from multiglandular pathology after careful bilateral exploration and identification of all four parathyroid glands.
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PMID:Cervical exploration for primary hyperparathyroidism. 844 Dec 55

Paraoxonase (PON) is an antioxidative enzyme, which eliminates lipid peroxides. PON has two common polymorphisms (M/L55 and R/Q192) that influence PON concentration and activity. We studied whether the M/L55 or R/Q192 genotype relates with the severity of atherosclerosis of the abdominal aorta, and the mesenteric and common iliac arteries in 123 consecutive autopsy cases (90 males and 33 females, aged 18-93 years). The severity of atherosclerosis in the arteries was evaluated, and the percentage of stenosis was measured. The intimal thickness in the internal elastic lamina (IEL) of the coeliac (CA), superior mesenteric (SMA) and inferior mesenteric (IMA) arteries were measured by light-microscopy. The LL homozygous men had more atherosclerotic plaques and complicated lesions in the common iliac arteries (56.8%) than the M allele carriers (28.3%, P=0.007). In logistic regression analysis, age (P<0.001) and the PON M/L55 genotype (P=0.015) were associated significantly with the severity of atherosclerosis in the common iliac arteries independent of smoking status, R/Q192 genotype, hypertension, diabetes mellitus, BMI and sex. The mean intima of the IMA was significantly thicker (P=0.035) and the number of stenotic lesions in SMAs significantly higher (P=0.008) in the LL homozygous men than M allele carriers. In turn, the R/Q192 genotype was not statistically significantly associated with plaque type, intimal thickness in the IEL or with the number of stenotic lesions. This study demonstrates that PON L55 homozygosity is an independent risk factor for autopsy-verified atherosclerosis in Finns.
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PMID:Paraoxonase producing PON1 gene M/L55 polymorphism is related to autopsy-verified artery-wall atherosclerosis. 1147 29

Thy-1 nephritis was induced in stroke-prone spontaneously hypertensive rats (SHR-SP) with unilateral nephrectomy (UNX) and normotensive same genetic strain Wistar-Kyoto (WKY) rats with UNX to evaluate whether the tubulointerstitial injury in Thy-1 nephritis is accelerated by long-term systemic and intraglomerular hypertension. SHR-SP that underwent UNX at twelve weeks of age were randomly assigned to receive monoclonal anti-thy 1.1 antibody (group SP), and normal saline (group SC). Age-matched normotensive WKY rats served as controls and were given the same dose of monoclonal anti-thy 1.1 antibody after UNX (group WK). In all groups, the blood pressure and renal function were assessed, and morphologic changes of tubulointerstitium were examined by using immunohistochemistry and light microscopy twelve weeks after Thy-1 nephritis induction (in groups SP and WK) and UNX alone (in group SC). In all groups, histological findings, the degree of monocyte/macrophage infiltration, interstitial expression of alpha-smooth muscle actin (alpha-SMA), which is a marker for myofibroblasts, and the degree of tubular cell proliferation were examined. In addition, assessments of blood pressure, serum creatinine and BUN levels, and the degree of proteinuria were made. In parallel to glomerular structural damage, interstitial fibrosis with predominant monocyte/macrophage influx, increased interstitial expression of alpha-SMA and tubular cell proliferation were observed in group SP. A significant increase in serum creatinine and proteinuria were also present in this group. In contrast, the changes observed in group SC were not so evident or extensive as in group SP. The level of proteinuria was lower than that in group SP. No evident tubulointerstitial changes were found in group WK. The results showed that tubulointerstitial injury was prominently progressed in the hypertensive model with Thy-1 nephritis. This suggests that sustained systemic and glomerular hypertension is not only ultimately responsible for the progression of immunologically mediated glomerular injury, but is also responsible for subsequent tubulointerstitial changes. Migration and proliferation of myofibroblasts and intense influx of monocytes/macrophages may contribute to the development of tubulointerstitial fibrosis.
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PMID:Tubulointerstitial injury of Thy-1 nephritis in uninephrectomized stroke-prone spontaneously hypertensive rats. 1150 77

Hypertension development, phenylephrine-induced contraction and Na(+),K(+)-ATPase functional activity and protein expression in aorta (AO), tail (TA) and superior mesenteric (SMA) arteries from ouabain- (25 microg day(-1), s.c., 5 weeks) and vehicle-treated rats were evaluated. Ouabain treatment increased systolic blood pressure (127+/-1 vs 160+/-2 mmHg, n=24, 35; P<0.001) while the maximum response to phenylephrine was reduced (P<0.01) in AO (102.8+/-3.9 vs 67.1+/-10.1% of KCl response, n=12, 9) and SMA (82.5+/-7.5 vs 52.2+/-5.8%, n=12, 9). Endothelium removal potentiated the phenylephrine response to a greater extent in segments from ouabain-treated rats. Thus, differences of area under the concentration-response curves (dAUC) in endothelium-denuded and intact segments for control and ouabain-treated rats were, respectively: AO, 56.6+/-9.6 vs 198.3+/-18.3 (n=9, 7); SMA, 85.5+/-15.4 vs 165.4+/-24.8 (n=6, 6); TA, 13.0+/-6.1 vs 39.5+/-10.4% of the corresponding control AUC (n=6, 6); P<0.05. The relaxation to KCl (1 - 10 mM) was similar in segments from both groups. Compared to controls, the inhibition of 0.1 mM ouabain on KCl relaxation was greater in AO (dAUC: 64.8+/-4.6 vs 84.0+/-5.1%, n=11, 14; P<0.05), similar in SMA (dAUC: 39.1+/-3.9 vs 43.3+/-7.8%, n=6, 7; P>0.05) and smaller in TA (dAUC: 62.1+/-5.5 vs 41.4+/-8.2%, n=12, 13; P<0.05) in ouabain-treated rats. Protein expression of both alpha(1) and alpha(2) isoforms of Na(+),K(+)-ATPase was augmented in AO, unmodified in SMA and reduced in TA from ouabain-treated rats. These results suggest that chronic administration of ouabain induces hypertension and regional vascular alterations, the latter possibly as a consequence of the hypertension.
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PMID:Alterations in phenylephrine-induced contractions and the vascular expression of Na+,K+-ATPase in ouabain-induced hypertension. 1183 25

The aim of the present study was to elucidate how transforming growth factor-beta(1) (TGF-beta(1)) can stimulate collagen deposition in cardiac tissue by interstitial cells via stimulation of fibroblasts, via myofibroblasts, or via differentiation of fibroblasts to myofibroblasts. The dose- and time-dependent stimulation of collagen production and of expression of alpha-smooth muscle actin (alpha-SMA), a marker of myofibroblasts, was studied in cultures of second-passage adult rat cardiac fibroblasts. The TGF-beta(1)-stimulated collagen production is positively correlated (r=0.68, P<0.001) with the appearance of alpha-SMA. Only at high concentrations (40 to 600 pmol/L) and after a long time (24 to 48 hours) of incubation, TGF-beta(1) increases the collagen production and stimulates the differentiation of fibroblasts to myofibroblasts. The maximal stimulation of the collagen production (2-fold, P<0.001) observed after incubation of cultures of fibroblasts with 600 pmol/L TGF-beta(1) for 48 hours is accompanied by a maximal stimulation of alpha-SMA expression (3.5-fold, P<0.001), when cultures consist mainly of myofibroblasts. The stimulation of collagen production cannot be reversed either after additional incubation of TGF-beta(1)-stimulated second-passage cultures for 2 days or in their offspring in the next third passage after incubation for 7 days without TGF-beta(1). The increased collagen production in these third-passage cultures cannot be further stimulated by TGF-beta(1). Our data suggest that TGF-beta(1)-stimulated collagen production in cultures of adult rat cardiac ventricular fibroblasts cannot be explained by a direct stimulation of the collagen production either in fibroblasts or in myofibroblasts. Instead, TGF-beta(1) induces the differentiation of fibroblasts to myofibroblasts, which have a higher activity for collagen production than fibroblasts.
Hypertension 2002 Feb
PMID:Stimulation of collagen production by transforming growth factor-beta1 during differentiation of cardiac fibroblasts to myofibroblasts. 1184 94


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