ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The fifth Joint National Committee report on the detection, evaluation, and treatment of high blood pressure (JNC-V) introduced a new system of blood pressure classification that incorporated systolic blood pressure (SBP) and established new diastolic blood pressure (DBP) cut points. With the previous JNC classification, subjects were classified according to DBP alone. In this study, our purpose was to assess the effect of the new staging system on the assessment of hypertension severity and to determine whether the new JNC-V staging system better identifies individuals at risk for hypertensive target-organ damage. We compared the assessment of hypertension severity using JNC-IV with that using JNC-V in 1158 subjects enrolled in the Harlem Hospital Hypertension Clinic database from 1975 to 1992. We used pretreatment DBP to classify subjects according to JNC-IV criteria. These subjects were reclassified into one of the four stages of JNC-V. The assessment of hypertension severity and prevalence of organ damage in subjects who remained in the same category of severity in both systems was compared with damage in subjects who were upstaged. With the JNC-V classification, 321 subjects remained in the same category, and 837 were upstaged. Six hundred and four subjects moved up because of the new cut points of DBP, and 275 were upstaged because of higher SBP. Upstaged subjects had more manifestations of hypertensive target-organ damage. With the new JNC-V classification system, hypertension is assessed as severe or very severe in more individuals than with JNC-IV. Subjects who are upstaged in JNC-V are more likely to have evidence of renal disease and other target-organ damage. (Hypertension. 1996;28:713-718.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Classification schemes for hypertension are necessary. They provide us with definitions for when hypertension begins and help us to assess risk, determine prognosis, and guide management. Systems in current use rely on either the level of blood pressure (diastolic, systolic, or both) and classify patients based on the level of relative risk (the proportional likelihood of cardiovascular events occurring as blood pressure rises), absolute risk (the actual odds that a patient or a population will develop an event), or both. Absolute risk reflects the sum of all the factors that contribute to the likelihood that a patient will experience cardiovascular disease. The system we propose stages hypertensive individuals on the basis of blood pressure level (as does the Fifth Joint National Committee report on the detection, evaluation, and treatment of high blood pressure [JNC-V] and the World Health Organization/International Society of Hypertension guidelines) but uses different levels for each stage than do the previous systems and then modifies the numerical stage with the subscript "c" for complicated (when target-organ damage and/or other cardiovascular risk factors are present) or "u" for uncomplicated (when they are absent). The data obtained from a complete medical history and physical examination and a few inexpensive laboratory tests provide the information a provider needs to classify an individual as being complicated or uncomplicated. This system also provides a guide to treatment, as drug therapy would be used sooner in individuals with complicated hypertension, and we propose that compensation for providers be higher when they are caring for a patient with complicated rather than uncomplicated hypertension. (Hypertension. 1996;28:719-724.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

We compared mean intra-arterial ambulatory blood pressure (IAMB), blood pressure (BP) diurnal profiles and variability, and postural measurements with casual sphygmomanometric measurements for the prediction of future BP. We studied 97 healthy, unmedicated men classified as normotensive (NT, n = 34), borderline hypertensive (BHT, n = 29), or mildly hypertensive (HT, n = 34) by repeated casual measurements during the 2 months before IAMB. Five years later, we reassessed 79 subjects (81%) using casual BP measurements and noninvasive ambulatory 24-hour BP monitoring (NAMB). IAMB level generally correlated well with follow-up BP and slightly better with NAMB level than with casual measurements (24-hour IAMB versus follow-up NAMB systolic BP [SBP], r = .64, P < .001; versus diastolic BP [DBP], r = .52, P < .001). NT and BHT subgroup correlations were of similar strength, but the relationship in the HT subgroup was not significant. Similarly, when we examined daytime and nighttime BP levels, nighttime BP correlated better with follow-up BP in NT and BHT but not in HT. The only measures that were significantly related to follow-up BP in HT were two BP variability measures, SD and the range of variability (RV80: 90th minus 10th percentile) (initial 24-hour IAMB SD and follow-up BP, r = .42 to r = .52, P < .05 to P < .01; RV80versus follow-up BP, r = .43 to r = .52, P < .05 to P < .01). Correlations of follow-up BP with postural BP were generally weaker than with casual BP or IAMB level. Linear stepwise regressions for SBP and DBP separately (including all IAMB variables) demonstrated that the best single predictor for follow-up BP was 24-hour IAMB SBP level, which explained 41% of follow-up NAMB SBP level variance (F = 52.6, P < .001). However, in a second analysis including casual values, casual SBP alone explained 44% of follow-up NAMB SBP variance (F = 62.5, P < .001), whereas IAMB SBP added only 4% (F = 5.5, P < .05). Predictions of follow-up DBP were always poorer. After 5 years, 70% of NT and 86% of HT were still in their initial classification group, but 67% of BHT had become hypertensive. In these new HT (n = 16), initial IAMB level correlated most strongly with follow-up NAMB level (24-hour SBP, r = .70, P < .01; 24-hour DBP, r = .55, P < .05). The only other significant demographic variable predicting future BP was change in weight over 5 years, which added 10% to the explanation of future casual SBP variance (F = 12.5, P = .0007) and 15% to casual DBP variance (F = 18.0, P = .0001); for NAMB, the percentages were lower. In logistic regression, those NT and BHT who became hypertensive (n = 22) had a 75% probability of becoming hypertensive if they gained 11.7 kg or more during 5 years (chi squared = 4.5, P = .03). To conclude, BP tended to increase in all groups, especially in BHT, during follow-up. Nominal differences were observed between casual measurements and BP level measures in the prediction of future BP, and their explanatory value for future BP was generally less than 50%. However, for BHT who became hypertensive, BP level and variability measurements somewhat improved the prediction of follow-up BP. Weight gain was an important additional predictor for future hypertension in both NT and BHT. (Hypertension. 1996;28:725-731.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The endothelium plays an important role in the circulation by modulating contractile responses of vascular smooth muscle. We designed this study to investigate the alterations of endothelial modulation in hypertension. Rings of femoral arteries were prepared from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), and changes in isometric tension were recorded. In rings with endothelium, norepinephrine (in either the presence or absence of yohimbine) evoked concentration-dependent contractions. Endothelium removal markedly enhanced the contraction; both the maximal response and sensitivity were increased, and these responses were less pronounced in SHR than WKY. In contrast to norepinephrine-induced contractions, the enhancement of prostaglandin F2alpha-or serotonin-induced contractions after endothelium removal was small and comparable in WKY and SHR; sensitivity was increased, but the maximal response was not. N (omega) -Nitro-L-arginine methyl ester enhanced the contractions induced by these agonists in arteries with but not without endothelium and thereby abolished the enhancement of the contractions after endothelium removal. Thus, the endothelium plays an inhibitory role against contractions in rat femoral arteries by releasing nitric oxide, but the characteristics of the endothelial inhibition are not identical against various types of contractions. The negative endothelial modulation is more pronounced during alpha1-adrenoceptor-mediated contractions than during contractions mediated by other receptors. The inhibitory role of the endothelium against alpha1-adrenoceptor agonist-induced but not serotonin- or prostaglandin F2alpha-induced contraction is impaired in hypertension. (Hypertension. 1996;28:732-737.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

We evaluated pressure-dependent stimulation of renin release in rats with sustained hypertension induced by chronic blockade of nitric oxide synthase with Nomega.05), in the hypertensive and normal control groups, respectively. Overall, these findings are consistent with the hypothesis that prolonged L-NAME administration attenuates pressure-dependent renin release by inhibiting nitric oxide formation, which may function as a paracrine mechanism inversely linking renal perfusion pressure with the stimulation of renin release. (Hypertension. 1996;28:738-742.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Alterations in nitric oxide signaling have been hypothesized to have an etiologic role in the development of hypoxic pulmonary hypertension. However, changes in the expression of nitric oxide synthase (NOS) in hypoxic lungs remains controversial. In this study, we used (1) Northern and Western analyses to measure NOS mRNA and protein expressions, (2) lung histology together with measurements of lung and heart weights to monitor pulmonary vascular remodeling, and (3) immunohistochemistry to localize NOS proteins. The data demonstrated that endothelial NOS mRNA and protein were upregulated over 1 to 7 days of hypoxia that temporally correlated with and preceded the vascular remodeling that occurred in the course of the development of hypoxic pulmonary hypertension. Hypoxia also induced brain NOS in bronchial epithelium and inducible NOS in vascular smooth muscle but did not affect inducible NOS expression in macrophages or basal guanylyl cyclase activity in the lung. These findings showed that upregulation of endothelial NOS was tightly correlated with the vascular remodeling induced by hypoxia, suggesting a role for nitric oxide in the development of pulmonary hypertension. (Hypertension. 1996;28:743-753.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

We examined accumulating evidence of the positive contribution of nitric oxide to the pharmacological effects of converting enzyme inhibitors in 36 rats rendered hypertensive, hyperinsulinemic, and hypertriglyceridemic by a fructose-enriched diet. We studied the response of blood pressure, insulin, and triglyceride levels to inhibition of either converting enzymekininase II, nitric oxide synthase, or both. Two weeks of the converting enzyme inhibitor enalapril (20 mg/kg) reduced blood pressure from 137 +/- 2 to 105 +/- 7 mm Hg, insulin from 7.6 +/- 2.0 to 2.2 +/- 1.1 pg/mL, and triglycerides from 292 +/- 37 to 163 +/- 37 mg/dL. Treatment with NG-nitro-L-arginine methyl ester (100 mg/kg) raised blood pressure from 144 +/- 7 to 170 +/- 8 mm Hg without affecting the other parameters. Two weeks of concomitant treatment with both agents blunted the hypotensive and beneficial metabolic effects of enalapril; thus, final blood pressure (141 +/- 7 mm Hg), insulin (6.4 +/- 2.4 pg/mL), and triglyceride (231 +/- 51 mg/dL) values were no different from those of untreated fructose-fed rats. These data suggest that persistent synthesis of nitric oxide contributes to the vasodilator and metabolic effects of enalapril in the fructose-fed rat model. (Hypertension. 1996;28:754-757.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The pathogenesis of preeclampsia is proposed to be due to uncharacterized circulating factors that activate endothelial cells. Support for this hypothesis is provided by in vitro activation of endothelial cells by plasma from preeclamptic women, eg, increased nitric oxide and prostacyclin generation. We performed molecular sizing, lipid extraction, and lipoprotein fractionation of plasma from normal pregnant and preeclamptic women and determined the ability of these plasma fractions to increase nitric oxide or prostacyclin generation by endothelial cells. Fractions from plasma of preeclamptic women were consistently more active than fractions from normal pregnant women, although characterization was qualitatively similar. The factors stimulating nitric oxide and prostacyclin were different. The factor (or factors) stimulating nitric oxide generation was extractable by charcoal and present in lipid extracts and lipoprotein isolates with a molecular weight greater that 1.5 million daltons, which is characteristic of a lipoprotein or lipoprotein aggregate. By contrast, activity to stimulate prostacyclin persisted after charcoal stripping or lipoprotein removal, partitioned to the aqueous fraction, and had a molecular weight of approximately 50 000 D. Two distinct factors in the blood of preeclamptic women alter endothelial function in vitro. This information should guide the search for circulating factors contributing to the pathophysiology of preeclampsia. (Hypertension. 1996;28:758-764.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

In this study we determined whether cAMP is metabolized to adenosine in vascular smooth muscle cells and whether cAMP-derived adenosine modulates vascular smooth muscle cell growth. Confluent smooth muscle cells were exposed to cAMP (0.01 to 30 micro mol/L) in the presence and absence of 3-isobutyl-1-methylxanthine (IBMX, 1 mmol/L; an inhibitor of both extracellular and intracellular phosphodiesterase), alpha, beta-methyleneadenosine 5'-diphosphate (AMP-CP, 100 micro mol/L; an ecto-5'-nucleotidase inhibitor), and 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX, 100 micro mol/L; a xanthine that can inhibit extracellular phosphodiesterase) for 0 to 60 minutes. Medium was then sampled and assayed for AMP, adenosine, and inosine. cAMP increased the amount of AMP, adenosine, and inosine in the medium in a time- and concentration-dependent manner. The conversion of cAMP to adenosine and inosine was inhibited by blockade of phosphodiesterase with IBMX, of ecto-phosphodiesterase with DPSPX, and of ecto-5'-nucleotidase with AMP-CP. To evaluate the physiological relevance of cAMP-derived adenosine in vascular smooth muscle cell proliferation, we studied the inhibitory effects of cAMP (10-4mol/L) and 8-bromo-cAMP (10-4mol/L) on fetal calf serum-induced DNA synthesis ([(3) Hydrogen]thymidine incorporation) in the presence and absence of erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA, an inhibitor of adenosine deaminase), dipyridamole (a blocker of adenosine transport), KF17837 (a selective A2adenosine receptor antagonist), and DPSPX (a nonselective adenosine receptor antagonist). cAMP inhibited DNA synthesis, and both EHNA and dipyridamole enhanced this effect. Both KF17837 and DPSPX significantly reduced the inhibitory effects of cAMP on DNA synthesis; however, they did not reduce the inhibitory effects of 8-bromo-cAMP on DNA synthesis. These results indicate that vascular smooth muscle cells metabolize cAMP to adenosine via the sequential action of ecto-phosphodiesterase and ecto-5'-nucleotidase and provide the first evidence that cAMP-derived adenosine can inhibit vascular smooth muscle cell growth. Hence, this cAMP-adenosine pathway may importantly contribute to the regulation of vascular biology. (Hypertension. 1996;28:765-771.)

ISSN:0194-911X    

出版商:OVID    

年代:1996

数据来源: OVID