ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

A workshop to describe and then seek possible causes for the increased stroke mortality in the southeastern United States briefly considered 30 suspected correlates and discussed in more detail the 10 thought to be most likely. Recent age-adjusted stroke mortality rates in adults from industrialized countries reveal marked geographic differences. Age-adjusted statewide stroke mortality rates also differ, and they are higher in the Southeast than elsewhere in the United States. For five southeastern coastal states in the heart of the "Stroke Belt," excess stroke mortality has been present at least since 1930. In a 20-year follow-up of 10 000 veterans, the Stroke Belt had a 25% increase in all-cause mortality and congestive heart failure. A potential cause of increased fatal stroke included hypertension, which was more frequent in the Stroke Belt. No consistent patterns of lifestyle differences or of differences in potassium or calcium intake seemed to explain the higher rates of fatal strokes in the Stroke Belt; however, detailed investigations of smaller populations in localized areas seem warranted. Some data suggest a relationship between socioeconomic status and the Stroke Belt effect. Other differences in the Southeast that could explain, at least partially, the Stroke Belt effect include presence of soft water throughout most of the area, decreased antioxidant intake, and differences in the use of medical care and in the response to antihypertensive drugs. On the basis of available information, the three most likely explanations or partial explanations for the Stroke Belt are increased levels of blood pressure, localized differences in socioeconomic status, and toxic environmental factor(s). Two major recommendations were made: (1) to encourage both patient and caregiver to use all currently available means of decreasing morbidity and mortality by controlling blood pressures at or below normal levels and by reducing other risk factors and (2) to seek precise information about relationships of identified possible causes of increased morbidity and mortality in the Stroke Belt. (Hypertension. 1998;31:1206-1215.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

We asked whether the altered cerebral vasculature associated with essential hypertension might dampen or redirect the regional cerebral blood flow (rCBF) response to cognitive work. Relative rCBF was assessed with [(15) O]water positron emission tomography during a working memory task, a memory span task, and two perceptual control tasks. Unmedicated hypertensive patients and control subjects differed in rCBF response during both memory tasks. Hypertensives showed relatively diminished rCBF responses in right hemisphere areas combined with compensatory activation of homologous areas in the left cerebral cortex. Essential hypertension appears to selectively influence the circulatory reserve of portions of cerebral cortex and secondarily induce recruitment of other cortical areas to process certain tasks. (Hypertension. 1998;31:1216-1222.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Hypertension as a risk factor for intracerebral hemorrhage (ICH) is poorly quantified, particularly in the setting of the use of modern antihypertensive agents. To investigate this, we studied 331 consecutive hospital cases of primary ICH verified by computed tomography or autopsy, occurring during the period 1990 through 1992, and 331 age- and sex-matched community-based control subjects in a city-wide study involving 13 hospitals. Hypertension approximately doubled the risk of ICH (adjusted odds ratio [OR], 2.45; 95% confidence interval [CI], 1.61 to 3.73). The OR associated with hypertension was significantly greater among those who had ceased taking medications, supervised and unsupervised (OR, 4.98; 95% CI, 2.25 to 11.02), compared with those who had not (OR, 1.95; 95% CI, 1.20 to 3.16), were under the age of 55 years (OR, 7.68; 95% CI, 2.65 to 22.5), or were current smokers (OR, 6.12; 95% CI, 2.29 to 16.35). The presence of hypertension did not influence size or location of the hemorrhage. However, those dying from ICH displayed a greater risk of ICH due to hypertension than survivors, with the ratio of the two ORs being 5.47 (95% CI, 1.23 to 24.44). These findings provide evidence for a greater increase in risk of ICH due to hypertension among younger persons, current smokers, and those discontinuing antihypertensive therapy. This is the first direct evidence for a link between stopping antihypertensive medication use and stroke risk; targeting these individuals for more intensive monitoring and education on the importance of risk factor modification may help to reduce the impact of this form of stroke. (Hypertension. 1998;31:1223-1229.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

or=to85th percentile for the US population. Using BMI rather than hypertension as a quantitative trait, we found significant linkage for the marker D7S504 (P=0.029) but not for the other markers. Significance strengthened in the overweight subset of sibships for this marker (P=0.001), and there was a trend of lower P values for the other three markers. However, multipoint analysis with the use of all four markers simultaneously to estimate linkage between BMI and the leptin locus did not demonstrate a statistically significant relationship. Analysis of the coding region of the leptin gene (exons 2 and 3) by single-strand conformational polymorphism revealed a rare Ile-Val polymorphism at amino acid 45 but revealed no other alterations. These results suggest that the OB gene is not a major contributor to the phenotype of essential hypertension in African Americans, although a minor contribution to the phenotype of extreme obesity in this group cannot be ruled out. (Hypertension. 1998;31:1230-1234.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

An abnormal hemodynamic response to stressful stimuli has been proposed as a mechanism involved in the higher prevalence of hypertension in blacks. Given the important role of nitric oxide (NO) in the regulation of cardiovascular homeostasis, we investigated the possibility of racial differences in vascular NO activity during mental stress. To test this hypothesis, we compared the forearm blood flow (FBF) response to mental stress in 14 white and 12 black healthy subjects during intra-arterial infusion of either saline or NO synthesis inhibitor NG-monomethyl-L-arginine(L-NMMA; 4 [micro sign]mol/min). We also examined vascular responses of the two groups to intra-arterial infusion of sodium nitroprusside (0.8 to 3.2 [micro sign]g/min), an exogenous NO donor. During saline infusion, the increase in FBF from baseline induced by mental stress was significantly higher in whites than in blacks (109 +/- 20% versus 58 +/- 8%; P=0.03). L-NMMA significantly reduced stress-induced increase in FBF in whites (from 109 +/- 20% to 54 +/- 11%; P=0.004) but not in blacks (from 58 +/- 8% to 42 +/- 10%; P=0.24); thus, the vasodilator effect of stress testing during L-NMMA was similar in whites and blacks (54 +/- 11% versus 42 +/- 10%; P=0.44). The vasodilator response to sodium nitroprusside was also lower in blacks than in whites (maximum flow, 6.9 +/- 2 versus 11.6 +/- 3.5 mL [center dot] min-1[center dot] dL-1; P=0.001) and was not significantly modified by L-NMMA in either group. Our findings indicate that blacks have a reduced NO-dependent vasodilator activity during mental stress. This difference seems related to reduced sensitivity of smooth muscle to the vasodilator effect of NO and may play some role in the increased prevalence of hypertension and its complications in blacks. (Hypertension. 1998;31:1235-1239.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The peptide hormone relaxin (RLX) has been shown to elicit a powerful vasodilatory response in several target organs. This response is mediated by the stimulation of intrinsic nitric oxide (NO) generation. The present study was designed to clarify whether RLX directly promotes the relaxation of vascular smooth muscle cells through stimulation of NO generation. Vascular smooth muscle cells from bovine aortas were incubated with RLX at concentrations ranging from 1 nmol/L to 1 [micro sign]mol/L. The expression and activity of NO synthase, production of NO, and the intracellular levels of cGMP and Ca2+were determined. The cell morphology and signal transduction mechanisms of these bovine aortic smooth muscle cells in response to RLX were also studied. RLX stimulated the ecpression of immunoreactive inducible NO synthase and increased significantly and in a concentration-related fashion inducible NO synthase activity, NO generation, and intracellular cGMP levels. Concurrently, RLX simnificantly decreased cytosolic Ca2+concentrations and caused changes in cell shape and the actin cytoskeleton that were consistent with cell relaxation. The signal transduction mechanisms leading to the enhanced expression of inducible NO synthase protein and activity caused by RLX involve the activation of tyrosine kinase, phosphatidylcholine-phospholipase C, and the transcription factor nuclear factor-kappa B, similar to bacterial endotoxins and proinflammatory cytokines. This study suggests that RLX is an endogenous agent capable of regulating vascular tone by activation of the L-argining-NO pathway in vascular smooth muscle cells. (Hypertension. 1998;31:1240-1247.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The available data on the role of the L-arginine/nitric oxide (NO) pathway in the genesis of hypertension in spontaneously hypertensive rats (SHR) are limited and contradictory. In an attempt to address this issue, male SHR were studied during the early phase of evolution of hypertension (age 8 to 12 weeks) to distinguish the primary changes of NO metabolism from those caused by advanced hypertension, vasculopathy, and aging late in the course of the disease. A group of age-matched male Wistar-Kyoto rats (WKY) served as controls. The SHR exhibited a marked rise in arterial blood pressure and a significant increase in urinary excretion and plasma concentration of NO metabolites (nitrite/nitrate [NOx]). Likewise, the SHR showed a significant elevation of thoracic aorta NO synthase (NOS) activity coupled with significant increases of kidney, aorta, inducible NOS (iNOS), and endothelial NOS (eNOS) proteins. In an attempt to determine whether the enhanced L-arginine/NO pathway is a consequence of hypertension, studies were repeated using 3-week-old animals before the onset of hypertension. The study revealed significant increases in urinary NOx excretion as well as vascular eNOS and renal iNOS proteins. In conclusion, the L-arginine/NO pathway is upregulated in young SHR both before and after the onset of hypertension. Thus, development of hypertension is not due to a primary impairment of NO production in SHR. On the contrary, NO production is increased in young SHR both before and after the onset of hypertension. (Hypertension. 1998;31:1248-1254.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The present study was conducted to determine the contribution of nitric oxide to angiotensin II (Ang II) reactivity of afferent and efferent arterioles from Ang II-infused hypertensive rats. Experiments were performed in vitro with the blood-perfused juxtamedullary nephron technique in kidneys harvested from hypertensive Sprague-Dawley rats (181 +/- 1 mm Hg) that had received 60 ng/min Ang II subcutaneously for 13 days. Superfusion with 0.1, 1, and 10 nmol/L Ang II reduced afferent arteriolar diameter (18.1 +/- 0.6 [micro sign]m; n=12) by 10.0 +/- 0.7%, 28.1 +/- 1.7%, and 52.8 +/- 1.9%, respectively, and efferent arteriolar diameter (17.2 +/- 1.4 [micro sign]m; n=8) decreased by 9.3 +/- 0.7%, 27.0 +/- 1.2%, and 50.4 +/- 1.6%, respectively. Nitric oxide synthase inhibition with 100 [micro sign]mol/L Nomega-nitro-L-arginine(NLA) reduced resting afferent and efferent arteriolar diameters to 14.7 +/- 0.4 and 14.3 +/- 1.2 [micro sign]m, respectively, and enhanced afferent but not efferent arteriolar reactivity to Ang II. The enhanced afferent arteriolar reactivity to Ang II was eliminated by addition of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP, 10 [micro sign]mol/L), which reversed the NLA-induced decrease in diameter. Addition of 10 [micro sign]mol/L SNAP, without NLA, blunted efferent but not afferent arteriolar reactivity to Ang II. Afferent (n=7) and efferent arteriolar diameters (n=6) decreased by 48.5 +/- 2.2% and 41.0 +/- 1.9%, respectively, in response to 10 nmol/L Ang II. These results suggest that in this model of hypertension, maintained nitric oxide production in afferent arterioles counteracts the enhanced afferent arteriolar reactivity that occurs in Ang II-induced hypertension. (Hypertension. 1998;31:1255-1260.)

ISSN:0194-911X    

出版商:OVID    

年代:1998

数据来源: OVID