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PubMed1994

Termination of endothelin signaling: role of nitric oxide.

Cellular mechanisms responsible for the termination of ET-1 signal are poorly understood. In order to examine the hypothesis that nitric oxide serves as a physiological brake of ET-1 signaling, Chinese hamster ovary (CHO) cells stably transfected with the ETA receptor cDNA (CHO-ET) were studied. CHO-ET responded to ET-1 with robust [Ca2+]i transients and developed a long-lasting homologous desensitization. Donors of nitric oxide (NO), 3-morpholino-sydnonimine HCl (SIN-1), or sodium nitroprusside (SNP) reduced the amplitude of these responses, accelerated the rate of [Ca2+]i recovery, and counteracted the development of homologous desensitization by a cyclic GMP-independent mechanism, suggesting an alternative mode for NO modulation of ET-1 responses. Stimulation of CHO-ET cells with mastoparan, a wasp venom acting directly on G proteins (bypassing receptor activation), was inhibited by NO, revealing a postreceptoral target for NO-induced modulation of [Ca2+]i mobilization. Using a lys9-biotinylated ET-1 (ET-1 [BtK9]), binding sites were "mapped" in CHO-ET cells. Receptor-ligand complexes did not exhibit spontaneous dissociation during 60-min observations. Quantitative fluorescence microscopy revealed that SNP or SIN-1 caused a rapid, concentration-dependent, and reversible dissociation of biotinylated ET-1 from ETA receptor (EC50 = 75 microM and 6 microM, respectively), an effect that was not mimicked by 8-bromo-cyclic GMP. "Sandwich" co-culture of endothelial cells with CHO-ET showed that activation of NO production by endothelial cells similarly resulted in dissociation of ET-1 [BtK9] from ETA receptors. We hypothesize that NO plays a role in physiological termination of ET-1 signalling by dual mechanisms: (1) displacement of bound ET-1 from its receptor, thus preventing homologous desensitization, and (2) interference with the postreceptoral pathway for [Ca2+]i mobilization, hence inhibiting end-responses to ET-1.

Animals↗
PubMed2001

Nitric oxide inhibits norepinephrine stimulated contraction of human internal thoracic artery and rat aorta.

The effect of nitric oxide (NO) on norepinephrine-induced vascular contraction was evaluated using segments of rat aorta and human internal thoracic artery (ITA) and the NO donor, SNAP. NO levels were measured directly using an amperometric probe. Concentrations of NO greater than 2 nM were required to reduce vascular contraction induced by 100 nM norepinephrine (NE). Exposure of the aortic rings to SNAP prior to, or after NE addition, resulted in a similar attenuation of NE-induced contraction. In contrast, increased relaxation of ITA segments in response to SNAP was observed relative to that of rat aorta and significant development of contractile tone following NE addition was not observed. Evaluation of cytoskeletal actin demonstrated marked loss of F-actin content in smooth muscle cells following NO exposure, suggesting that NO may have direct and indirect effects on contractile tone. These data taken together suggest that vascular responsiveness to contractile agents may be significantly attenuated by prior or subsequent exposure to NO, and mechanisms in addition to vascular relaxation are likely to contribute to this effect.

Animals↗
PubMed2003

The contribution of hip fracture to risk of subsequent fractures: data from two longitudinal studies.

BACKGROUND: The contribution of hip fracture to the risk of subsequent fractures is unclear. METHODS: Data from the Baltimore Hip Studies and the Established Populations for Epidemiologic Studies of the Elderly (EPESE) were used. Baltimore subjects enrolled at the time of hip fracture ( n=549) and EPESE subjects without previous fractures at baseline ( n=10,680) were followed for 2-10 years. Self-reported nonhip skeletal fracture was the outcome, and hip fracture was a time-varying covariate in a survival analysis stratified by study site. The model was adjusted for race, sex, age, BMI, stroke, cancer, difficulty walking across a room, dependence in grooming, dependence in transferring, and cognitive impairment. RESULTS: The rate of all subsequent self-reported fractures after hip fracture was 10.4 fractures/100 person-years. The unadjusted hazard of nonhip skeletal fracture was 2.52 (95% confidence interval 2.05 to 3.12) for subjects with hip fracture compared with subjects without; when adjusted for other known fracture risk factors the hazard ratio was 1.62 (1.30 to 2.02). Men and women had a similar relative risk increase. The increased risk of secondary fracture after hip fracture persisted over time. CONCLUSIONS: A hip fracture is associated with a 2.5-fold increased risk of subsequent fracture, which is not entirely explained by prefracture risk factors. Careful attention to secondary prevention is warranted in these patients.

Aged↗
PubMed2003

Predictors of bone loss after hip fracture.

Although accelerated bone mineral density (BMD) loss follows hip fracture, little is known about factors associated with this loss. We examined potential predictors of BMD loss in a cohort of community-dwelling women who had sustained hip fracture and who were followed for 1 year after fracture. BMD was measured at the femoral neck, intertrochanteric region, and total body, during hospitalization and 2, 6, and 12 months later. Demographic, health, lifestyle, clinical, surgical, and functional characteristics at baseline, and postfracture activity were evaluated for associations with baseline BMD and BMD 1 year later. To examine possible BMD-dependent effects, high and low baseline BMD groups were defined. None of the studied factors consistently predicted either baseline BMD or BMD at 1 year after fracture, among women with either high or low baseline BMD. Baseline BMD was the only factor that substantially and consistently predicted change, explaining 70% to 90% of variation. These results suggest that BMD will not be preserved by general rehabilitative measures and that prompt, specific intervention to minimize bone loss after hip fracture is an essential element of clinical management of the hip fracture patient.

Absorptiometry, Photon↗
PubMed2006

Women with hip fracture have a greater rate of decline in bone mineral density than expected: another significant consequence of a common geriatric problem.

INTRODUCTION: Hip fracture is a major public health problem, annually affecting over 350,000 persons in the United States and 1.6 million worldwide. Consequences include decreased survival, loss of independence, and increased risk of subsequent fractures. A substantial decline in bone mineral density (BMD) also occurs, yet the magnitude of the decline specifically attributable to hip fracture has not been documented. METHODS: To determine the amount of BMD decline attributable to hip fracture, the rate of decline in BMD in a cohort of hip fracture patients was compared with that in a cohort of women of similar age and BMD but without hip fracture. All subjects were community dwelling when enrolled. Hip fracture patients in the Baltimore Hip Studies (BHS) came from two hospitals in Baltimore, Maryland, from 1992 through 1995; comparison subjects came from the Study of Osteoporotic Fracture (SOF) enrolled in four areas of the United States during the same period. Eighty-four white, female hip fracture patients 65 years and older from the BHS were compared with 168 SOF participants matched on age, race, and BMD at baseline. BMD of the femoral neck and total hip was measured by dual-energy x-ray absorptiometry. RESULTS: Hip fracture patients had a greater decline in BMD during the 12-month postfracture follow-up than that expected on the basis of the nonfracture cohort: 4.9% vs. 0.4% at the femoral neck and 3.5% vs. 0.7% for the total hip. The decline in BMD in hip fracture patients was 11.8 times the amount expected at the femoral neck (matched on age and baseline BMD and adjusted for between-cohort differences in smoking prevalence) and 4.9 times that expected for the total hip at the end of 1 year after the hip fracture. CONCLUSION: In this sample of older women, bone loss over the year following hip fracture far exceeded that expected and is an important clinical management concern.

Activities of Daily Living↗
PubMed2000

Loss of bone density and lean body mass after hip fracture.

Few studies of bone loss have assessed the amount of loss directly after a hip fracture. The present prospective study was conducted to determine changes in bone mineral density (BMD) and muscle mass shortly after fracture and through 1 year to assess short-term loss and related factors. The setting was two acute care teaching hospitals in Baltimore, Maryland, and subjects were 205 community-dwelling women with a new fracture of the proximal femur between 1992 and 1995. Bone density of the nonfractured hip and whole-body and body composition were measured by dual-energy X-ray absorptiometry at 3 and 10 days and 2, 6 and 12 months after admission. Mean BMD of the femoral neck was 0.546 +/- 0.007 g/cm(2) at baseline. Average loss of femoral neck BMD from baseline was 2.1% at 2 months, 2.5% at 6 months and 4.6% at 12 months. The average loss of BMD in the intertrochanteric region was 2.1% at 12 months. Total lean body mass decreased by 6% while fat mass increased by 3. 6% by 1 year after the fracture. These findings indicate that significant loss in BMD and lean body mass occur shortly after hip fracture while body fat increases. Continued loss was evident throughout the 1 year of follow-up. This loss of both bone density and muscle mass may lead to new fractures.

Absorptiometry, Photon↗
PubMed1999

The prevalence of osteoporosis in nursing home residents.

This study describes the prevalence of osteoporosis in a statewide sample of nursing home residents. Composite forearm bone mineral density (BMD) (including the distal radius and the distal ulna) of 1475 residents aged 65 years and older from 34 randomly selected, stratified nursing homes was assessed. BMD was expressed with reference to World Health Organization diagnostic criteria. Trends with age, gender and race were consistent with other populations. However, prevalence estimates were higher than community-based age-specific rates. The prevalence of osteoporosis for white female residents increased from 63.5% for women aged 65-74 years to 85.8% for women over 85 years of age. Only 3% had composite forearm BMD within 1 standard deviation of the young adult mean. The significance of the high prevalence of low BMD in nursing home residents is the increased fracture risk it may confer. In community cohorts of white women, the risk of hip fracture increases approximately 50% for every 1 standard deviation decrease in bone mass. However, the degree to which BMD contributes to fracture risk in this population has not been well established.

Black or African American↗
PubMed2003

Hip fracture: risk factors and outcomes.

Hip fracture is an important public health and personal burden, and this burden is anticipated to increase over the next several decades. Although white women experience the greatest lifetime risk of hip fracture, risk extends to men and to nonwhite populations. Bone strength, risk of falling, and individual clinical characteristics combine to affect the risk of hip fracture. Nearly $9 billion were expended in 1995 in the United States for the management of hip fractures. Hip fracture has important sequelae, including loss of bone and muscle mass. Mortality is significantly increased after hip fracture, and functional recovery is limited to less than 50% of those who fracture. About 25% of patients reside in long-term care facilities for a year or more after fracture, and the impact of hip fracture on health-related quality of life is considerable and long lasting.

Accidental Falls↗
PubMed2006

Post-operative considerations in hip fracture management.

Hip fractures are among the most important causes for disability, reduced quality of life, and death in older persons. Hip fracture patients are typically characterized by older age and a large complexity in their underlying conditions, comorbidities, and clinical histories. Therefore, large, well-designed studies are difficult to perform and the available evidence for most treatments is limited compared with other disease entities of this magnitude. This paper illuminates the current issues and recommendations for post-operative hip fracture care. Efforts to improve osteoporosis assessment and management, the multidisciplinary team approach, and clinical pathways are areas that have received attention recently.

Accidental Falls↗
PubMed1991

Evaluation of endothelin receptor populations using endothelin-1 biotinylated at lysine-9 sidechain.

Optimal conditions for biotinylation of endothelin-1 (Et-1) were determined using biotinylating reagents of variable linker arm length and mono- vs dual-biotinylated Et-1. Specific modification of lysine-9 sidechain with NHS-LC-biotin (Et-1[BtK9]) produced a derivative with maximal binding and retention of vascular smooth muscle contractile activity. The Et-1[BtK9] probe bound to Chinese hamster ovary cells transfected with EtA receptor cDNA (CHO[EtR]), but not untransfected cells. Binding to rat vascular smooth muscle cells (VSMC) was detectable at 0.01 nM with maximal binding at 1 nM. Displacement of 1 nM Et-1 [BtK9] binding by Et-1 indicated an IC50 value of 6 +/- 3 nM. Et-1 displaced Et-1[BtK9] binding to VSMC and CHO[EtR] to a greater extent than endothelin-3, indicating predominant expression of EtA receptor sub-type. Thus, biotinylation of Et-1 at the lysine-9 sidechain may be of general use for localization and typing of Et-receptor populations.

Animals↗
PubMed1996

Morphine stimulates nitric oxide release from invertebrate microglia.

Morphine stimulates nitric oxide (NO) release in human endothelial cells. To determine whether this mechanism also occurs in invertebrates, the mussel Mytilus edulis was studied. Exposure of excised ganglia to morphine for 24 h resulted in a significant dose-dependent decrease in microglial egress that was naloxone sensitive. In coincubating the excised ganglia with morphine and the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), an increase in microglial egress was observed, suggesting that morphine may stimulate microglia to release NO. Morphine exposure to these cells in vitro resulted in NO release (39.4 +/- 4.9 nM), a phenomenon found to be naloxone sensitive (10(-6) M; NO level = 5.9 +/- 2.6 nM) and L-NAME sensitive (10(-4) M; NO level = 2.8 +/- 1.8 nM). Opioid peptides did not stimulate NO release, indicating that the process was mediated by the opiate alkaloid selective mu 3 receptor. Coincubation of microglia with L-arginine or the superoxide scavenger, superoxide dismutase, resulted in significantly higher NO levels observed following morphine stimulation. Taken together, the data demonstrate that morphine can stimulate NO release in cells obtained from an invertebrate that represents an animal 500 million years divergent in evolution from man, underscoring the significance of this process and further substantiating the critical importance of morphine as a naturally occurring signal molecule.

Animals↗
PubMed1993

Endothelin-receptor interactions. Role of a putative sulfhydryl on the endothelin receptor.

The mechanism of action of endothelin-receptor interactions was studied, using radioligand binding assays and SDS-PAGE, to investigate the possibility of disulfide interchange. Electrophoretic analysis suggested involvement of disulfide bond(s) in the receptor-ligand complex. Treatment of Et receptors with sulfhydryl-specific alkylating reagents (NEM or others) resulted in decreased ability to bind [125I]Et-1. [Dpr1-Asp15]Et-1, an antagonist homologous to Et but with an amide link replacing one of the disulfides, bound to Et receptors reversibly, but binding of Et-1 was less reversible. Preincubation of receptors with Et-1, but not with [Dpr1-Asp15]Et-1, protected receptors from alkylation with [14C]NEM. The data suggest that the Et receptor has a sulfhydryl group at or near the Et binding site. A model is proposed in which the role of the putative sulfhydryl group is discussed.

Animals↗
PubMed1996

Protease activated receptors modulate aortic vascular tone.

The effect of agonists of the known protease activated receptors (PAR), the thrombin and the PAR-2 receptors, on vasoactive mediator release and vascular tone were studied using rings of rat aorta. Stimulation of aortic rings with the thrombin receptor agonist, Trap-14, or the PAR-2 agonist, SLIGRL, resulted in a rapid release of nitric oxide. Trap-14 and SLIGRL-induced nitric oxide release was reduced by pre-treatment with BQ-788, an ETB endothelin receptor-specific antagonist. Consistent with a role for endothelin-1 receptor activation in Trap-14 and SLIGRL-induced nitric oxide release, endothelin-1 levels were increased significantly following 5 min treatment of aortic rings with Trap-14 or SLIGRL. Cumulative addition of Trap-14 to aortic rings denuded of endothelium resulted in dose-dependent contraction with an EC50 value of 23 +/- 5 microM, whereas SLIGRL addition failed to induce aortic contraction. These data suggest that the known protease activated receptors are functionally coupled to nitric oxide release. In addition, the thrombin receptor appears to modulate both vasodilator and contractile responses, whereas the PAR-2 receptor is linked only to vasodilation.

Animals↗
PubMed1988

Patient-proxy response comparability on measures of patient health and functional status.

The present study evaluates the response comparability between 361 elderly hip fracture patients admitted from the community to seven Baltimore area hospitals between 1984 and 1986 and interviewer selected proxies on items pertaining to patients' pre-fracture health and functional status. Agreement across items ranges from very poor to good and varies with respect to the health or functional area assessed. Proxies tend to overestimate patient disability relative to the patients themselves, especially with regard to capacity to perform instrumental activities of daily living. Although proxies who report the greatest contact with patients respond most comparably to the patients, when they do disagree, proxies with the greatest patient contact tend to overestimate patient disability. The authors suggest that attention to item construction and phrasing may improve response comparability.

Activities of Daily Living↗
PubMed1995

Detection of endothelial cell-derived nitric oxide: current trends and future directions.

The vascular endothelium is a significant site of NO release that inhibits cellular adhesion and maintains a non-thrombogenic surface. Use of newly described technology suggests for the first time that the maximal release of NO induced by cNOS and iNOS activation may be quite similar, implying that it is the duration of NO release and not the concentration of NO produced from stimulated endothelial cells that accounts for the different biological activities of the enzymes. The respective roles of cNOS and iNOS must be carefully evaluated since both enzymes may have potent biological effects at local sites of production.

Animals↗