UMLS:C0020538 - FACTA Search

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Despite the relatively high incidence of essential hypertension and pregnancy-induced hypertension, the etiologies of these disorders remain enigmatic. A link between stretching of neural structures in the lower body and the induction of hypertension in these disorders is hypothesized. Hypertension has been documented in patients undergoing femoral and tibial lengthening procedures; in experimental models the stretching of lower extremity nerves appeared to be responsible for the increase in blood pressure with bone lengthening. The upright posture of humans puts an added strain on nerves and an increased pressure on lumbar disks may put increasing tension on the nerve roots. The resultant nerve stretch in pregnant women may be exacerbated by the hormone relaxin. A possible link between the stretching of neural structures and the genesis of essential hypertension or pre-eclampsia/eclampsia is hypothesized.
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PMID:Lower body nerve stretch: a role in essential hypertension or pre-eclampsia? 891 Aug 84

The overall rate of induction of labor in the United States in 1993 was 134 per 1,000 live births, or over 527,000 of the four million births that occur annually in the United States. Indications for labor induction include postdate pregnancy, premature rupture of membranes (PROM), and maternal medical complications, such as diabetes mellitus and pregnancy-induced hypertension. This article briefly reviews common indications for induction of labor and the importance of cervical ripening. It then addresses methods used to hasten cervical ripening and to induce labor, ranging from the more "natural" and noninvasive methods, such as nipple stimulation, to the newest commercially available formulation of prostaglandin. Methods well documented in the scientific literature, as well as those commonly used but less well studied, are included. Although one may argue about the "invasive" nature of these methods, they are addressed, in general, from the most natural methods to the latest pharmacologic methods, and they include the following: sexual intercourse, nipple/breast stimulation, herbal preparations, homeopathic solutions, castor oil, enemas, acupuncture, membrane sweeping or stripping, mechanical dilation (balloon catheters, laminaria, and synthetic osmotic dilators), amniotomy, and pharmacologic hormonal preparations (prostaglandin E2, oxytocin, misoprostol, mifepristone, and relaxin).
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PMID:Methods of cervical ripening and labor induction. 910 14

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 micromol/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 expression 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 significantly 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-kappaB, 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-arginine-NO pathway in vascular smooth muscle cells.
Hypertension 1998 Jun
PMID:Relaxin activates the L-arginine-nitric oxide pathway in vascular smooth muscle cells in culture. 962 36

The mechanisms involved in cardiovasular changes during human pregnancy and the complicated aetiology of gestational hypertension are unclear. Reproductive hormones have known effects on the cardiovascular system in the non-pregnant state and in animal systems, but their effects in human pregnancy are uncertain. In this study of pregnant women, the effects of serum concentrations of relaxin, progesterone and oestradiol on arterial blood pressure were studied. Higher serum concentrations of progesterone and relaxin, but not oestradiol, in early pregnancy were related to lower mean systolic blood pressures in the second and third trimesters. No relationship was found between hormonal concentrations and diastolic blood pressures. However, women with a diastolic blood pressure of >90 mmHg in late pregnancy showed statistically significant lower relaxin concentrations in early pregnancy in comparison with women whose diastolic blood pressure was </=90 mmHg. In a multivariate analysis, the mean systolic blood pressure (P: < 0.0001) and serum relaxin (P: < 0.01) in early pregnancy, but not progesterone, were independently related to systolic blood pressure in late pregnancy. The results support previous experimental and clinical studies. The effect of relaxin may be explained by a possible vasodilatatory action seen in animal studies and appears to be moderate.
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PMID:Reproductive hormones and blood pressure during pregnancy. 1147 81

Before 1980 research on the kidney and hypertension during pregnancy was neglected, although these diseases, especially hypertension, are major causes of morbidity to mother and child. The past 20 years, however, has witnessed a striking reversal of this neglect. This review focuses on recent progress in renal physiology, kidney disease, and hypertension as relates to pregnancy. Why do renal hemodynamics increase markedly in pregnancy? Studies have suggested roles for nitric oxide synthase, prostaglandins, endothelin and relaxin. This area of research is exciting, as unraveling why glomerular filtration rate and renal plasma flow increase in pregnancy may eventually help all patients with acute and chronic renal function loss. Concerning other advances: Micropuncture studies in rats, and the interpretation of fractional dextran clearances in humans show that the hyperfiltration that occurs during normal gestation is not associated with increased glomerular capillary pressure. Finally, description of changes in osmoregulation and in the metabolic disposal of arginine vasopressin in human pregnancy led to identification and appropriate treatment of a new group of disorders termed "transient diabetes insipidus of pregnancy." Chronic renal disease of any severity once led to proscription or interrupting of pregnancy. Clinical-pathological correlation studies and long-term follow-up of the mothers have revealed that most of these gestations succeed with little risk of worsening the natural history of the kidney disorder. This is also true in allograft recipients, and we now have guidelines to counsel both groups of patients. Progress relating to hypertension in pregnancy has been in 2 broad areas; systematic attempts to accurately define and differentiate the various disorders and population studies to predict, prevent, and improve the management of preeclampsia. There has also been considerable progress in unraveling the pathophysiology and identifying the cause of preeclampsia.
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PMID:The kidney and hypertension in pregnancy: twenty exciting years. 1124 79

The first part of this report on the Australian Health and Medical Research Congress, held November 25-29, 2002, in Melbourne, Australia, considers some of the symposia and three plenary lectures: Neurosteroids: Nature's Valium, G-Protein-Coupled Receptors and the Mike Rand Memorial Lecture. In the new era in relaxin research symposium, we learned that relaxin is a general antifibrotic agent rather than just a hormone of pregnancy. The drugs discussed in the drug discovery symposium included drugs from natural products, allosteric modulators, antibodies to cytokines and AM-336, an N-type Ca(2+) channel blocker. In the matrix proteases symposium, we learned of the importance of these enzymes in bone, endometrial remodeling and cardiovascular disease. The emphasis of the cytokine antagonist symposium was the involvement of cytokines in rheumatoid arthritis and how these effects could be inhibited with cytokine antagonists. The second part of this report is on the cardiovascular components of the meeting. One of the major strengths of Australian research is the cardiovascular area. Thus, it was not surprising that there were three major symposia with a cardiovascular theme this congress. Although the clinical trials of the NHE1 inhibitors in ischemia and reperfusion have been disappointing to date, evidence was presented in the sodium-hydrogen exchanger symposium that these agents might be beneficial in hypertrophy and heart failure. The discussion in the vessel wall biology in diabetes symposium ranged from molecular aspects to clinical trials. In this, and the NAD(P)H oxidases symposium, many new potential drug targets were discussed. The plenary lecture of the High Blood Pressure Research Council concerned the pathophysiology and management of obesity hypertension, and included a discussion of the drugs for weight reduction.
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PMID:Health and medical research down under in 2002. 1294 54

Preeclampsia, the de novo occurrence of hypertension and proteinuria after the 20th week of gestation, continues to exert an inordinate toll on mothers and children alike. Recent clinical trials, new physiologic insights, and novel observations on pathogenesis have altered the thinking about preeclampsia. The mechanisms surrounding relaxin and its effects on the circulation and on matrix metalloproteinases have been elucidated. The growth factor's receptor, fms-like tyrosine kinase 1, has been shown to exist in a soluble form that is able to inactivate vascular endothelial-derived growth factor and human placental growth factor. Compelling evidence has been brought forth suggesting that fms-like tyrosine kinase 1 is a circulating factor that can cause preeclampsia. Preeclamptic women have high circulating levels of asymmetric dimethyl arginine that could account for the generalized endothelial dysfunction observed in preeclampsia. Preeclamptic women also produce novel autoantibodies that may serve to activate angiotensin receptors. These new observations raise the possibility that the treatment of preeclamptic women will soon be improved.
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PMID:New aspects in the pathophysiology of preeclampsia. 1533 93

The antifibrotic effects of the peptide hormone relaxin on cardiac and renal fibrosis were studied in 9- to 10-month-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Rats (n=8 to 9 per group) were allocated into 3 groups: WKY controls, vehicle-treated SHR (SHR-V), and relaxin-treated SHR (SHR-R). Relaxin (0.5 mg/kg per day) was administered via subcutaneously implanted osmotic mini-pumps over 2 weeks before hearts and kidneys were harvested for analysis. Collagen content was analyzed by hydroxyproline assay, gel electrophoresis, and quantitative histology. Zymography was used to determine matrix metalloproteinase (MMP) expression and Western blotting to determine proliferating cell nuclear antigen (PCNA) expression and alpha-smooth muscle actin (alpha-SMA)/myofibroblast expression, whereas cardiac hypertrophy was assessed by myocyte size and real-time polymerase chain reaction of associated genes. The left ventricular (LV) myocardium of SHR-V contained increased collagen levels (by 25+/-1%, P<0.01 using biochemical analysis and 3-fold; P<0.01 using quantitative histology), enhanced expression of PCNA (by 70+/-8%; P<0.01), alpha-SMA (by 32+/-2%; P<0.05), and the collagen-degrading enzyme MMP-9 (by 70+/-6%; P<0.05) versus respective levels measured in WKY controls. The kidneys of SHR-V also contained increased collagen (25+/-2%, P<0.05 using biochemical analysis and 2.4-fold; P<0.01 using quantitative histology). Relaxin treatment significantly normalized collagen content in the LV (P<0.01) and kidney (P<0.05), completely inhibited cell proliferation (P<0.01) and fibroblast differentiation (P<0.05) in the LV, and increased MMP-2 expression (by 25+/-1%; P<0.05) without affecting MMP-9 in the LV compared with that measured in SHR-V. Thus, relaxin is a potent antifibrotic hormone with a rapid-occurring efficacy that may have therapeutic potential for hypertensive disease.
Hypertension 2005 Aug
PMID:Relaxin reverses cardiac and renal fibrosis in spontaneously hypertensive rats. 1596 69

Chronic administration of recombinant human relaxin (rhRLX) to conscious, normotensive rats (male and female) increases cardiac output (CO) and global arterial compliance (ACg) and reduces systemic vascular resistance (SVR) with no change in mean arterial pressure (MAP). Effects (magnitude and temporal pattern) of relaxin on systemic hemodynamics and arterial properties in hypertensive animal models are not known. Accordingly, the major goal of the present study was to determine the cardiovascular effects of rhRLX in hypertensive rats using 2 models: Long-Evans rats chronically administered angiotensin II (AII) and spontaneously hypertensive rats (SHR). CO and systemic arterial load, as quantified by SVR and ACg, were obtained using methods reported previously by us. In rats with AII-induced hypertension, acute rhRLX administration (up to 6 hours) significantly increased CO and ACg (24.9+/-3.9 and 34.3+/-12.6% above baseline, respectively) and significantly decreased SVR (17.2+/-3.5%) without changing MAP. In contrast, acute rhRLX administration to SHR and normotensive rats for up to 6 hours failed to produce any significant changes in CO, ACg, SVR, or MAP. However, chronic rhRLX administration (1 to 7 days) to SHR yielded significant changes (24.0+/-8.1 and 22.3+/-6.6% increases in CO and ACg, respectively, and a 13.3+/-5.3% decrease in SVR, with no change in MAP). In conclusion, rhRLX increases CO and reduces arterial load in hypertensive rats without reducing MAP. However, the time course of response to rhRLX treatment is dependent on the model of hypertension such that rats characterized by AII-mediated hypertension responded more rapidly to rhRLX administration than SHR.
Hypertension 2005 Oct
PMID:Relaxin increases cardiac output and reduces systemic arterial load in hypertensive rats. 1617 27

Systemic sclerosis (SSc) is a multi-system disease characterized by skin fibrosis and visceral disease. Therapy is organ and pathogenesis targeted. In this review, we describe novel strategies in the treatment of SSc. Utilizing the MEDLINE and the COCHRANE REGISTRY, we identified open trials, controlled trials, for treatment of SSc from 1999 to April 2005. We used the terms scleroderma, systemic sclerosis, Raynaud's phenomenon, pulmonary hypertension, methotrexate, cyclosporin, tacrolimus, relaxin, low-dose penicillamine, IVIg, calcium channel blockers, losartan, prazocin, iloprost, N-acetylcysteine, bosentan, cyclophosphamide, lung transplantation, ACE inhibitors, anti-thymocyte globulin, and stem cell transplantation. Anecdotal reports were omitted. Methotrexate, cyclosporin, tacrolimus, relaxin, low-dose penicillamine, and IVIg may be beneficial in improving the skin tightness in SSc. Calcium channel blockers, the angiotensin II receptor type 1 antagonist losartan, prazocin, the prostacyclin analogue iloprost, N-acetylcysteine and the dual endothelin-receptor antagonist bosentan may be beneficial for Raynaud's phenomenon. Epoprostenol and bosentan are approved for therapy of pulmonary hypertension (PAH). Other options under investigation include intravenous or aerolized iloprost. Cyclophosphamide (CYC) pulse therapy is effective in suppressing active alveolitis. Stem cell and lung transplantation is a viable option for carefully selected patients. Renal crisis can be effectively managed when hypertension is aggressively controlled with angiotensin converting enzyme (ACE) inhibitors. Patients should continue taking ACE inhibitors even after beginning dialysis in hope of discontinuing dialysis. Antithymocyte globulin and mycophenolate mofetil appear safe in SSc. The improvement in skin score and the apparent stability of systemic disease during the treatment period suggest that controlled studies of these agents are justified. Stem cell transplantation is under investigation for severe disease. Novel therapies are currently being tested in the treatment of SSc and have the potential of modifying the disease process and overall clinical outcome. The evaluation of these studies is still a difficult process.
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PMID:New therapeutic strategies for systemic sclerosis--a critical analysis of the literature. 1629 21

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