Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients in different stages of diabetic nephropathy (DN) frequently present cardiac disease expressed by myocardial ischemia and/or diabetic cardiomyopathy. These changes are already present at early stages of DN, probably even before urinary albumin excretion (UAE) reaches the traditionally diagnostic levels of microalbuminuria. The cardiac changes are responsible for a significant proportion of the increased death rates in patients with DN and can be reduced through multiple intervention on the several risk factors present in these patients. Cardiac disease assessment should ideally be performed in every patient, irrespective of renal status, through specific methods to detect ischemia and myocardial dysfunction, besides routinely performing 24-h ambulatory blood pressure monitoring. In patients with advanced atherosclerosis, other arteries (aorta, carotid, renal) should be evaluated as well. Intensive treatment of arterial hypertension, and use of cardioprotective drugs, correction of the associated dyslipidemia and anemia, and use of antiplatelet agents can reduce the elevated cardiovascular mortality in patients with DN.
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PMID:[Diabetic nephropathy and cardiac disease]. 1750 31

We demonstrated previously that, in mice with chronic angiotensin II-dependent hypertension, gp91phox-containing NADPH oxidase is not involved in the development of high blood pressure, despite being important in redox signaling. Here we sought to determine whether a gp91phox homologue, Nox1, may be important in blood pressure elevation and activation of redox-sensitive pathways in a model in which the renin-angiotensin system is chronically upregulated. Nox1-deficient mice and transgenic mice expressing human renin (TTRhRen) were crossed, and 4 genotypes were generated: control, TTRhRen, Nox1-deficient, and TTRhRen Nox1-deficient. Blood pressure and oxidative stress (systemic and renal) were increased in TTRhRen mice (P<0.05). This was associated with increased NADPH oxidase activation. Nox1 deficiency had no effect on the development of hypertension in TTRhRen mice. Phosphorylation of c-Src, mitogen-activated protein kinases, and focal adhesion kinase was significantly increased 2- to 3-fold in kidneys from TTRhRen mice. Activation of c-Src, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, and focal adhesion kinase but not of extracellular signal regulated kinase 1/2 or extracellular signal regulated kinase 5, was reduced in TTRhRen/Nox1-deficient mice (P<0.05). Expression of procollagen III was increased in TTRhRen and TTRhRen/Nox1-deficient mice versus control mice, whereas vascular cell adhesion molecule-1 was only increased in TTRhRen mice. Our findings demonstrate that, in Nox1-deficient TTRhRen mice, blood pressure is elevated despite reduced NADPH oxidase activation, decreased oxidative stress, and attenuated redox signaling. Our results suggest that Nox1-containing NADPH oxidase plays a key role in the modulation of systemic and renal oxidative stress and redox-dependent signaling but not in the elevation of blood pressure in a model of chronic angiotensin II-dependent hypertension.
Hypertension 2008 Feb
PMID:Renal redox-sensitive signaling, but not blood pressure, is attenuated by Nox1 knockout in angiotensin II-dependent chronic hypertension. 1819 61

Abdominal compartment syndrome was initially described as a cascade of physiopathological events triggered by the increase in intra-abdominal pressure induced by a surgical procedure for aneurysm of the abdominal aorta. In practice, it is a complication that can arise after various procedures; it has a multi-organ impact and can lead to exitus. We retrospectively analyzed a total of 9 patients with abdominal compartment syndrome. In 5 cases onset of the syndrome was due to a secondary complication of a vascular procedure (3 mesenteric, 2 renal). The clinical data characterizing the disease included abdominal distension and reduced diuresis. In all cases the finding of increased necrosis scores (LDH, CPK) was evident, while the appearance of leukocytosis occurred only in 4 (44%). The basic treatment was surgical decompression. In one case we obtained an excellent result with medical treatment alone, consisting in steroids and PGE1; these were useful in all cases in which an inflammatory bowel component played a role. Our experience encourages us to stress the importance of early assessment of abdominal hypertension in patients with a potential risk of abdominal compartment syndrome. In this phase, appropriate medical and supportive treatment could limit the surgical indications or at any rate favour the healing process after surgical decompression, the basic treatment indicated for this syndrome.
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PMID:Abdominal compartment syndrome: a situation thet needs to be better known. 1870 76

We found previously that selective blockade of endothelin ETA receptors is superior to nonselective ET(A)/ET(B) in attenuating hypertension and survival rate in Ren-2 transgenic rats (TGR). In the present pilot study, we were interested in whether similar effects will be found in TGR with inducible malignant hypertension (iTGR; official strain name Cyp1A1-Ren-2rats), which were derived from the original Ren-2 transgenic rat strain. Studies were performed in three-month old male iTGR. Treatment with either bosentan, a non-selective ET(A)/ET(B), or with atrasentan, a selective ET(A) receptor blocker, was started on day 2 of the experiment. Feeding with indole-3-carbinole (13C; 03% in rat chow), a natural xenobiotic which activates the Cyplal promoter of the mouse Ren-2 gene, began on day 3 and lasted for 4 days until day 6. Systolic BP, body weight, plasma ANG II and tissue ANG II and ET-1 concentrations were determined daily. Severe hypertension developed as early as 1 day after beginning of 13C feeding which was accompanied by a significant reduction in body weight and by increases in plasma and tissue ANG II and left ventricle ET-1 concentrations. Atrasentan or bosentan had no effects on the rise in BP or plasma and tissue ANG II concentrations but prevented the rise in heart ventricle ET-1 concentration. Our data show that blockade of the ET system does not prevent or attenuate the rapid development of severe hypertension in iTGR; a long-term protective effect of ET blockade on cardiac (and renal) damage, however, cannot be excluded and awaits further investigations.
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PMID:Endothelin receptor blockade does not affect blood pressure or angiotensin II levels in CYP1A1-Ren-2 transgenic rats with acutely induced hypertension. 1956 37

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit production of prostaglandins by acting on cyclooxygenase (COX) isoenzymes 1 and 2. Nonselective NSAIDs inhibit both COX 1 and 2 isoenzymes (eg, ibuprofen and naproxen). Selective NSAIDs act on COX-1 (eg, aspirin) or COX-2 (eg, celecoxib) isoenzymes, respectively. Prostaglandins are produced in platelets and gastric mucosal cells through constitutively expressed COX-1 isoenzyme. They are involved in the regulation of hemostasis, functional integrity of the gastrointestinal and renal tracts, platelet function, and macrophage differentiation. Inhibition of COX-1 isoenzymes impedes platelet aggregation, impairs maintenance of protective gastric mucosal barrier, and affects renal function. Prostaglandin production in inflamed tissue results from de novo induction of COX-2 expression by inflammatory cytokines and other noxious stimuli. Thus, COX-2 isoenzyme inhibition either selectively or nonselectively helps in reducing inflammation in the setting of musculoskeletal disorders. Safety and efficacy of NSAIDs are related to their relative actions on COX-1 or COX-2 inhibition. Given the multisystem (gastrointestinal, hematopoietic, and renal) adverse effect profile of COX-1 inhibition, formulation of NSAIDs with relative COX-2 selectivity became a highly desirable target during the 90's. However, studies in the first half of this decade revealed adverse effects of COX-2 inhibition on the cardiovascular system, including increased risks of myocardial infarction, exacerbation of stable congestive heart failure, and worsening high blood pressure. Randomized trials and meta-analyses confirmed these findings, which led to withdrawal of some of the COX-2 inhibitors from the market by the federal Food and Drug Administration a few years ago. Here, we review the effects of COX-2 isoenzyme inhibitors on the cardiovascular system to provide a safe strategy for prescribing these agents in patients with existing cardiovascular disease. We did not find adequate long-term randomized controlled trials appropriately powered to evaluate cardiovascular outcomes. Potentially, all NSAIDs possess a fair risk of adverse effects on gastrointestinal, cardiovascular, and renal systems. Until more evidence for safety via randomized trials is available, we recommend caution in prescribing COX-1 and 2 inhibitors for musculoskeletal disorders in patients with existing gastrointestinal or cardiovascular conditions.
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PMID:Use of nonsteroidal anti-inflammatory drugs in patients with cardiovascular disease: a cautionary tale. 2053 4

For 50 years aldosterone has been thought to act primarily on epithelia to regulate fluid and electrolyte homeostasis. Mineralocorticoid receptors (MR), however, are also expressed in nonepithelial tissues such as the heart and vascular smooth muscle. Recently pathophysiologic effects of nonepithelial MR activation by aldosterone have been demonstrated, in the context of inappropriate mineralocorticoid for salt status, including coronary vascular inflammation and cardiac fibrosis. Consistent with experimental studies, clinical trials (RALES, EPHESUS), have demonstrated a reduced mortality and morbidity when MR antagonists are included in the treatment of moderate-severe heart failure. The pathogenesis of MR-mediated cardiovascular disease is a complex, multifactorial process that involves loss of vascular reactivity, hypertension, inflammation of the vasculature and end organs (heart and kidney), oxidative stress and tissue fibrosis (cardiac and renal). This review will discuss the mechanisms by which MR, located in the various cell types that comprise the heart, plays a central role in the development of cardiomyocyte failure, tissue inflammation, remodelling and hypertension.
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PMID:Mechanisms of mineralocorticoid salt-induced hypertension and cardiac fibrosis. 2193 Jan 86

All types of acute kidney injury (AKI) (functional /pre-renal, parenchymal/intra-renal, obstructive/post-renal) result in a sharp drop of the glomerular filtration rate, with variable reversibility according to the initial cause. In one case out of five, drug intake can be related to the onset of AKI. Antibiotics, analgesics and nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists are the agents mostly involved, as well as iodinated radio-contrast agents. Mechanisms are often complex: toxic cellular effect directed on a nephron segment (tubular necrosis) associated or not with intraglomerular hemodynamic changes, or immune process leading to acute tubule-interstitial nephritis. Each underlying risk factor (age > 60 year, cardiac or hepatic failure, hypertension, diabetes, intra-vascular volume depletion, preexisting or unknown chronic kidney disease) must be taken into consideration by the prescribing physician because it reduces the chance of functional recovery and worsens the renal and the overall prognosis. A pre-renal additional component is often present and avoidable thanks to a strict hemodynamic monitoring. The present article summarizes some recent physiopathological aspects of AKI and makes the link between clinical situations and currently prescribed drugs. Lessons from the radio-contrast induced nephropathy are examined by taking into account prevention aspects and risk factors screening. An effective collaboration between the general practitioner and the nephrologist would benefit in optimizing the treatment of difficult cases.
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PMID:[Acute kidney injury and drug-induced nephropathies]. 2203 61

Systemic mastocytosis (SM) is a rare, clonal disorder of the mast cell (MC) and its precursor cells. It is characterized by proliferation and accumulation of MCs within various organs, most commonly the skin. The clinical course is variable with indolent or smouldering and aggressive forms being described. We report the case of a middle-aged male patient with smouldering SM presenting with atypical recurrent life-threatening crises. The patient reported a 19-year history of chronic symptoms. The patient had four inpatient stays due to atypical life-threatening crises, during which he has shown end organ damage (cardiac and renal). With each crisis the patient reported acute symptoms. The management of each of these episodes was complex and made more challenging by the patient's longstanding history of hypertension and ischaemic heart disease. In short, SM can present with unexplained life-threatening crises which can be confused for an infectious disease being acute in nature.
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PMID:Smouldering systemic mastocytosis presenting with cryptic life-threatening crises: case report and literature review. 2240 24

The prevalence of hypertension among the paediatric population is 1%-2%. The emergency physician should recognise potentially harmful blood pressure (BP) levels and ensure they are adequately treated, in order to avoid life-threatening complications. A hypertensive emergency is a severely elevated BP complicated by target organ dysfunction (cardiovascular, cerebrovascular and/or renal). Hypertensive urgency, however, is a severe elevation in BP without target organ dysfunction. This distinction is critical for the clinical approach. The authors present a case of a severe hypertension due to primary focal segmental glomerulosclerosis. In this case, the lack of BP measurement in the infant surveillance and the devaluation of an albuminuria detected in a previous routine urine examination, have culminated in a late diagnosis of a severe hypertension, with subsequent effects on target organs.
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PMID:How important it is to determine the blood pressure in paediatric patients? 2278 90

Hypertension in children is an important often under diagnosed condition. There are no absolute values of normal blood pressure in children as it varies with age, gender and height. Normative blood pressure data is available for different ages, sexes and heights, the diagnosis of hypertension should be based on these values. It is recommended that all children over the age of 3 years should have blood pressure measured whenever seen by a doctor. Essential hypertension can occur in children, but hypertension secondary to an underlying cause (most often renal) is more likely. Secondary hypertension tends to be more severe, sustained and at times uncontrolled. Evaluation includes a thorough history and physical examination and certain basic laboratory tests. All attempts should be made to look for the etiology in cases where secondary hypertension is suspected. Management of hypertension in children must incorporate non pharamacological measures including weight reduction, exercise and dietary modifications. Pharamacological treatment is indicated for; a) symptomatic hypertension, b) if there is evidence of end organ damage and c) for those unresponsive to nonpharmacological treatment. A number of drugs are available for children with hypertension; commonly used ones are calcium channel blockers, beta blockers, angiotensin converting enzyme inhibitors and diuretics. Choice of a drug depends on the underlying cause of hypertension and presence of comorbidity, if any.
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PMID:Hypertension in children: approach to management. 2318 86


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