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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microalbuminuria (urinary albumin excretion between 20 and 200 micrograms/min) and endothelial dysfunction coexist in patients with essential hypertension. To evaluate whether the two phenomena are related and the determinants of that association, we recruited 10 untreated males with essential hypertension and microalbuminuria without diabetes to be compared with an equal number of matched patients with essential hypertension excreting albumin in normal amounts and 10 normal controls. The status of endothelial function was inferred from circulating von Willebrand Factor antigen (vWF), a glycoprotein secreted in greater amounts when the vascular endothelium is damaged. vWF concentrations were higher in hypertensive patients with microalbuminuria than in hypertensive patients without and controls. Individual vWF and urine albumin-excretion values were correlated (r = 0.55, p < 0.002). Blood pressure correlated with both urinary albumin excretion and vWF. Left ventricular mass index and minimal forearm vascular resistances were comparable in patients with hypertension and higher than in controls; total and low-density lipoprotein cholesterol, triglycerides, lipoprotein-a, Factor VII, and plasminogen activator inhibitor-1 did not differ. Fibrinogen was higher and creatinine clearance lower in microalbuminurics. Albuminuria in essential hypertension may reflect systemic dysfunction of the vascular endothelium, a structure intimately involved in permeability, haemostasis, fibrinolysis, and blood pressure control. This abnormality may have important physiopathological implications and expose these patients to increased cardiovascular risk.
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PMID:Microalbuminuria and endothelial dysfunction in essential hypertension. 798 Jul 88

There is a new, potentially fatal disorder that is infrequently reported. The apparent rareness may be because of a lack of recognition of the syndrome or its predisposing factors. Fluoxetine (Prozac, Dista Products Co, Division of Eli Lilly Co, Indianapolis, IN), sertraline (Zoloft, Roerig Division, Pfizer Inc, New York, NY), and paroxetine (Paxil, SmithKline Beecham Pharmaceuticals, Philadelphia, PA) belong to a new class of antidepressant medication: the serotonin reuptake-inhibitors (SRIs). The relative safety profile of the SRIs has led to their widespread use. However, a syndrome of excessive serotonergic activity, the "serotonin syndrome" (SS), has recently been recognized. It is characterized by changes in mental status, hypertension, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor. A high index of suspicion is required to make the diagnosis in these acutely ill patients. The most common agents implicated in SS are the monoamine oxidase inhibitors in combination with L-tryptophan or fluoxetine. A case of a patient with significant peripheral vascular disease who developed SS while taking paroxetine and an over-the-counter cold medicine is reported. There have been no prior reports of this interaction. Discontinuation of the offending agents, sedation, and supportive care are the mainstays of treatment. The interactions of serotonin with platelets and vascular endothelium are also discussed.
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PMID:The serotonin syndrome associated with paroxetine, an over-the-counter cold remedy, and vascular disease. 766 67

Transgenic rats carrying the mouse Ren-2 gene (Ren-2d)27 provide a unique model to study the interplay between the renin-angiotensin system and estrogen in the pathogenesis of hypertension. In this study we measured the effects of ovariectomy and estrogen replacement on blood pressure and the contribution of vascular endothelium relaxing factor, nitric oxide, in female transgenic hypertensive rats and normotensive Sprague-Dawley (SD) rats. Both groups of animals were either ovariectomized or sham-operated at 12 weeks of age. Ovariectomized rats were treated with either 17 beta-estradiol (70 micrograms/day) or placebo for 4 weeks, whereas sham-operated rats received placebo alone. Mean arterial blood pressure measured in conscious rats directly by an arterial catheter was significantly higher in ovariectomized rats, compared with ovariectomized rats given estrogen replacement therapy for both transgenic (167 +/- 5 v 154 +/- 4 mm Hg, P < .05) and SD rats (125 +/- 4 v 113 +/- 5 mm Hg, P < .05). The contribution of endothelium-derived nitric oxide to the maintenance of blood pressure was examined by acute systemic injection of NG-monomethyl-L-arginine (L-NMMA, 10 mg/kg). L-NMMA caused a significantly greater increase in blood pressure in sham-operated transgenic as compared to SD rats (34 +/- 3 v 14 +/- 3 mm Hg, P < .05). The response in ovariectomized transgenic rats was markedly reduced (13 +/- 3 mm Hg), reaching levels that were no different from sham-operated SD rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Estrogen augments the contribution of nitric oxide to blood pressure regulation in transgenic hypertensive rats expressing the mouse Ren-2 gene. 794 57

The effect of vascular endothelium, endocardium, and coronary endothelium on vascular tone and myocardial contraction-relaxation sequence in heart failure is discussed. Vascular endothelium affects underlying vascular smooth muscle through paracrine secretion of relaxing and constricting factors. In heart failure, systemic vasoconstriction results not only from neuroendocrine activation, but also from disturbed local endothelial control of vascular tone because of impaired endothelial-dependent vasodilation and because of increased plasma concentration of endothelin. Experimental evidence obtained in isolated cardiac muscle strips established the influence of endocardial endothelium on the duration of myocardial contraction and on the onset of myocardial relaxation. By analogy to vascular endothelium, both diffusible agents that abbreviate (endothelial-derived relaxation factor-like substance) and those that prolong (endocardin) myocardial contraction have been shown to be released from the endocardium. Similar agents are released from the coronary endothelium and, because of the close proximity of capillaries and myocytes, could exert a major effect on myocardial performance. Endothelial dysfunction and concomitant lack of release of myocardial relaxant factors could explain left ventricular relaxation abnormalities observed in the cardiac allograft or in arterial hypertension. Since endothelial-derived relaxation factor or nitric oxide mediates the coronary reactive hyperemic response, a negative inotropic action of nitric oxide could contribute to left ventricular failure when left ventricular wall stress is elevated, as occurs after myocardial infarction in the noninfarcted zone and during left ventricular volume or pressure overload in the absence of adequate hypertrophy.
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PMID:Endothelial control of vascular and myocardial function in heart failure. 794 59

Our appreciation of the vascular endothelium has changed considerably over the last decade. This organ, finally recognized as such, participates actively in vasomotor regulation and haemostasis. It secretes several relaxing and contracting factors which act locally to determine resting vascular tone. One of the relaxing factors, EDRF/NO plays an important physiological role as it contributes to the rapid adaptation of blood flow to various pharmacological and mechanical stimuli, thereby ensuring maintenance of adequate tissue perfusion. Nitric oxide (NO) is an ubiquitous factor which was crowned "molecule of the year 1992" by the scientific review Science. Its effects extend well beyond those on the cardiovascular system. Endothelial dysfunction is observed in many pathological states such as atherosclerosis, reperfusion injury, postangioplasty endothelial regeneration, degeneration of venous bypass grafts, pure spastic angina, hypertension and diabetes. It is associated with decreased production of EDRF/NO, which probably contributes significantly to the aggravation of endothelial and parietal lesions and to the natural progression of atherosclerotic disease in general. This article describes the principal vasoactive factors secreted by the endothelium and goes on to list the physiologic cardiovascular effects of EDRF/NO in detail, and to review the different pathologies associated with a disorder of secretion of this factor.
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PMID:[EDRF/NO and endothelial functions]. 801 Aug 61

Impairment of the vascular endothelium and its functions is a common sign of several serious diseases (atherosclerosis, hypertension, vascular spasms, thromboses) and is the initial stage of vascular affection in diabetes mellitus. The endothelium plays an important role in the transformation of some substances with a cardiovascular action and it secretes itself vasoactive substances. Vascular affections in diabetes are characterized by impaired homeostasis of vasoactive substances of endothelial origin--raised levels of vasoconstrictor factors (endothelins, thromboxanes) and reduction of vasodilatating factors (prostacyclin, EDRF--endothelin derived relaxing factor) as well as disorders of their interrelations. Vasoactive agents lead at the same time also to alteration of the growth and proliferation potential of smooth muscle cells of the vascular wall and thus to remodelling of the vascular structure in diabetes. At present possible ways how to influence these processes in a favourable way are intensely studied and discussed.
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PMID:[Endothelial dysfunction in diabetes mellitus]. 806 97

The vascular endothelium plays a vital role in the control of the circulation. It metabolizes various vasoactive substances, coverts angiotensin I to angiotensin II and secretes the potent vasodilators prostacyclin and EDRF (NO) and the vasoconstrictor peptide endothelin-1. The balance between these mediators determines the responses of the cardiovascular system in diseases such as hypertension, atherosclerosis and myocardial infarction.
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PMID:The Croonian Lecture, 1993. The endothelium: maestro of the blood circulation. 814 36

Modulation of vascular tone is one important function of the endothelium. This can occur via two principal mechanisms: by modulating the local concentration of circulating vasoactive substances (e.g. adenine nucleotides, angiotensin II, biogenic amines, bradykinin), and by synthesizing and releasing vasoactive autacoids. The most important endothelium-derived vasodilator autacoids are nitric oxide (NO) and prostacyclin (PGI2). By counteracting neuro- and myogenic vasoconstriction, the continuous release of these autacoids from the vascular endothelium represents a sensitive and highly effective local system for maintaining an adequate blood flow to the organs. Impaired production of NO (and PGI2), either as a result of endothelial injury or dysfunction, has been implicated in the pathology of a variety of cardiovascular diseases, such as hypertension, hypercholesterolaemia, atherosclerosis and diabetes. Therefore, the prevention and/or reversal of the functional and morphological changes of the endothelium associated with these diseases is an important therapeutic goal. This brief overview covers current knowledge concerning the intracellular pathways that link endothelial activation by receptor-dependent and -independent stimuli to the formation of NO and PGI2.
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PMID:Signal transduction in endothelium-dependent vasodilatation. 829 77

Recent observations indicate that pre-eclampsia is a disease, which occurs because of a partially defective maternal immune response against the fetal (paternal) antigen expressed on trophoblast tissue. The resulting defective or insufficient placentation can cause ischaemic changes, which seem to act in a harmful way on the vascular endothelium, initially locally in the utero-placental circulation, but later with universal systemic effects. The resulting endothelial dysfunction and concommitant thrombocyte activation seems to account for an important part of the pathophysiology of pre-eclampsia. Hypertension is presumably a secondary phenomenon. The definitive treatment of pre-eclampsia is delivery, which is always indicated in cases of severe pre-eclampsia after 32 weeks of pregnancy. In milder cases and before 32 weeks it is reasonable to await delivery, if necessary starting anti-hypertensive treatment. Treatment of hypertension has to balance the risks of maternal cerebral complications against the risks of reduced utero-placental bloodflow with resulting intra-uterine growth retardation. Low-dose acetylsalicylic acid treatment could in theory constitute a prophylactic principle, but the results of new, large, well-conducted, randomised trials advise against using such treatment prophylacctically at present. The effect of fish-oil supplements is not yet clarified, whereas mineral supplements such as calcium and magnesium are unlikely to have prophylactic effects on the development of pre-eclampsia, at least not in western industrialized society.
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PMID:[Pre-eclampsia. Etiology--physiopathology--treatment]. 831 41

Endothelin is a recently isolated 21 amino acid peptide with vasoconstrictor activity. It seems to be part of the "hormonal" production by the vascular endothelium and might play a key role in the regulation of vasomotricity. The principal property of endothelin is that it induces an intense and prolonged arterial and venous contraction. Endothelin is secreted by endothelial cells under the influence of various stimuli (thrombin, adrenaline, shearing stress, hypoxia, etc.), then binds to specific membrane receptors thereby increasing the intracellular free calcium concentration. Endothelin has many other vascular and extravascular properties: it has positive inotropic and chronotropic effects, increases renal vascular resistances and reduces the glomerular filtration rate, contracts bronchial and gastrointestinal smooth muscle, induces proliferation of the vascular smooth muscle cells as well as that of fibroblasts and glomerular mesangial cells. Compared with experimental data in animals, human data are still scantly. Plasma endothelin concentration rises in acute renal failure and in chronic renal failure treated by dialysis, diabetes mellitus, essential arterial hypertension, pre-eclampsia and asthma. The development of specific antagonists and endothelin in synthesis inhibitors should soon enable us to specify the modes of regulation of endothelin production before considering applications to therapy.
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PMID:[Endothelin: the vasoconstrictor of the 1990's?]. 837 53


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