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

The role of EDRF in the modulation of blood pressure and vascular reactivity in estrogen-treated rats was investigated both in vivo and in vitro studies. In vivo, long-term subcutaneous injection of ethinyl estradiol (EE2, 0.2 micrograms/day, s.c.) for 6 weeks significantly induced an elevation of systolic blood pressure from 117.1 +/- 2.7 to 129.9 +/- 3.6 mmHg. In vitro, the endothelium-dependent relaxation of ACh (10(-8)-10(-5) M) in intact aortic rings from EE2-treated rats was significantly blunted compared with normal control rats. Meanwhile, the contractile responses to PE (10(-8)-10(-5) M) was no difference between intact and denuded aortic rings from EE2-treated rats. The results indicate that the reduction of vasodilator response to ACh and the loss of enhanced contractile responses to PE in denuded rings may be due to altered endothelial function after long-term treatment with EE2. Furthermore, the high potassium (12.5-62.5 mM) induced-contraction and nitroglycerin (3 x 10(-8)-3 x 10(-6) M) induced-relaxation were not different between EE2 and control groups. These results indicate that the function of vascular smooth muscle did not alter after long-term treatment with EE2. In conclusion, the alteration of function of endothelium may play an important role in the modulation of estrogen-induced mild hypertension.
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PMID:The role of EDRF in the modulation of blood pressure and vascular reactivity in estrogen-treated rats. 795 10

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

Cardiac events are a major cause of death in dialysed patients. This is due, at least in part, to the high prevalence of atherosclerotic coronary heart disease. To a large extent, however, coronary lesions are acquired in the predialytic phase of chronic renal failure. The susceptibility of the heart to ischaemia is modulated by a number of factors, e.g. microvascular abnormalities, increased cardiac pulsatile workload, disturbed cardiac glucose metabolism, imbalanced autonomic innervation. The paradoxical result of there being no relationship of cardiac death in dialysis patients to blood pressure may be explained by confounding factors. Intradialytic hypotension appears to be an independent risk factor. The dialysis patient is exposed to hypertension and dyslipidaemia, two potent risk factors of atherosclerosis. Although no definite information is available, it is conceivable that factors related to dialysis procedures may also influence early or late events in atherogenesis. Such potential factors include oxidative modification of lipids, modulation of insulin resistance or glucose metabolism by non-insulin-dependent pathways, expression of adhesion molecules and activation of potential effector cells in atherogenesis, particularly monocytes and platelets, changes of synthesis and/or response to endothelin and nitroxide (EDRF), and possibly also accelerated formation of advanced plaques by hyperphosphataemia and/or hyperparathyroidism. Such proatherogenic mechanisms must be balanced against factors potentially protecting against atherogenesis; these comprise altered arachidonic acid metabolism (increased prostacyclin and decreased thromboxane synthesis), impaired platelet aggregation, antiatherosclerotic effects of heparin, and diminished concentrations of 1,25(OH)2D3, i.e. of a proatherogenic compound.
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PMID:Atherogenesis and cardiac death: are they related to dialysis procedure and biocompatibility? 806 10

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

An elevation in mean blood pressure was found in rats treated with low lead (0.01%) for 6 months and then only water for an additional 6 months (discontinuous low lead). No change in blood pressure was found in rats similarly treated with high lead (0.5%) (discontinuous high lead). Administration of DMSA (0.5% in drinking water), for 5 days every 2 months following cessation of lead administration, resulted in a significant lowering of blood pressure in both groups of animals. In the low-lead but not the high-lead group, this was associated with an increase in plasma cyclic GMP (acting as a second messenger for endothelium-derived relaxing factor, EDRF) and a decrease in the plasma concentration of a 12-kDa hypertension-associated protein. Plasma endothelin-3 (ET-3) levels were decreased in discontinuous high-lead rats, increased in discontinuous low-lead rats, but were unaltered by DMSA treatment. We infer that the elevated blood pressure in the discontinuous low-lead rats is related to an increase in the putative vasoconstrictors, ET-3 and the hypertension-associated protein, without a change in the vasodilator, EDRF. With DMSA treatment, plasma cyclic GMP in low-lead rats increased above normal, and the hypertension-associated protein decreased, resulting in lowered blood pressure. DMSA was shown to act as an antioxidant in vitro. Thus the DMSA effect on plasma cGMP (EDRF) may occur via a scavenging effect on EDRF-inactivating reactive oxygen species.
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PMID:Effect of chelation treatment with dimercaptosuccinic acid (DMSA) on lead-related blood pressure changes. 816 87

Morphological examination of renal biopsies from 90 women with preeclampsia (PE), assessment of the clinical data and clinicomorphological correlations produced the following results: 1. By light-microscopy the renal lesions in PE imitate a picture of glomerulonephritis of mesangial type with different degrees of severity. 2. Morphometric investigations confirmed the impression gained by light-microscopy of swelling of endothelial cells and podocytes as well as endocapillary cell proliferation and enlargement of the glomeruli. 3. The immunohistological findings are non-specific and argue against immune complex deposition, but are suggestive of insudative processes. In addition immunohistological investigations of fibronectin and factor VIII-associated antigen reveal a pathogenetic relevant alteration of endothelial cell. 4. Electronmicroscopy is the most valid diagnostic method allowing subdivision of the quantitative different lesions in various degrees of severity. Furthermore the use of this method allows elucidation of the dynamics of the underlying disease process, which progresses through successive stages i.e. early, fully developed and late stage, supporting the reversibility of these glomerular lesions. 5. Close correlations are found between the clinical parameters and morphological findings in nephropathy in pregnancy-induced hypertension. The hypertension, proteinuria and nephrotic syndrome, which characterize the clinical picture, correlate with the severity of the glomerular lesions and the further course of the disease. Moreover, hypertension also correlates with mesangial and subendothelial deposits and with focal segmental hyalinosis and sclerosis, occurring in some cases. The focal segmental hyalinosis and sclerosis should be regarded as hyperperfusion-lesions indicating benign nephrosclerosis and developing only facultatively in PE. 6. The first morphological substrate of nephropathy in pregnancy-induced hypertension with the key to pathogenesis present itself as endothelial lesion, possibly caused by oxygen free radicals, lipid-peroxides or hyperfusion. In result of the endothelial lesion an imbalance of the different mediator systems i.e. thromboxane-prostacyclin, endothelin-EDRF with dominance of vasoconstrictive reactions would be effective. Thus the following induction of coagulative, vasoconstrictive and proliferative processes results in the characteristic glomerular lesions in PE.
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PMID:[Nephropathy in pregnancy--an endothelial lesion?]. 817 90

Gou-teng is a drug used for treatment of hypertension in Chinese medicine. Its antihypertensive action has been previously confirmed in the spontaneously hypertensive rat (SHR). Here, its vasorelaxing effect and the mechanisms of actions were studied in vitro. Gou-teng extract (GTE) relaxed the norepinephrine (NE)-precontracted aortic ring preparations isolated from Wistar Kyoto rats (WKY) with and without intact endothelium; the latter was significantly less sensitive than the former. The GTE-induced endothelium-dependent relaxation was significantly inhibited by NG-monomethyl-L-arginine (NMMA) in a dose-dependent manner while indomethacin did not affect the relaxation. Atropine inhibited the acetylcholine (ACh)-induced endothelium-dependent relaxation but did not the GTE-induced one. Furthermore, once GTE was applied, the following NE-induced contraction was significantly reduced even after repeated washout. NMMA effectively reduced and rather reversed this residual effect of GTE. From these results, it is concluded that GTE relaxes the NE-precontracted rat aorta through endothelium-dependent and, to lesser extent, -independent mechanisms. The endothelium-dependent component would be mediated by EDRF/NO pathway in which the muscarinic cholinoceptors were not involved. Thus, GTE appears to be a potent and long-lasting vasodilator mainly through EDRF/NO release.
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PMID:Gou-teng (from Uncaria rhynchophylla Miquel)-induced endothelium-dependent and -independent relaxations in the isolated rat aorta. 820 63

During the last decade, a multitude of experimental arguments have led to the concept that EDRF is nitric oxide (NO), a messenger not only involved in the control of vasomotor tone but also in vascular homeostasis, neuronal and immunological functions. Regardless of its origin, endogenous NO is produced through the conversion of L-arginine to L-citrulline by NO-synthase (NOS) from which several isoforms have recently been isolated, purified and cloned. NOS-type I (isolated from brain) and type III (isolated from endothelial cells) are termed "constitutive-NOS" and produce picomolar levels of NO from which only a small fraction elicits physiological responses. These isoforms are regulated by Ca(2+)-calmodulin with NADPH, FAD/FMN and tetrahydrobiopterin as co-factors and reveal a high degree of homology with the amino-acid sequence of cytochrome P450 reductase within the C-terminal domain. Functionally, neuronal-NOS type I is important in neurotransmission (modulation of NMDA receptor), the central control of vascular homeostasis and possibly learning and memory. In the peripheral nervous system, NOS appears to be linked to nonadrenergic noncholinergic (NANC) neuronal pathways. Endothelial-NOS type III is essential for the control of vascular tone in response to the release of endogenous mediators, although shear stress is the major trigger of endothelial-NOS activity under physiological conditions. NOS-type III also contributes to the prevention of abnormal platelet aggregation. NOS-types II and IV (isolated from macrophages) are Ca(2+)-calmodulin independent and are termed "inducible-NOS" since their activation is only promoted under pathophysiological situations where macrophages exert cytotoxic effects in response to cytokines. In contrast with NOS-types I and III, activation of NOS-type II in these cells induces the formation of nanomolar levels of NO which act as a defense mechanism of the immune system. Dysfunctions of the L-arginine-NO pathway have been characterized in multiple diseases (atherosclerosis, hypertension, diabetes, sepsis, cerebral ischemia, etc) and the design of more selective activators/inhibitors of NOS isoforms is a new challenge for the understanding of their pathophysiology and treatment.
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PMID:Nitric oxide: an ubiquitous messenger. 829 80

Endothelium-derived vasoactive factors are produced by the endothelium activated by effective stimulus, and with paracrine regulatory activity of the tone/proliferation of the vascular smooth muscle and platelet function. They are divided in two groups: endothelium-derived relaxing and contracting factors. Among the endothelium-derived relaxing factors, PG I2, EDRF (NO or other nitrous compound) and EDHF (still unidentified) have been considered Synthetized by the endothelium after stimulation by plasmatic, platelet-derived and endothelium-derived substances and mechanisms, towards the vascular smooth muscle (myorelaxing/cytostatic) and the platelets (antiaggregation). The endothelium-derived contracting factors include the EDCF1 (endothelins, 21 amino acids peptides), EDCF2 (O2-) and TxA2. Its production, induced by stimulus similar to those for relaxing factors, promotes constriction/mitogenesis of the vascular smooth muscle and platelet aggregation. Probably, endothelin-1 has indirect actions over hormonal mechanisms of cardiovascular and renal regulation. The vascular system establishes a tight regulation over the production of these endothelium-derived vasoactive factors. Its loss (usually due to alteration of endothelial responsiveness to stimulation) allows local or generalized modifications of the vascular tone. These can depend on hypertension, atherosclerosis, ischemia-reperfusion lesion, diabetes, inflammation and situations of farmacotoxicity (all developing vasoconstriction/vasospasm) or by septicemia (leading to vasodilation). This disregulation is also involved in the pathogenesis of hypertension, atherosclerosis and ischemia-reperfusion. The vascular tone regulation by endothelium also leads to systemic consequences. Essentially by decreasing cardiac, cerebral and renal blood flow it implies morphologic and functional modifications of these organs.
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PMID:[Vasoactive endothelial factors]. 833 93


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