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

Investigations on singleton and twin pregnancies show different functional behaviour on maternal-fetal relationship. In some ways twin pregnancies may be considered at risk and they may develop associated pathologies such as hypertension. The aim of this work was to evaluate the morpho-functional behaviours of umbilical cord veins in twin and singleton gestations to better understand the role of these extra-embryonic tissues in the regulation of pregnancies. The umbilical cords were studied from singleton pregnancies and from dichorionic twin pregnancies. Biochemical and morphological investigations were carried out. A significant decrease in the anisotropy values was observed in endothelial cells from twins compared with singletons. Our ultrastructural data show immaturity features at the vein vessel wall level in twins. Furthermore, immunohistochemical investigations showed a lower degree of expressivity concerning adhesion molecules such as ICAM-1 and ELAM. Morphogenetic extracellular glycoproteins like fibronectin and tenascin seem over-expressed in twin pregnancies. Our morpho-functional data well testify the lower maturation degree of umbilical cord veins in twins with respect to singletons.
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PMID:Umbilical veins in dichorionic twins. A morpho-functional assessment. 755 55

DOCA-NaCl treatment causes hypertension, accelerates development of proteinuria, and leads to glomerulosclerosis in rats with autoimmune Heymann nephritis. To study the mechanisms of kidney injury induced by renal haemodynamic load in chronic nephritis, we studied by immunohistochemistry the local expression of various cytokines, growth factors and adhesion molecules in the kidneys of Heymann nephritic rats with or without DOCA-NaCl-induced hypertension. The DOCA-NaCl-nephritis group developed hypertension and marked renal enlargement as compared with the nephritis group, the DOCA-NaCl group, and the controls. Albuminuria appeared earlier and was heavier in the DOCA-NaCl-nephritis group compared with the nephritic rats without DOCA-NaCl. Expression of IL-6, TNF-alpha, GM-CSF, b-FGF, NGF, TGF-beta, and ICAM-1 was enhanced in the kidneys of the DOCA-NaCl-nephritis group as compared with other groups, localized mainly in the glomerular mesangium (IL-6, GM-CSF, TGF-beta), glomerular and peritubular endothelium (ICAM-1), and collecting ducts (TNF-alpha, b-FGF, NGF, TGF-beta), possibly associated with the observed tubulointerstitial mononuclear cellular infiltration. Thus in autoimmune Heymann nephritis, DOCA-NaCl treatment causes hypertension and increased renal mass together with upregulation of local cytokine and growth factor production, which may further aggravate hypertension and accelerate progression of renal damage.
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PMID:Increased renal expression of cytokines and growth factors induced by DOCA-NaCl treatment in Heymann nephritis. 880 10

How an increase in blood pressure, in and of itself, induces hypertensive nephrosclerosis is unclear. In an earlier study we found that leukocyte infiltration, proximal tubular cell proliferation, matrix deposition and interstitial fibrosis occur in the unclipped kidney of 2 K 1 C Goldblatt hypertensive rats. In this study we tested the hypothesis that the cell surface adhesion molecule ICAM-1 is expressed on the vascular endothelium and tubular epithelium of unclipped kidneys at 4 weeks. As a positive control, we examined the clipped kidney as well. We found that systolic blood pressure was significantly elevated in renovascular hypertensive rats compared to sham-operated controls after 4 weeks (198 +/- 5 mmHg vs 121 +/- 2 mmHg, P < 0.001). Furthermore, quantitative (densitometry) measurements showed that ICAM-1 expression on vascular endothelium and on tubular cells was significantly increased in unclipped kidneys compared to controls (P < 0.05). The same was true for monocyte and granulocyte infiltration (P < 0.05). These same variables were even more prominent in the clipped kidneys, compared to unclipped and control kidneys (P < 0.05). Our data show that ICAM-1 is expressed in unclipped kidneys exposed to hypertension as well as in clipped kidneys exposed to ischemia. We suggest that mechanical injury induced by increased blood pressure is responsible for an inflammatory adhesion molecule-mediated response and concomitant renal injury.
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PMID:Leukocyte infiltration and ICAM-1 expression in two-kidney one-clip hypertension. 917 41

Lysis of aortic endothelial cells (EC) by neutrophils from spontaneously hypertensive rats (SHR) was investigated using a nonradioactive cytotoxicity assay. Interleukin-1-activated EC, but not unstimulated EC, were effective target cells for lysis by SHR neutrophils. Supernatants from activated neutrophil did not exert a cytotoxic effect on EC. Inhibitors of reactive oxygen species did not affect the cytotoxicity of neutrophils on EC. In contrast, inhibitors of serine protease and elastase markedly inhibited the cytotoxicity of neutrophils on EC. Antibodies against the endothelial cell surface ligands ICAM-1 (CD54) and E-selectin (CD62E) inhibited the adhesion and cytotoxicity of activated neutrophils on EC. The cytotoxicity of neutrophils required direct cell-to-cell contact because separating them with a microporous membrane abrogated the neutrophil-mediated cytotoxic activity. These results demonstrate that SHR neutrophils possess potent cytotoxicity against cytokine-activated EC. Neutrophil-mediated damage of EC could contribute to organ damage in hypertension under conditions of local or systemic activation of neutrophils.
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PMID:Neutrophil-mediated damage to vascular endothelium in the spontaneously hypertensive rat. 917 19

In health, the vascular endothelium forms a multifunctional interface between the circulating blood and various tissues and organs of the body. It constitutes a selectively permeable barrier for macromolecules, as well as a nonthrombogenic and nonadhesive container that actively maintains the fluidity of blood. It is a metabolically active endocrine organ, serving as the source of multiple factors and mediators that are critical for normal homeostasis. These include vasodilators (nitric oxide, prostacyclin, endothelium-derived hyperpolarizing factor), vasoconstrictors (endothelin-1, thromboxane A2, prostaglandin H2 and components of the renin angiotensin system), various pro- and antithrombotic factors (e.g. tissue factor, platelet activating factor--PAF, von Willebrand factor), fibrinolytic activators and inhibitors (e.g. tissue plasminogen activator, plasminogen activator inhibitor-1), potent arachidonate metabolites (prostanoids), leukocyte adhesion molecules (e.g. E-selectin, P-selectin, intercellular adhesion molecule-1--ICAM-1, vascular cell adhesion molecule-1--VCAM-1), and multiple cytokines with activities of growth stimulators and inhibitors, transforming growth factors, proinflammatory and antiinflammatory mediators, tumour necrosis factors and chemotactic factors (chemokines). Besides these essential activities controlling the cardiovascular system, the endothelial cells represent an important part of the immune system as well. They have a pivotal role in the initiation and development of defensive and damaging inflammatory responses. Therefore endothelium can be considered as being the central equipment for the mutual exchange of life important information between the cardiovascular and immune systems. This in turn is leading to rapid advances in understanding the pathogenesis of some of the most serious and most common diseases, including inflammation, atherosclerosis and hypertension. (Tab. 7, Ref. 89.)
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PMID:[Vascular endothelium as a factor in information transfer between the cardiovascular and immune systems]. 958 73

Plasma concentrations of the circulating adhesion molecules ICAM-1 (CD54), VCAM-1 (CD106) were determined in 31 women with pre-eclampsia, 9 women with HELLP syndrome, and 13 women with transient pregnancy induced hypertension (PIH). Data were compared with a control group of 157 healthy pregnant women of the same gestational age. Furthermore, concentrations of circulating E-selectin (CD62E), P-selectin (CD62P), and PECAM-1 (CD31) were determined in a subpopulation of 17 women with pre-eclampsia. Plasma concentrations of circulating ICAM-1, VCAM-1, E-selectin, and PECAM-1 were significantly elevated in women with pre-eclampsia compared to healthy control pregnant women. Circulating ICAM-1 and VCAM-1 levels were also significantly elevated in the pre-eclampsia group compared to women with PIH. Concentrations of circulating P-selectin varied strongly in all experimental groups (SD > 70% of the mean), most likely reflecting various degrees of thrombocyte degranulation in the individual samples. Finally, longitudinal profiles of cICAM-1 and cVCAM-1 concentrations were determined in 123 healthy pregnant women between the 16th and the 42nd week of gestation. This analysis identified cICAM-1 and cVCAM-1 as tightly regulated plasma parameters that varied in a small concentration range. Concentrations of cICAM-1 and cVCAM-1 did not vary during pregnancy and the determined concentrations corresponded to the reported reference levels of nonpregnant individuals.
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PMID:[Soluble adhesion molecules in patients with pre-eclampsia]. 965 98

Angiotensin (Ang) II-induced organ damage has fascinated students of hypertension since the work of Wilson and Byrom. We are investigating a double transgenic rat (dTGR) model, in which rats transgenic for the human angiotensinogen and renin genes are crossed. These rats develop moderately severe hypertension but die of end-organ cardiac and renal damage by week 7. The heart shows necrosis and fibrosis, whereas the kidneys resemble the hemolytic-uremic syndrome vasculopathy. Surface adhesion molecules (ICAM-1 and VCAM-1) are expressed early on the endothelium, while the corresponding ligands are found on circulating leukocytes. Leukocyte infiltration in the vascular wall accompanies PAI-1, MCP-1, and VEGF expression. The expression of TGF-beta and deposition of extracellular matrix proteins follows, which is accompanied by fibrinoid vasculitis in small vessels of the heart and kidneys. Angiotensin-converting enzyme inhibitors and AT1 receptor blockers each lowered blood pressure and shifted pressure natriuresis partially leftward by different mechanisms. When combined, they normalized blood pressure, pressure natriuresis, and protected from vasculopathy completely. Renin inhibition lowered blood pressure partially, but protected from vasculopathy completely. Endothelin receptor blockade had no influence on blood pressure but protected from vasculopathy and improved survival. We show evidence that Ang II stimulates oxidative stress directly or indirectly via endothelin 1 and that NFkappaB is upregulated in this model. We speculate that the transcription factors NFkappaB and AP-1 are involved with initiating chemokine and cytokine expression, leading to the above cascade. The unique model and our pharmacological probes will enable us to test these hypotheses.
Hypertension 1999 Jan
PMID:Hypertension-induced end-organ damage : A new transgenic approach to an old problem. 993 Nov 7

Adhesion molecules on the endothelial cell membrane play an important role in the pathogenesis of atherosclerosis. Levels of soluble forms of cell adhesion molecules are reportedly elevated in patients with peripheral artery vessel disease and in patients with an atherosclerotic aorta. The present study investigated the association of serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble intercellular adhesion molecule 1 (sICAM-1), and soluble P-selectin (sP-selectin) with coronary heart disease (CHD) and the extent of coronary atherosclerosis, and examined the influence of serum levels of lipids, lipoproteins and apolipoproteins (apo) in subjects with (n=52, M/F:43/9) and without (controls, n=40, M/F:25/15) angiographically proven coronary atherosclerosis. After controlling for age and gender, levels of sVCAM-1 (least squares mean +/- std error: 565+/-36 ng/ml vs 540+/-41 ng/ml, ns), sICAM-1 (261+/-17ng/ml vs 247+/-19ng/ml, ns), and sP-selectin (142+/-8ng/ml vs 149+/-10 ng/ml, ns) in patients with coronary atherosclerosis were not different from those in controls, as assessed by an analysis of covariance. After also adjusting for body mass index, hypertension, diabetes mellitus, and smoking by a multiple logistic function analysis, the association of sVCAM-1, sICAM-1, and sP-selectin with CHD was still not significant. Levels of sVCAM-1, sICAM-1, and sP-selectin were also not related to the extent of coronary atherosclerosis as judged by the number of stenosed vessels. However, inverse (p<0.05) relationships were observed between sVCAMs and serum levels of HDL3-cholesterol, apo A-II, and lipoprotein containing apo A-I and A-II, between sICAMs and levels of apo A-II and Lp A-I/A-II (Lp A-I/A-II), and between sP-selectin and lipoprotein containing only apo A-I. In conclusion, serum levels of soluble VCAM-1, ICAM-1, and P-selectin were not related to CHD or the extent of coronary atherosclerosis, but were inversely related to serum levels of high-density lipoprotein-related lipoproteins.
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PMID:Levels of soluble cell adhesion molecules in patients with angiographically defined coronary atherosclerosis. 1008 83

Cell-bound adhesion molecules are involved in immune and inflammatory responses. Soluble forms of adhesion molecules (s.a.m.) can be detected in the blood. The elevated blood levels of s.a.m. were found as a response to variety disease processes (e.g. septic shock, acute graft rejection, atherosclerosis). The objective of the present study was to measure the serum levels of s.a.m. in patients with chronic renal allograft rejection and in recipients with a stable graft function. Evaluated was also the effect of activity of graft rejection (ch. g. r.) and risk factors of graft lesion on the levels of the investigated s.a.m. 34 patients with ch.g.r. were examined (Group I), 50 patients with a stable allograft function (Group II), and 25 healthy subjects (control). Group I patients were 76 +/- 34 months and Group II patients were 59 +/- 36 months after transplantation. Both groups of patients were treated with immunosuppressive drugs (CsA, azathioprine and prednisone) Group I patients had a higher plasma levels of creatinine and uric acid, increased arterial blood pressure and triglycerides concentrations, and lower plasma levels of HDL cholesterol, as compared to Group II patients. In all the examined subjects, serum concentrations of s.a.m. from the immunoglobulin and selectin families (s.ICAM-1, s.VCAM-1, s.E-selectin) were measured by the immunoenzymatic method. The investigations of s.a.m. in ch.g.r. patients revealed a statistically significant increase the serum levels of s.ICAM-1, s.VCAM-1 and s.E-selectin. Some disorders of the release of s.a.m. into blood were also found in patients without graft disfunction. In this patients were observed: increased levels of s.VCAM-1 and s.E-selectin. S.ICAM-1, s.VCAM-1 and s.E-selectin serum levels showed a correlation with plasma uric acid concentration and arterial pressure, whereas the other two molecules with the plasma level of triglycerides. Each of the three molecules had a negative correlation with the HDL cholesterol level. The regression analysis revealed a correlation of s.ICAM-1 and s.VCAM-1 with IL-6. The correlation of the molecules with chemokines (s.VCAM-1 and s. E-selectin with IL-8, and s. E-selectin with MCP-1) may results from their release in the course of the inflammatory process. The increased levels of circulating s.VCAM-1 and s.E-selectin found in renal allograft patients suggest a chronic stimulation and activation of the endothelium. Non-immunological mechanisms (such as arterial hypertension or metabolic disorders) contributed to the generation of the s.a.m. in patients with ch.g.r. and in those with stable graft function. The negative correlation of HDL with s.a.m. (s.ICAM-1, s.VCAM-1) suggests a protective role of HDL on the vascular endothelium by inhibiting the generation of these mediators.
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PMID:[Soluble cell adhesion molecules in chronic renal graft rejection]. 1041 May 74

The objective of the present study was to determine whether long-term arterial hypertension renders the microvasculature more vulnerable to the deleterious inflammatory responses elicited by ischemia and reperfusion (I/R). Intravital fluorescence microscopy was used to monitor leukocyte adherence and emigration, platelet-leukocyte aggregation, and albumin extravasation in mesenteric postcapillary venules of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) after 10 minutes of ischemia and subsequent reperfusion. Significant and comparable increases in leukocyte adherence/emigration and the formation of platelet aggregates were elicited by I/R in both WKY and SHR. Albumin extravasation was enhanced after I/R in SHR, but not in WKY. Monoclonal antibodies directed against the adhesion glycoproteins CD18, P-selectin, or ICAM-1 showed similar patterns of protection against the I/R-induced inflammatory responses in WKY and SHR. The enhanced albumin extravasation noted in postischemic venules of SHR was prevented by immunoneutralization of either CD18 on leukocytes or ICAM-1 on endothelial cells. These results suggest that, whereas long-term arterial hypertension does not significantly modify the leukocyte and platelet recruitment normally elicited in venules by I/R, it does result in an exaggerated albumin leakage response, which is mediated by an interaction between beta(2) (CD18) integrins on leukocytes and ICAM-1 on endothelial cells.
Hypertension 1999 Aug
PMID:Microvascular responses to ischemia/reperfusion in normotensive and hypertensive rats. 1045 43


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