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

We examined erythropoietin (EPO) gene expression and EPO production during hypoxia in two Sprague-Dawley rat strains with divergent polycythemic responses to hypoxia. Hilltop (H) rats develop severe polycythemia, severe hypoxemia, and pulmonary artery hypertension. The H rats often die from a syndrome indistinguishable from chronic mountain sickness (CMS) in humans. Madison (M) rats develop polycythemia and pulmonary artery hypertension that is modest and suffer no excess mortality. We tested the hypothesis that these rat strains have different stimulus-response characteristics governing EPO production. Rats of each strain were exposed to hypoxia (0.5 atm, 73 Torr inspired PO2), and renal tissue EPO mRNA and EPO levels, plasma EPO, ventilation, arterial and renal venous blood gases, and indexes of renal function were measured at fixed times during a 30-day hypoxic exposure. During extended hypoxic exposure, H rats had significantly elevated renal EPO mRNA, renal EPO, and plasma EPO levels compared with M rats. Ventilatory responses and indexes of renal function were similar in the strains during the hypoxic exposure. H rats had greater arterial hypoxemia from the onset of hypoxia and more severe renal tissue hypoxemia and greater polycythemia after 14 days of hypoxic exposure. When EPO responses were expressed as functions of renal venous PO2, the two strains appeared to lie on the same dose-response curves, but the responses of H rats were shifted along the curve toward more hypoxic values. We conclude that H rats have significantly greater polycythemia secondary to poorer renal tissue oxygenation, but the stimulus-response characteristics governing EPO gene expression and EPO production do not seem to differ between M and H rats. Finally, the regulation of EPO levels during hypoxia occurs primarily at the transcriptional level.
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PMID:Polycythemic responses to hypoxia: molecular and genetic mechanisms of chronic mountain sickness. 951 90

Hypertension is a common finding after renal transplantation, and it has a variety of underlying mechanisms. One reason is the type of immunosuppressive therapy, with a higher prevalence of hypertension in cyclosporine-treated patients. Cyclosporine interferes with several humoral and neural systems which are involved in blood pressure regulation such as the renin-angiotensin system, endothelins, nitric oxide, prostaglandins and the sympathetic nervous system. Other pathomechanisms for posttransplant hypertension are uncontrolled renin secretion of the native kidneys, polycythemia, recurrence of renal disease in the graft and renal failure. Renal transplant artery stenosis is a potentially treatable cause of post-transplant hypertension and several techniques such MRT angiography, Doppler sonography and conventional angiography are available. The diagnosis and treatment of hypertension are of high importance in general for the transplanted patient, and especially for the long-term prognosis of graft function.
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PMID:Hypertension in the transplanted patient. 980 33

A modified Casson equation was established, verified satisficatorily for real conditions and suggested for use in clinical hemorheology. It provides 5 Casson parameters, i.e., Casson yield stress, Casson viscosity, the first critical point of shear rate to cause rouleaux to be broken down into smaller units, the second critical point of shear rate to completely disaggregate into individual erythrocytes, the difference between the two critical points, and also gives two series of the 5 above-mentioned Casson parameters, respectively, under original hematocrit and the standardized hematocrit of 45%. This equation not only reveals the apparent abnormalities of hypertensive patients and normalities of the healthy persons, but also reveals hidden abnormalities for patients with either low or high hematocrit. For 20 cases of hypertensive patients with low hematocrit, the 5 Casson parameters have lower values than control, but the modified equation reveals their hidden higher values than control when their hematocrit is standardized to 45%. For 7 cases of polycythemia complicated with hypertension, the 5 Casson parameters are higher at their original hematocrit, and the modified equation reveals the higher parameters than control also when the hematocrit is standardized to 45%. For 8 cases of polycythemia without complications, the 5 Casson parameters are higher at their original hematocrit than control, while the modified equation still reveals their normalities when standardizing their hematocrit to 45%.
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PMID:A modified Casson equation to characterize blood rheology for hypertension. 984 24

We previously demonstrated augmented endothelium-derived nitric oxide (EDNO)-dependent pulmonary arterial dilation and increased arterial endothelial nitric oxide synthase (eNOS) levels in chronic hypoxic (CH) and monocrotaline (nonhypoxic) models of pulmonary arterial hypertension. Therefore, we hypothesized that the long-term elevation of arterial eNOS levels associated with CH is related to pulmonary hypertension or some factor(s) associated with hypertension and not directly to hypoxia. To test this hypothesis, we examined responses to the EDNO-dependent dilator ionomycin in U-46619-constricted, isolated, saline-perfused lungs from control rats, CH (4 wk at 380 mmHg) rats, and rats previously exposed to CH but returned to normoxia for 4 days or 2 wk. Microvascular pressure was assessed by double-occlusion technique, allowing calculation of segmental resistances. In addition, vascular eNOS immunoreactivity was assessed by quantitative immunohistochemistry, and eNOS mRNA abundance was determined by RT-PCR assays. Our findings indicate that 4-day and 2-wk posthypoxic rats exhibit persistent pulmonary hypertension, likely due to maintained arterial remodeling and polycythemia associated with prior exposure to CH. Furthermore, arterial dilation to ionomycin was augmented in lungs from each experimental group compared with controls. Finally, arterial eNOS immunoreactivity and whole lung eNOS mRNA levels remained elevated in posthypoxic animals. These findings suggest that altered vascular mechanical forces or vascular remodeling contributes to enhanced EDNO-dependent arterial dilation and upregulation of arterial eNOS in various models of established pulmonary hypertension.
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PMID:Maintained upregulation of pulmonary eNOS gene and protein expression during recovery from chronic hypoxia. 995 Aug 73

The twin-to-twin transfusion syndrome (TTS) results from an unbalanced blood supply through placental anastomoses in monochorionic twins. It induces growth restriction, renal tubular dysgenesis, and oliguria in the donor and visceromegaly and polyuria in the recipient. A better understanding of its pathophysiology could contribute to improving the management of TTS, which still carries a high perinatal mortality in both twins. As well as several other candidates, the renin-angiotensin system might be involved in TTS. To evaluate its role in the pathogenesis of the syndrome, we studied the kidneys of 21 twin pairs who died from TTS at 19 to 30 weeks, compared with 39 individuals in a control group, using light microscopy, immunohistochemistry, and in situ hybridization. The overexpression of the renin protein and transcript with frequent evidence of renin synthesis by mesangial cells was observed in the donor kidneys, presumably as a consequence of chronic renal hypoperfusion. This upregulation of renin synthesis might be beneficial to restore euvolemia. In severe cases of TTS, however, angiotensin-II-induced vasoconstriction acts as an additional deleterious factor by further reducing the renal blood flow in donors. In recipients, renin expression was virtually absent, possibly because it was down-regulated by hypervolemia. However, in addition to congestion and hemorrhagic infarction, there were severe glomerular and arterial lesions resembling those observed in polycythemia- or hypertension-induced microangiopathy. We speculate that fetal hypertension in the recipient might be partly mediated by the transfer of circulating renin produced by the donor, through the placental vascular shunts.
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PMID:Twin-to-twin transfusion syndrome. Role of the fetal renin-angiotensin system. 1066 92

461 consecutive inborn babies, delivered during the period September 1993-March 1994 were subjected to a microhematocrit assessment at 6 hours of age to determine the incidence of polycythemia. 47 babies (inborn and out born), admitted to the neonatal unit with confirmed polycythemia were studied for clinical and laboratory abnormalities. These 47 babies were then randomly assigned to receive partial exchange transfusion with either normal saline or fresh plasma. The incidence of polycythemia was 27 of 461 (5.8%). 23 of 27 (85.1%) were term babies and 15 of 27 (55.5%) were small for gestational age. 14 of 27 (51.1%) babies had mothers who had pregnancy induced hypertension. Feeding problems (16/47) and lethargy (25/47) were the commonest symptoms (34% and 51% respectively). 25 of 47 (51%) babies had hypoglycemia and 5 of 47 (10.6%) had hypocalcemia. Thrombocytopenia was seen in 13/47 (27.65%) of cases. 24 babies received normal saline and 23 received fresh plasma for partial exchange transfusion. The immediate post-exchange fall in hematocrit was significant in both groups and this was well sustained over the following 48 hours. However, improvement in clinical and laboratory parameters was more remarkable with fresh plasma. Polycythemia appears to be a real clinical entity in neonates in India and babies with known risk factors should be actively screened for this condition. Once diagnosis is established special attempts should be made to rule out hypoglycemia. For treatment of polycythemia fresh plasma is preferable for partial exchange transfusion but normal saline appears to be an adequate substitute.
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PMID:Neonatal polycythemia. 1077 85

With current immunosuppression, elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this are impairment of renal function (secondary to chronic allograft nephropathy or less frequently recurrence of primary renal disease), the use of calcineurin inhibitors as immunosuppressants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenosing lesions of the transplant artery (or the upstream arteries of the recipient), polycythemia, and genetic predisposition to hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, angiotensin converting enzyme inhibitors are indicated in treatment, but given the causal role of sodium retention and graft vasoconstriction, diuretics and calcium channel blockers remain mainstays of antihypertensive treatment in the renal allograft recipient.
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PMID:Hypertension after renal transplantation. 1155 80

A 32-year-old Japanese man was hospitalized for evaluation of unconsciousness. He was diagnosed as having primary pulmonary hypertension (PPH) with severe systemic hypertension, Raynaud's phenomenon and relative polycythemia. Hemostatic studies revealed increased coagulation and decreased fibrinolysis, similar to findings of chronic disseminated intravascular coagulation (DIC). Although activation of coagulation and systemic hypertension were improved after treatment with phlebotomy and administration of nifedipine, enerapril and warfarin, pulmonary hypertension was unchanged, suggesting that irreversible change had already occurred in the pulmonary arteries. Those complications could modify the process of pulmonary hypertension by inducing a hyperviscosity state.
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PMID:Primary pulmonary hypertension with severe systemic hypertension, Raynaud's phenomenon and relative polycythemia. 1157 54

The introduction of new immunosuppressive regimens results in the significant improvement in the outcome of patients after kidney transplantation. However, about 5 percent of renal transplants are lost every year. Not only immunological (alloantigendependent) but also nonimmunological (alloantigen-independent) factors are involved in late graft loss. Among them, hypertension, hyperlipidemia, proteinuria, genetic predisposition, viral infection and nephrotoxicity of immunosuppressive drugs contribute to the development and to the progression of chronic post-transplant nephropathy. Hypertension can be both the cause and the consequence of chronic allograft failure. Hypertension is frequently observed before transplantation, persists after grafting and increases the risk of chronic allograft nephropathy. Hypercholesterolemia, obesity, atheromatosis, polycythemia, and excessive salt intake are factors contributing in post-transplant hypertension. However, in some cases, hypertension can be transferred with the grafted kidney, as observed in normotensive patients before renal transplantation. In 1 to 12 percent of cases, the cause of post transplant hypertension is the stenosis of the transplant artery. Sometimes the presence of hypertension in renal recipients may result from the recurrence of glomerulonephritis or from the development of glomerulonephritis de novo in the graft. Also immunosuppressive treatment with corticosteroids and cyclosporine A contributes to the increased prevalence of hypertension by 20-30 percent. The development of the graft nephroarteriolosclerosis as a consequence of hypertension accelerates the progression of the post-transplant nephropathy. Adequate control of the arterial pressure (< 140/90) should be achieved in all renal transplant recipients. Reduction in protein and salt intake is important to reduce hyper-filtration and slows the progression of transplant nephropathy. However, pharmacological treatment is usually needed. Angiotensin-converting-enzyme inhibitors, angiotensin II type I receptor antagonists exhibit beneficial hemodynamic effect leading to the reduction of glomerular hypertension and proteinuria. Calcium antagonists besides their systemic antihypertensive effect, can protect renal grafts from vascular and renal toxicity of CyA. Sometimes, combined therapy with these and other antihypertensive drugs and diuretics is necessary.
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PMID:[Post-transplant nephropathy and arterial hypertension]. 1186 48

We report a 72-year-old right-handed man who was diagnosed as having crossed aphasia. He had polycythemia, hypertension and an old cerebral infarction in the right occipital lobe. He was admitted to our hospital because of muscle weakness in the left extremities at the age of 71. In the laboratory data, red blood cells(689 x 10(4)/microliter) and platelets(87.6 x 10(4)/microliter) were increased in number. Brain CT detected a right putaminal hematoma and an old infarct in the occipital lobe on the right. After admission, he developed non-fluent speech, and impairments of auditory comprehension, writing and naming due to the infarction in his right cerebral hemisphere including the middle cerebral artery distribution. The standard language test of aphasia(SLTA) revealed marked impairments in the language function, except for reading kana and kanji words. This writing was severely impaired compared with other language dysfunctions. Auditory comprehension, repetition and reading were impaired at the sentence level rather than at the kana word level. Furthermore, he suffered from left hemiparesis and left unilateral spatial neglect. We diagnosed his impairments of language function as crossed aphasia based on his right-handedness, CT findings and the results of SLTA. His language center was considered to be located in both cerebral hemispheres. Compared with typical findings in reported cases of crossed aphasia, the presence of both non-fluent speech and mutism were consistent with previous observations. However, the marked impairments of auditory comprehension, repetition and naming were different. Polycythemia and hypertension were considered to be the risk factors of cerebral infarction in our patient.
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PMID:[A case of crossed aphasia in a dextral patient with polycythemia]. 1199 62


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