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

In order to investigate the combined effects of diabetes and hypertension on the pathogenesis of cardiovascular disease, adult male and female SHR rats which develop hypertension spontaneously were given a single, 10 mg or 15 mg/100 g body wt. injection of alloxan s.c. to induce moderate or severe diabetes. Insulin was deliberately withheld. Animals were examined by autopsy daily for 7 days post-alloxan and after 4 and 8 weeks. Mortality was high--only 52% of the males survived as against 80% of the females. Most deaths occurred on Day 5 and were associated with adrenal haemorrhage and hyperplasia, thymus galnd involution, fatty liver and marked hypotension despite elevated aldosterone levels. During the first week, corticosterone levels increased significantly in the male; in females they showed little change. After 4 weeks, the severly diabetic animals became emaciated and moribund; corticosterone and aldosterone levels fell to very low levels despite adrenal hyperplasia. The beta cells of the moderately diabetic animals eventually lost their ability to secrete insulin and these animals too became cachetic and moribund with concomitant elevation of lipid, glucose and BUN levels, as well as myocardial infarction, fatty liver, and generalized hyalin arteriolo-, arterio-, and nephrosclerosis. It is suggested that the combined hormonal and metabolic alterations of diabetes and hypertension reinforced one another in these spontaneously hypertensive rats, leading to intense stimulation of the hypothalamic-pituitary-adrenal system, the exacerbation of those cardiovascular degenerative changes known to be associated with uncontrolled diabetes or hypertension, eventual impaired adrenocortical steroidogenesis, hypotension and death.
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PMID:Alloxan diabetes in spontaneously hypertensive rats: gravimetric, metabolic and histopathological alterations. 86 Nov 67

NZB nice spontaneously develop a high blood pressure and hypertensive vascular disease in the heart and the kidney. Treatment with cyclophosphamide decreased the level of blood pressure; congenital athymic nude NZB mice failed to develop a high blood pressure. These findings suggest that thymus and the thymus-dependent immune reactions have pathogenic importance for the spontaneous hypertension in these mice.
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PMID:Spontaneous hypertension and hypertensive vascular disease in the NZB strain of mice. 89 91

Repeatedly bred male rats which develop arteriosclerosis spontaneously were subjected to unilateral nephrectomy, 1% saline drinking water, and 2 mg subcutaneous injections of deoxycorticosterone acetate per animal weekly for 7 weeks to induce severe hypertension (+/- 175 mmHg systolic). Acute cerebral ischemia was induced by ligating one carotid artery. Two days later, experimental animals were subjected to acute myocardial ischemia by injecting them subcutaneously with a single dose of isoproterenol (25 mg/100 g body weight). All of the experimental animals died within 4 hours of the injection of isoproterenol. During this same period, blood pressure, body weight, thymus, kidney, and testicular weights were reduced, whereas heart and adrenal gland weights increased markedly. Serum enzymes (CPK, SGOT, and LDH), lipids (triglycerides and free fatty acids), glucose, BUN, and corticosterone rose progressively. Fatty infiltration of the liver, adrenal hyperplasia, myocardial thrombi, renal degenerative changes, and cerebral edema became progressively more severe. A hypothalamic-pituitary-adrenal axis component may be involved in the reaction to the stress of acute cerebral or myocardial ischemia, which is intensified when the two ischemias are combined, and chronic hypertension may exacerbate both.
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PMID:Acute cerebrovascular and myocardial ischemia superimposed upon chronically hypertensive and arteriosclerotic male Sprague-Dawley rats. 90 14

Acute hemorrhage in a normal thymus in neonates and infants has been reported in the literature. These patients were known to have an antecedent cause or defects in coagulation. The case of an adult who developed acute hemorrhage in a normal thymus and who was known not to have any defects in coagulation, hypertension, or other underlying cause is reported.
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PMID:Spontaneous thymic hemorrhage in an adult. 91 54

Treatment with desoxycorticosterone acetate (DOCA) and 1 per cent saline as drinking water for 21 days caused a significant and similar increase in blood pressure in haired mice, with a normal thymus function, as in nude mice with genetical aplasia of the thymus. After 57 and 78 days there was, however, a significantly more pronounced increase in blood pressure in haired than in nude mice. A marked degree of round cell infiltration around intrarenal vessels and degenerative changes including wedge-shaped infarcts were observed in the kidneys of the haired mice, commencing after 57 days of treatment, while no such changes were found in nude mice. Thymus grafting in nude mice, successively treated with DOCA and salt, conferred the ability to react with chronic hypertension and intrarenal vascular disease, equal to the reaction seen in haired mice. The present investigation has provided evidence for the existence of an initial thymus independent and a chronic thymus dependent phase of DOCA and salt hypertension in mice. It still remains an unsolved problem whether the secondary blood pressure fall observed in nude athymic mice is a direct consequence of the lack of perivascular cellular immune reactions, or caused by other defects in this strain of mice.
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PMID:Evidence for an initial, thymus independent and a chronic, thymus dependent phase of DOCA and salt hypertension in mice. 99 51

1. Bilateral compression of adrenal glands combined with unilateral nephrectomy and followed by imposition of a high sodium chloride intake caused severe hypertension in all rats, accompanied by enlargement of the heart, kidneys and adrenal glands, atrophy of the thymus and severe nephrosclerosis. 2. Digitoxin treatment delayed the onset, reduced the incidence and ameliorated the magnitude of the hypertensive response in such rats; it also reduced the degree of cardiac hypertrophy, the severity of nephrosclerosis and completely prevented enlargement of the adrenals and kidneys or atrophy of the thymus.
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PMID:Delayed onset and reduced severity of adrenal-compression hypertension in rats treated with digitoxin. 107 96

Partial infarction of one kidney and contralateral nephrectomy was followed by a rapid and significant increase in blood pressure both in haired mice with a normal thymus function and in nude mice with genetical aplasia of the thymus. The level of blood pressure and the prognosis were not influenced by the presence of thymus within the first 3 months after partial infarction of the kidney; but a significantly more pronounced increase in blood pressure after 4 months was observed in a small group of haired mice than in a similarly treated small group of nude mice. A marked degree of round cell infiltration around intrarenal arteries was only found in the haired mice, commencing 2 months after partial infarction of the kidney. Degenerative changes were observed in the kidneys of the haired mice 2-4 months after infarction. Very few of these lesions were found in the nude mice. Atempts to transfer the hypertension by means of viable lymph node cells from hypertensive donors to normotensive syngeneic recipients failed. The results support the assumption that high intravascular pressure induces thymus-dependent immune reactions against substances in teh vascular walls which, in turn, may have a prognostic significane; the results give no support for the assumption that the earlier phase of the hypertension which follows partial infarction of the kidney and contralateral nephrectomy is thymus-dependent.
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PMID:The role of thymus for the development and prognosis of hypertension and hypertensive vascular disease in mice following renal infarction. 127 88

The effects of gamma-interferon (gamma-IFN) on protein kinase C (PKC) levels and immunosuppression in the spontaneously hypertensive rat (SHR) were examined. First, an abnormal PKC distribution was found in spleen, thymus and aorta from SHRs relative to normotensive controls. Biweekly injections of rat recombinant gamma-IFN (1000 U/kg) restored basal or resting PKC levels to those found in normotensive Wistar-Kyoto (WKY) rats. We also examined the effects of in vivo gamma-IFN treatment on nuclear PKC (nPKC) activation in purified, isolated splenocyte nuclei. It was found that basal nPKC levels were higher in untreated SHRs than gamma-IFN SHRs or WKYs. Also, while nuclei from untreated SHRs were relatively unresponsive to various immunoreactive substances and PKC activators, gamma-IFN treatment significantly restored activity. Last, the proliferative response to mitogen challenge of isolated splenocytes from untreated SHRs, gamma-IFN-treated SHRs and WKYs was studied. Although gamma-IFN treatment did not restore the proliferative response to that of WKYs, the mitogen response was significantly enhanced by treatment with gamma-IFN. The data show that gamma-IFN acts to restore normal immune function and corrects aberrant PKC levels and adds to the growing body of knowledge suggesting a role for immune dysfunction in the etiology of hypertension.
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PMID:Gamma-interferon corrects aberrant protein kinase C levels and immunosuppression in the spontaneously hypertensive rat. 146 74

Immune dysfunction has been reported in spontaneously hypertensive rats (SHR), particularly in mature animals with established hypertension. The current study examined the time course of development of immune dysfunction and defined its cellular basis in male SHR and control normotensive Wistar-Kyoto rats (WKY). Mitogen-induced proliferative responses in lymphoid cells obtained from induced proliferative responses in lymphoid cells obtained from SHR thymus and spleen before (age 4 wk) and during the development of (ages 8 and 12 wk) hypertension and in age-matched normotensive WKY were monitored. A 50% reduction in concanavalin A (Con A)-induced proliferative responses was seen in SHR thymocytes compared with those of WKY at 12 wk only, suggesting differences in immature T-cell populations. Con A-induced T-cell proliferative responses in splenocytes also differed between strains: greatest (as much as 8-fold) decreases were found in 12-wk-old SHR. Similar findings were obtained in splenocytes stimulated with lipopolysaccharide (LPS), indicating differences in B-cell function. Mononuclear cells depleted of their adherent cell population were prepared from SHR and WKY at 12+ wk of age and assayed for their proliferative responses to LPS and Con A. The remaining nonadherent mononuclear cells of SHR had proliferative responses equal to or greater than those of WKY. Further, when SHR splenic mononuclear cells were allowed to adhere to plastic, and the adherent fraction was co-cultured with either SHR G-10 nonadherent or unfractionated SHR splenic mononuclear cells, proliferative responses were suppressed by as much as 88%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneously hypertensive rat: lymphoid depression is age dependent and mediated via a mononuclear cell subpopulation. 173 28

Experimental hypertensive vascular damage in rats resembles periarteritis nodosa microscopically and thus resembles immunologically produced cell infiltration. The immune system in patients with hypertension has, therefore, been investigated. High serum concentrations of immune globulins and increased prevalence of auto-antibodies have been found. Immune complexes and deposition of complement are present in the renal arteries. On transfer of lymphocytes from hypertensive experimental animals, normotensive animals develop hypertension and vascular changes resembling periarteritis nodosa. The leucocyte-migration-inhibition test demonstrates a cell-mediated immunological reaction to vascular wall antigens. Normal thymus function is essential for maintenance of the chronic phase of hypertension and for development of vascular wall changes. The genetic conditions are still obscure but a definite association to the C3F gene has, however, been found. The investigation reveals immunological reactions occur in arterial hypertension. It is not yet possible to differentiate between immunological reactions in the pathogenesis of hypertension and immunological reactions caused by hypertensive vascular damage. According to one of the hypotheses about the mechanisms of action, the immunological processes are mediated by complement. Complement activation may be initiated by a virus inter alii. Thus, hypertension may possibly be compared with other auto-immune disease where virus infections and genetic conditions are of great significance in the pathogenesis.
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PMID:[Immunologic reactions in essential hypertension]. 218 47


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