title: [Immunologic reactions in essential hypertension].
abstract: 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.
authors.forename: U O
authors.initials: UO
authors.lastname: Andersen
mesh_terms: D000818:Animals; D000906:Antibodies / Q000032:analysis; D003167:Complement Activation / Q000235:genetics; D006801:Humans; D006973:Hypertension / Q000276:immunology*; D007111:Immunity, Cellular / Q000235:genetics; D051381:Rats
chemical_list: D000906:Antibodies
vernacular_title: Immunologiske reaktioner ved essentiel hypertension.