The secondary and tertiary inflammatory cellular reaction in arterioles damaged by acute angiotensin-hypertension in rats.

When rats were treated repeatedly with series of intravenous injections of angiotensin, intervals between the series covering at least one week, the cellular reaction in the arterioles damaged by the hypertension differed from that to be found after only one series of injections (primary reaction). While the primary reaction showed equal numbers of mononuclear cells and polymorphous leucocytes at onset of the luminal cellular reaction and a duration of about 72 hours, the secondary and tertiary reactions differed (in identical way) with dominance of mononuclear cells from onset and to termination of the cellular reaction, with appearance of polymorphous leucocytes in the adventitia, and with a markedly prolonged duration of the reaction, up to more than 96 hours. Finally, the total number of mononuclear cells which infiltrated the damaged arterioles after the termination of the second and third hypertensive period was 3–10 times higher than that found after the first hypertensive period. It was found that the changed reaction was not caused by a development of impaired areas of the arterioles damaged during the first hypertensive period. As the secondary reaction has much in common with a delayed type of hypersensitivity the possible antigen was discussed, and angiotensin was found not to be responsible.

[1]  F. Olsen Lysosomes and pyroninophilia in mononuclear cells in hypertensive arterioles. Studies on the blood, arterioles and regional lymph nodes in experimental angiotensin-hypertension in rats. , 2009, Acta pathologica et microbiologica Scandinavica. Section A, Pathology.

[2]  F. Olsen Type and course of the inflammatory cellular reaction in acute angiotensin-hypertensive vascular disease in rats. , 2009, Acta pathologica et microbiologica Scandinavica. Section A, Pathology.

[3]  F. Milgrom,et al.  Rabbit autoantibodies to aorta. , 1969, Journal of immunology.

[4]  F. Olsen Penetration of circulating fluorescent proteins into walls of arterioles and venules in rats with intermittent acute angiotensin-hypertension. , 2009, Acta pathologica et microbiologica Scandinavica.

[5]  G. Pickering,et al.  The production and resolution of hypertensive vascular lesions in the rabbit. , 1967, Clinical science.

[6]  F. Paronetto IMMUNOCYTOCHEMICAL OBSERVATIONS ON THE VASCULAR NECROSIS AND RENAL GLOMERULAR LESIONS OF MALIGNANT NEPHROSCLEROSIS. , 1965, The American journal of pathology.

[7]  A. Grollman,et al.  EXPERIMENTAL PERIARTERITIS NODOSA IN THE RAT. , 1964, Archives of pathology.

[8]  B. Waksman,et al.  RADIOAUTOGRAPHIC STUDY OF CELLULAR MECHANISMS IN DELAYED HYPERSENSITIVITY: II. Experimental Allergic Encephalomyelitis in the Rat , 1963, Journal of neuropathology and experimental neurology.

[9]  B. Waksman,et al.  Radioautographic study of cellular mechanisms in delayed hypersensitivity. I. Delayed reactions to tuberculin and purified proteins in the rat and guinea-pig. , 1963, Immunology.

[10]  G. Schloss Die Histogenese und Pathogenese der Gefäβveränderungen beim experimentellen renalen Drosselungshochdruck der Ratte , 1948, Pathobiology.

[11]  P. Zeek,et al.  Periarteritis Nodosa in Experimental Hypertensive Rats and Dogs. , 1944, The American journal of pathology.