Key result
Experimental hypertension triggers splenic amyloid deposits in up to ~20% of mice.
Why the study?
The relationship between experimental hypertension and secondary amyloidosis development in mice was not well characterized.
Does the induction of experimental hypertension cause amyloidosis in mice?
Does the induction of experimental hypertension cause amyloidosis in mice?
Experimental hypertension in mice can induce secondary amyloidosis, suggesting hypertensive vascular disease stimulates the reticuloendothelial system.
Splenic amyloidosis arises in some hypertensive mouse models; leaves open any role in human disease.
Following the induction of three different forms of experimental hypertension, deposits of amyloid were found in the spleens of 5-20 per cent of the mice late in the course of the hypertension, Amyloidosis was found in nude (with genetical aplasia of the thymus) as well as in haired (normal) mice. The highest frequency of amyloidosis was observed in mice with hypertension due to partial infarction of one kidney and contralateral nephrectomy. The hypertensive vascular disease, involving lesion of the vessels and of the organs supplied by the affected vessels, is believed, to represent a stimulus for the reticulo endothelial system (RES) with development of amyloidosis as a secondary event.
No takes yet. Share an insight, caveat, or question.
Ulrik Gerner Svendsen (1977) studied Experimental hypertension. Induction of experimental hypertension was evaluated on Deposits of amyloid in the spleens. Following the induction of experimental hypertension, amyloid deposits were found in the spleens of 5-20% of mice, with the highest frequency in those with partial kidney infarction.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: