Cardiovascular effects of allylamine and β-aminopropionitrile exposure in rats

In rats exposure to allylamine (AA, 3-aminopropene) and β-aminopropionitnle (βAPN) produces a profound vascular synergism with medial smooth muscle necrosis and development of aortic aneurysm. To further characterize AA and βAPN toxicity, cardiovascular parameters were measured during a ten-day AA and βAPN exposure (100 mg·kg^-1 and 1 g·kg^-1 by gavage) in male rats (180-200 g; n=8). AA and βAPN significantly decreased heart rate, systolic blood pressure and body mass. Thoracic aortic rings (∼3 mm) were removed, and reactivity to contractile and relaxant agonists was tested in vitro. Aortic rings from treated rats were contracted significantly less by high potassium (50 mM) and by norepmephrine (NE, 10 μM) than anatomically-matched control rat aortic rings There was a decrease in aortic NE sensitivity but no change in the percentage relaxation with acetylchohne (10 μM) or sodium mtroprusside (100 μM) in treated rat aortic rings Treated rats with severe aortic medial smooth muscle necrosis had the greatest reduction in systolic blood pressure and aortic contractility The data show that AA and βAPN-stimulated medial smootn muscle necrosis is accompanied by an overall reduction in cardiovascular function.