The influence of the pituitary on arterial intimal proliferation in the rat.
The formation of arteriosclerotic fibromusculoelastic intimal thickening following arterial de-endothelialization is well documented. Recent findings, both in vitro and in vivo, suggest that platelets are a major participant in the pathogenesis of this lesion by releasing a mitogen to medial smooth muscle cells (SMC). This mitogen results in SMC migration to and proliferation within the intima. A similar mitogen has been described as originating in brain and pituitary tissue. We now report that, in hypophysectomized rats with normal platelet counts, intimal hyperplasia is markedly delayed; pair-fed intact controls normally develop lesions. It therefore appears that the pituitary gland plays a significant role in the experimental arteriosclerotic response.
D000818:Animals; D001011:Aorta / Q000473:pathology; D001161:Arteriosclerosis / Q000209:etiology* / Q000473:pathology; D001792:Blood Platelets / Q000378:metabolism; D004727:Endothelium / Q000473:pathology; D006965:Hyperplasia / Q000473:pathology; D007016:Hypophysectomy; D008297:Male; D008934:Mitogens / Q000378:metabolism; D010902:Pituitary Gland / Q000378:metabolism / Q000502:physiology*; D051381:Rats
D008934:Mitogens