Neural and non-neural mechanisms in spontaneous hypertension.
1. The pathogenesis of hypertension in spontaneously hypertensive rats (SHR) is considered to consist of neurogenic and non-neurogenic factors, both of which contribute to initiation and maintenance mechanisms. 2. Neurogenic factors have been demonstrated by the destruction of the central nervous system, sympathectomy, recording of sympathetic discharge, hind-limb perfusion and study of noradrenaline. These factors are mainly involved in the initiation of hypertension, and they appear to diminish in importance after the establishment of hypertension, as indicated by the noradrenaline-turnover study. 3. The non-neurogenic factors have been demonstrated haemodynamically by increased peripheral vascular resistance remaining even after sympathectomy. They have also been demonstrated histologically by the narrowing of resistance arteries with medial hyperplasia or hypertrophy. These factors appear to participate in maintenance mechanisms. 4. Increased incorporation of labelled amino acid into non-collagenous and collagenous protein of the arterial walls precedes medial hypertrophy and hyertensive arteriosclerosis. It seems to play a role therefore both during neurogenic initiation and later non-neurogenic maintenance of blood pressure. 5. Non-collagenous protein metabolism of arterial walls is increased in young SHR, and it is partly dependent on neural innervation as detected by surgical or pharmacological sympathectomy. It indicates a close linkage between neurological and structural changes in the initiation of spontaneous hypertension.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D008638:Mesenteric Arteries / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D051381:Rats; D013153:Splanchnic Nerves / Q000502:physiology; D013562:Sympathectomy; D014655:Vascular Resistance
D011506:Proteins; D009638:Norepinephrine