Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that "noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem" (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-β-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ("adaptive metabolic change", Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development o hypertension (neurovascular linkage, Yamori, 1975). From these findings, it can be concluded that labile hypertension primarily caused by neurogenic mechanisms is stabilized or maintained by medial hypertrophy of the arterial walls as well as by hypertensive diffuse arteriosclerosis. This hypertrophy is induced by increased noncollagenous protein synthesis due to pressure load or to increased vasomotor tone. Arteriosclerosis is induced secondarily by the increased collagenous protein metabolism due to hypertension. The accelerated vascular protein metabolism preceding structural alteration of the arterial walls is "the final common mechanism", important for the maintenance mechanism of various hypertensions. It obscures the primary cause of hypertension in spontaneous hypertension as well as probably in essential hypertension in man.