[Mechanisms of hypertension in the central nervous system].
This article reviews studies by the author on central mechanisms of hypertension. Spontaneously hypertensive rats (SHR) have been developed as a rat model of genetic hypertension, and central acetylcholine has been implicated in hypertension in SHR. The rostral ventrolateral medulla (RVL), a major source of efferent sympathetic activity, has cholinergic pressor systems. The release of acetylcholine is enhanced in the RVL of SHR, leading to hypertension. The alteration of the RVL cholinergic system in SHR results from enhanced angiotensin systems in the anterior hypothalamic area (AHA). Angiotensin II-sensitive neurons are present in the AHA and they are tonically activated by endogenous angiotensins. The basal activity of AHA angiotensin II-sensitive neurons is enhanced in SHR, mainly due to enhanced sensitivity of AHA neurons to angiotensin II. The AHA angiotensin system is also responsible for hypertension induced by emotional stress and central Na(+) increases. These findings suggest that the AHA angiotensin system may play a critical role in the development of hypertension.
Kubo
Takao
T
Showa Pharmaceutical University, Machida City, Japan. t.kubo@cityfujisawa.ne.jp
D000109:Acetylcholine / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007032:Hypothalamus, Anterior / Q000502:physiology / Q000503:physiopathology*; D008526:Medulla Oblongata / Q000378:metabolism*; D009474:Neurons / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D012084:Renin-Angiotensin System / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D013315:Stress, Psychological / Q000503:physiopathology
D000804:Angiotensin II; D012964:Sodium; D000109:Acetylcholine