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高血壓成因的研究－由自發性高血壓鼠得來的線索
Studies on the Mechanisms of Essential Hypertension-Informations from the Spontaneously Hypertensive Rat (SHR)
摘要
自從Goldblatt于1934年成功地在動物身上引發腎性高血壓之後，許多型式的高血壓陸續在動物身上產生，這些高血壓的型式類似人類不同病因的續發性高血壓。1963年，Okamoto及Aoki成功地培育了一種日本（京都）種的遺傳性或自發性高血壓鼠（稱為SHR），以SHR為主的若干遺傳性高血壓鼠或兔在近來年成為研究人類本態性高血壓成因的動物模式。SHR及另外一種紐西蘭種（GHR）因為遺傳的因子而對環境及情緒的刺激過度敏感，因而引發交感神經興奮，神經的因素，特別是較高級中樞的刺激在引發高血壓的初期扮演重要腳色。另外一種米蘭種高血壓鼠（MHR）則可能因為遺傳性的腎功能異常，也代表了一部人類本態性高血壓（特別是低腎素高血壓）的型式。不論初期引發因素的性質為何，血管構造上的改變，諸如管壁肥厚，平滑肌以及膠質與纖維物質增生等，均可在SHR，MHR及其他遺傳性或非遺傳性高血壓動物身上發生，這些由於長期高血壓的續發性血管變化成為後期加速及維持高血壓狀態的主要因素。而且血管的變化加強了初期的引發因素，更與高血壓之間形成一正性迴饋的關係。在早期當血管的續發變化尚未十分嚴重之前，藥物的降血壓治療有良好的效果，而且可以減少血管之變化以及高血壓之惡化。一旦血管的變化繼續加重而成為不可逆性的病變時，藥物的降血壓治療則通常無法令人滿意。雖然對於人類本態性高血壓的成因仍有許多未解決之問題，但是由自發性高血鼠之研究結果中供給我們不少線索。
關鍵字
無資料並列摘要
Since Goldblatt produced renal hypertension in 1934, many types of hypertension which resemble secondary hypertension in man have been reproduced in animals. In 1963, Okamoto and Aoki developed a Japanese (Kyoto) strain of spontaneously hypertensive rats (SHR). Several strains of genetically hypertensive rats, primarily SHR, have been the subject for studies on the mechanisms of human essential hypertension. The SHR and New Zealand strain (GHR) are genetically overactive to environmental and emotional stimuli that induce sympathetic activation. Neurogenic factors, mainly of higher central origin, play an important role in the initiation of hypertension. Another strain of genetically hypertensive rats, the Milan hypertensive rats (MHR), on the other hand, illustrates a genetic deviation of renal function, which may simulates some variants of low-renin hypertension in man. Regardless of the nature of initiating factors, structural vascular changes such as thickening of the vascular wall with proliferation of smooth muscle and increased amount of collagenous and fibrous elements have been demonstrated in SHR, MHR and other genetically or nongenetically hypertensive animals. The vascular changes secondary to long term hypertension are responsible for the acceleration and maintenance of hypertensive state. They reinforce the initiating factors and have a positive feedback relationship with the blood pressure. Antihypertensive treatment with pharmacological agents is effective at early age when the vascular alterations are still minimal. Once the structural changes of vascular beds progress and become irreversible, antihypertensive treatment is always not satisfactory. Although there are still questions remain unresolved, studies on the SHR and other genetically hypertensive strains provide ample informations to the understanding of essential hypertension in man.