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一般认为自发性高血压(SH)鼠主要是由于血管平滑肌的钙代谢异常,导致外周血管收缩性改变所致。其神经机制可能是下丘脑引起交感神经活动升高。压力感受性反射损害也可能加重交感神经活动异常。但也可能存在使血管平滑肌的钙代谢异常和引起其收缩性改变的体液因素。作者已从(SH)鼠的红细胞中抽提到一种酸性的钙依赖性肽。应用分离到的酸性肽给6周龄的正常血压鼠脑室内注射0.1nmol,就引起血压升高25mmHg,持续3～5天之久。如果连续注射
Is generally believed that spontaneous hypertension (SH) rats are mainly due to abnormal calcium metabolism of vascular smooth muscle, resulting in changes in peripheral vasoconstriction caused. Its neural mechanism may be caused by hypothalamus sympathetic activity. Baroreflex damage may also worsen sympathetic activity. However, there may also be humoral factors that alter the calcium metabolism of vascular smooth muscle and cause changes in its contractility. The authors have extracted an acidic calcium-dependent peptide from mouse erythrocytes (SH). Application of isolated acidic peptides to 6-week-old normolamice injected intracerebroventricularly with 0.1 nmol resulted in an increase of 25 mmHg in blood pressure for 3 to 5 days. If continuous injection