Chapman I D, Leach J T, Bhoola K D
Adv Exp Med Biol. 1986;198 Pt B:219-24. doi: 10.1007/978-1-4757-0154-8_27.
Urinary kallikrein excretion, active (A) and total (T), was significantly reduced in the Okamato spontaneously hypertensive rat (SHR). The renal content of A and T soluble tissue kallikrein was clearly greater in this strain. Arginine vasopressin stimulated the release of both A and T kallikrein from renal cortical slices of the normotensive (N) Wistar strain, this response was not observed in the SHR. PGE2 stimulated release of A kallikrein in the N strain and both A and T enzyme in the SHR. It is suggested that urinary kallikrein excretion values may not necessarily reflect the endogenous levels of the enzyme in the kidney. Both the level and release of renal tissue kallikrein may become altered either in response to or as a result of chronically elevated blood pressure.
在冈本自发性高血压大鼠（SHR）中，尿激肽释放酶排泄量，包括活性（A）和总量（T），显著降低。该品系中A和T可溶性组织激肽释放酶的肾含量明显更高。精氨酸加压素刺激正常血压（N）的Wistar品系肾皮质切片释放A和T激肽释放酶，但在SHR中未观察到这种反应。前列腺素E2刺激N品系中A激肽释放酶的释放，以及SHR中A和T激肽释放酶的释放。提示尿激肽释放酶排泄值不一定反映肾脏中该酶的内源性水平。肾组织激肽释放酶的水平和释放可能会因慢性血压升高而发生改变，或者是慢性血压升高的结果。
