Tissue Kallikrein Levels Research Articles

Tissue kallikrein and tonin levels in submandibular glands of STZ-induced diabetic rats and the effects of insulin

Tissue kallikrein and tonin levels in submandibular glands of STZ-induced diabetic rats and the effects of insulin

Bioregulatory role of the kallikrein-kinin system in the normal pituitary gland and its tumours.

Tissue kallikrein, a serine protease, is present in the prolactin-secreting cells of the normal anterior pituitary gland and pituitary adenomas. It is mainly located in the Golgi apparatus, but is also present in secretory granules. There is a distinct sexual dimorphism, with amount of tissue kallikrein being greater in anterior pituitary tissue from female rats. The intracellular levels of tissue kallikrein are increased by estradiol and in pituitary tumours, and decreased by ovariectomy, dopamine and its agonists. There is preliminary in vitro evidence that tissue kallikrein may be involved in the intracellular processing of the prolactin molecule before secretion. Tissue kallikrein synthesizes kinins which are present in the anterior pituitary and are capable of stimulating prolactin and growth hormone secretion by activating the phosphoinositide second messenger system. Prolactin physiology is uniquely linked to the kallikrein-kinin system in the normal pituitary and its tumours. Tissue kallikrein may have an important role in the pathophysiology of prolactin-secreting pituitary adenomas.

Protective effect of cicletanine on hypertension-induced decreases in the renal kallikrein-kinin and prostaglandin systems in stroke-prone spontaneously hypertensive rats.

We investigated the effect of two oral (p.o.) doses of cicletanine (5 and 30 mg/kg/day) for 4 weeks on urinary excretion (UKE), renal concentration (RKC) of kallikrein, and prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha urinary excretion of stroke-prone (SP) spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) rats submitted to a high sodium intake (1%). Both doses of cicletanine induced a significant antihypertensive effect in treated SHR as compared with hypertensive untreated controls (HC). After 4-week treatment, a significant difference in mortality was observed between normotensive controls (NC) (0%) and HC (84%). Both doses of cicletanine reduced the mortality of hypertensive animals (8% SHR with 5 mg and 24% SHR with 30 mg vs. 84% in HC). Whereas UKE and RKC were decreased in HC during the progression of untreated hypertension from week 1 to week 4, both doses of cicletanine administration significantly prevented this decrease. Consistently with maintenance of UKE during the course of hypertension, the level of tissue kallikrein was higher in hypertensive cicletanine-treated than in untreated SHR. This increased RKC was associated with a significantly higher rate of kallikrein biosynthesis. The increased level of the urinary excretion and tissue concentration of PGE2 and 6-keto-PGF1 alpha in cicletanine-treated SHR as compared with untreated animals was also of interest. This protective effect on PG excretion correlated with that on kallikrein excretion. The results confirm the efficiency of cicletatine as an antihypertensive treatment. The antihypertensive action includes protective effects on potential vasodepressor kallikrein-kinin and prostaglandin systems.(ABSTRACT TRUNCATED AT 250 WORDS)