Exocrine and endocrine release of kallikrein after reflex‐induced salivary secretion

Wiley - Tập 139 Số 1-2 - Trang 29-37 - 1990
Torill Berg1, Liv Johansen2, Knud Poulsen3
1Institute of Physiology, University of Oslo, Norway
2Neurochemical Laboratory, University of Oslo, Norway
3Department of Biochemistry, Royal Dental School, Copenhagen, Denmark

Tóm tắt

Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and β‐adrenergic stimulation but greatly increased after α‐adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex‐induced salivary gland response.Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P < 0.005). Only heat stress increased circulating glandular kallikrein (12.7 ± 0.8 ng ml‐1 before heat exposure and 53.3 ± 14.1 ng ml‐1 40 min afterwards, P < 0.005). There were no indications that the endocrine release of kallikrein was due to non‐specific leakage. Atropine abolished heatinduced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P < 0.05). However, phentolamine did not, which may indicate an as yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P < 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.

Từ khóa


Tài liệu tham khảo

10.1113/jphysiol.1982.sp014050

BÆKKELUND PEDERSEN E., 1983, Aggression‐provoked huge release of submaxillary mouse renin to saliva, Acta Endocrinol, 104, 510

10.1177/28.8.7003006

BERG T., 1985, Enzymatic activity of glandular kallikrein released into the vascular compartment after autonomic stimulation of the rat submandibular gland, Am J Physiol, 249, H1134

10.1161/01.HYP.14.1.73

10.1016/0006-2952(71)90292-9

10.1038/2081102a0

10.1113/jphysiol.1958.sp006011

10.1139/y71-074

10.1016/0022-1759(83)90192-8

10.1016/0022-1759(84)90323-5

10.1111/j.1476-5381.1982.tb09318.x

MALING H. M., 1972, Salivation in mice as an index of adrenergic activity. III. Partial dependency of adrenergic activity, Arch Int Pharmacodyn, 199, 344

10.1152/ajpendo.1978.234.5.E480

MENZIE J. W., 1974, Sympathetic nervous system and renin release from submaxillary glands and kidneys, Am J Physiol, 227, 1281, 10.1152/ajplegacy.1974.227.6.1281

10.3109/00016358209019806

10.3109/00016358709097539

10.1111/j.1748-1716.1978.tb06298.x

10.1111/j.1748-1716.1977.tb05919.x

ØRSTAVIK T. B., 1975, Cellular localization of kallikreins in rat submandibular and sublingual salivary glands. Immunofluorescence tracing related to histological characteristics, Acta Histochem, 54, 183

ØRSTAVIK T. B., 1982, Kallikrein–kinin system in regulation of submandibular gland blood flow, Am J Physiol, 242, H1010

10.1161/01.RES.51.3.385

10.1161/01.HYP.5.2.180

10.1161/01.RES.52.6.635

SCHACHTER M., 1979, Handbook of Experimental Pharmacology: Bradykinin, Kallidin and Kallikrein, 400

10.1016/S0074-7696(08)61277-2

TOMI«‐BELESLIN N., 1983, The effect of anticholinesterases on salivation in cats. lugoslav, Physiol Pharmacol Acta, 19, 230

TOMI«‐BELESLIN N., 1983, Central cholinoceptive receptors and salivation, Period Biol, 85, 160

Thông tin
Thông tin xuất bản

Wiley

Tập 139 Số 1-2

29-37

Thông tin tác giả