Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release.
نویسندگان
چکیده
We evaluated whether the brain kallikrein-kinin system plays a role in the regulation of adrenocorticotropin (ACTH) release in rats. Intracerebroventricular (icv) injection of bradykinin (0.24 nmol) increased plasma immunoreactive ACTH (irACTH) levels (from 93 +/- 4 to 200 +/- 12 pg/ml, P less than 0.01). This effect was prevented by icv kinin antagonist at 15.4 nmol/h (from 98 +/- 5 to 108 +/- 6 pg/ml; not significant). The antagonist did not alter the increase in plasma irACTH levels induced by icv corticotropin-releasing factor (CRF), arginine vasopressin, or prostaglandin E2. Melittin (7 nmol/h icv) increased plasma irACTH from 95 +/- 4 to 268 +/- 7 pg/ml (P less than 0.01). This effect was prevented by icv kinin antagonist (15.4 nmol/h), kallikrein antibodies (13 pmol/h), or indomethacin (0.28 mmol/h). ACTH response to melittin was not altered by antagonists of CRF or vasopressin. Intra-arterial injection of insulin (0.3 IU/kg body wt) reduced plasma glucose levels to a similar extent in rats given icv kinin antagonist or vehicle; the ACTH response to insulin-induced hypoglycemia was slightly less in rats given kinin antagonist than in those given vehicle (55 +/- 5 vs. 86 +/- 4 pg/ml, P less than 0.05). The brain kallikrein-kinin system may play a role in the regulation of ACTH secretion in stimulated conditions.
منابع مشابه
The brain kallikrein-kinin system. A possible role in blood pressure regulation.
During the last decade, the actions of central nervous system peptides on blood pressure and volume homeostasis have been the subject of intense investigation. There is evidence that central mechanisms of cardiovascular control could be modulated by brain peptides. Kinins are biologically active peptides released from kininogen by either glandular or plasma kallikrein. Kinins in the central ner...
متن کاملA Possible Role in Blood Pressure Regulation
During the last decade, the actions of central nervous system peptides on blood pressure and volume homeostasis have been the subject of intense investigation. There is evidence that central mechanisms of cardiovascular control could be modulated by brain peptides. Kinins are biologically active peptides released from kininogen by either glandular or plasma kallikrein. Kinins in the central ner...
متن کاملTowards understanding the kallikrein-kinin system: insights from measurement of kinin peptides.
The kallikrein-kinin system is complex, with several bioactive peptides that are formed in many different compartments. Kinin peptides are implicated in many physiological and pathological processes including the regulation of blood pressure and sodium homeostasis, inflammatory processes, and the cardioprotective effects of preconditioning. We established a methodology for the measurement of in...
متن کاملRole of the kallikrein–kinin system in traumatic brain injury
Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite improvements in acute intensive care, there are currently no specific therapies to ameliorate the effects of TBI. Successful therapeutic strategies for TBI should target multiple pathophysiologic mechanisms that occur at different stages of brain injury. The kallikrein-kinin system is a promising therape...
متن کاملSpatial reference memory deficits precede motor dysfunction in an experimental autoimmune encephalomyelitis model: The role of kallikrein–kinin system
Multiple sclerosis (MS) is a progressive T cell-mediated autoimmune demyelinating inflammatory disease of the central nervous system (CNS). Although it is recognized that cognitive deficits represent a manifestation of the disease, the underlying pathogenic mechanisms remain unknown. Here we provide evidence of spatial reference memory impairments during the pre-motor phase of experimental auto...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- The American journal of physiology
دوره 262 3 Pt 1 شماره
صفحات -
تاریخ انتشار 1992