Cell volume and peptide hormone secretion.
In general way cell swelling evokes and shrinking inhibits exocytosis of proteins and peptides stored in secretory vesicles from various types of cells. Dynamics of this type of hormone secretion is indistinguishable from that induced by specific secretagogue. Peculiarities of swelling-induced secretion indicate an involvement of the unique signaling pathway. Hyposmotic stimulation of insulin secretion is independent from the extra- and intracellular Ca(2+), does not involve other intracellular mediators of glucose stimulation, and could not be inhibited by noradrenaline. Swelling-induced peptide secretion is not essential for cell volume control. Hyposmotic stimulation is a useful research tool when natural or pharmacological secretagogue is unknown: Thyrotropin releasing hormone release from the heart slices, pancreatic islets and various brain structures was characterized by the stimulation by hypotonic medium. Swelling-induced exocytosis possesses limited selectivity; cells involved in water and salt regulation retain their specific response to osmotic stimuli; hypotonic medium evokes thyrotropin releasing hormone but not oxytocin (OT) release from hypothalamic paraventricular nucleus. Specific response (release after hyperosmotic stimulation) of intranuclear OT secretion in the paraventricular nucleus and the supraoptic nucleus could be obviated by GdCl(3) and at these conditions OT release to swelling-inducing stimuli emerged. Swelling-induced hormone secretion can have pathophysiological implications. For example, a shift to anaerobic glycolysis and production of metabolites occurring in ischemia results in the increased intracellular osmolarity and cell swelling. Peptides and proteins released after swelling could play an important role in the pathophysiology of ischemia and be mediators of local or remote preconditioning when factors released at the place of ischemia have protective effect against ischemia-reperfusion injury. Moreover, the ischemic disruption of the osmotic receptors could result in a syndrome of inappropriate hormone secretion.
Strbák
Vladimír
V
Institute of Experimental Endocrinology, Centre of Excellence Acknowledged by European Commission, Slovak Academy of Sciences, Institute of Normal and Pathological Physiology, Slovak Medical University, Bratislava, Slovakia.
D000222:Adaptation, Physiological; D000818:Animals; D001692:Biological Transport / Q000502:physiology; D015220:Calcium Channels / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000502:physiology; D048429:Cell Size; D005110:Extracellular Space / Q000378:metabolism; D042541:Intracellular Space / Q000378:metabolism; D009997:Osmotic Pressure; D036361:Peptide Hormones / Q000378:metabolism*; D051381:Rats; D012680:Sensitivity and Specificity; D015398:Signal Transduction / Q000502:physiology*; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism; D014882:Water-Electrolyte Balance / Q000502:physiology*
D015220:Calcium Channels; D036361:Peptide Hormones; D013973:Thyrotropin-Releasing Hormone