Title

Regulation of renin processing and secretion: chemiosmotic control and novel secretory pathway

UMMS Affiliation

Department of Psychiatry; Department of Physiology

Publication Date

1993-08-01

Document Type

Article

Subjects

Animals; Biological Transport; *Carbohydrate Epimerases; Carrier Proteins; Cytoplasmic Granules; Enzyme Precursors; Enzymes; Humans; Ion Channels; Osmosis; Receptors, Cell Surface; Renin; Signal Transduction

Disciplines

Psychiatry

Abstract

The renin-angiotensin-aldosterone system (RAAS) plays an important role in cardiovascular and electrolyte regulation in health and disease. Juxtaglomerular cells in the kidney regulate endocrine RAAS by physiologically controlling conversion of prorenin and secretion of renin. The classical baroceptor, neurogenic, and macula densa mechanisms regulate renin expression at the cellular level by Ca2+, adenosine 3',5'-cyclic monophosphate (cAMP), and chemiosmotic forces (K+, Cl-, and water flux coupled to H+ movement). The baroceptor mechanism (through Ca2+) activates K+ and Cl- channels in the surface membrane and deactivates a KCl-H+ exchange chemiosmotic transporter in the secretory granular membrane. The neurogenic mechanism (through cAMP) promotes prorenin processing to renin. The macula densa mechanism (through K+ and Cl-) involves the processing of prorenin to renin. Ca2+, by inhibiting the KCl-H+ exchange transporter, prevents secretory granules from engaging in chemiosmotically mediated exocytosis. cAMP, on the other hand, by stimulating H+ influx, provides the acidic granular environment for prorenin processing to renin. It is concluded that, in the presence of a favorable chemiosmotic environment, prorenin is processed to renin, which may then be secreted by regulative degranulation or divergence translocation, a novel secretory pathway used by several secretory proteins, including renin.

Source

Am J Physiol. 1993 Aug;265(2 Pt 1):C305-20.

Journal/Book/Conference Title

The American journal of physiology

Related Resources

Link to Article in PubMed

PubMed ID

7690183

Link to Full Text

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