1932

Abstract

In the adult organism, systemically circulating renin almost exclusively originates from the juxtaglomerular cells in the afferent arterioles of the kidneys. These cells share similarities with pericytes and myofibro-blasts. They store renin in a vesicular network and granules and release it in a regulated fashion. The release mode of renin is not understood; in particular, the involvement of SNARE proteins is unknown. Renin release is acutely increased via the cAMP signaling pathway, which is triggered mainly by catecholamines and other G-coupled agonists, and is inhibited by calcium-related pathways that are commonly activated by vasoconstrictors. Renin release from juxtaglomerular cells is directly modulated in an inverse fashion by the blood pressure inside the afferent arterioles and by the chloride content in the tubule fluid at the macula densa segment of the distal tubule. Renin release is stimulated by nitric oxide and by prostanoids released by neighboring endothelial and macula densa cells. Steady-state renin concentrations in the plasma are determined essentially by the number of renin-producing cells in the afferent arterioles, which changes in parallel with challenges to the renin-angiotensin-aldosterone system.

Loading

Article metrics loading...

/content/journals/10.1146/annurev-physiol-012110-142238
2011-03-17
2024-06-19
Loading full text...

Full text loading...

/content/journals/10.1146/annurev-physiol-012110-142238
Loading
/content/journals/10.1146/annurev-physiol-012110-142238
Loading

Data & Media loading...

  • Article Type: Review Article
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error