Intra-Renal Factors in Renin Release
W. S. Peart
Abstract
W. S. Peart
Abstract
Renin release is believed to depend more on vasodilatation in the afferent arteriole than on any other factor. This allows for opposing effects of vasoconstriction and vasodilatation produced by sympathetic nerve stimulation by drugs or by autoregulation, to be interpreted in relation to the study of stretch of the afferent arteriole. This reduces but does not remove the necessity for alternate control through the macula densa. A final common pathway for all these stimuli is suggested through alterations in net calcium flux in the juxtaglomerular cell where increased intracellular calcium inhibits, and decreased intracellular calcium increases, renin release.
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Renin release is believed to depend more on vasodilatation in the afferent arteriole than on any other factor. This allows for opposing effects of vasoconstriction and vasodilatation produced by sympathetic nerve stimulation by drugs or by autoregulation, to be interpreted in relation to the study of stretch of the afferent arteriole. This reduces but does not remove the necessity for alternate control through the macula densa. A final common pathway for all these stimuli is suggested through alterations in net calcium flux in the juxtaglomerular cell where increased intracellular calcium inhibits, and decreased intracellular calcium increases, renin release.
Key concepts: Afferent arterioles, Macula densa, Arteriole, Vasodilation, Tubuloglomerular feedback, Vasoconstriction, Renin–angiotensin system, Autoregulation