Kenneth D. Mitchell

TL;DR: There has been an explosive growth of interest in the multiple interacting paracrine systems that influence renal microvascular function, and this review first discusses the membrane activation mechanisms for renal vascular control and discusses unique mechanisms that may be responsible for differential regulation of medullary blood flow by locally formedParacrine agents.

TL;DR: The data obtained from perfused tubules indicate that the proximal tubule adds substantial amounts of ANG II or a precursor into the tubular lumen, providing further evidence that intratubular ANG II concentrations are in the nanomolar range and are regulated independently of the plasma ANG II levels.

TL;DR: Findings indicate that proximal tubular fluid contains nanomolar concentrations of angiotensin I as well as angiotENSin II, which greatly exceed the plasma and kidney levels and likely reflect net secretion of the angiotsin peptides by proximal Tubular fluid cells.

TL;DR: It is suggested that qualitatively different mechanisms may be responsible for the elevated intrarenal angiotensin I and Ang II levels during the initial and maintenance phases of renal hypertension.

TL;DR: The augmentation of intrarenal ANG II is due to receptor-mediated internalization and continued ANG II formation, which provide a hypertensinogenic stimulus.