Tubule-vascular feedback in renal autoregulation

Abstract

Afferent arteriole (Af-Art) diameter regulates pressure and flow into the glomerulus, which are the main determinants of the glomerular filtration rate. Thus, Af-Art resistance is crucial for Na+ filtration. Af-Arts play a role as integrative centers, where systemic and local systems interact to determine the final degree of resistance. The tubule of a single nephron contacts an Af-Art of the same nephron at two locations: in the transition of the thick ascending limb to the distal tubule (macula densa) and again in the connecting tubule. These two sites are the anatomic basis of two intrinsic feedback mechanisms: tubule-glomerular feedback and connecting tubule-glomerular feedback. The cross communications between the tubules and Af-Arts integrate tubular Na+ and water processing with the hemodynamic conditions of the kidneys. Tubule-glomerular feedback provides negative feedback that tends to avoid salt loss, and connecting tubule-glomerular feedback provides positive feedback that favors salt excretion by modulating tubule-glomerular feedback (resetting it) and increasing glomerular filtration rate. These feedback mechanisms are also exposed to systemic modulators (hormones and the nervous system); however, they can work in isolated kidneys or nephrons. The exaggerated activation or absence of any of these mechanisms may lead to disequilibrium in salt and water homeostasis, especially in extreme conditions (e.g., high-salt diet/low-salt diet) and may be part of the pathogenesis of some diseases. In this review, we focus on molecular signaling, feedback interactions, and the physiological roles of these two feedback mechanisms.

Safety analysis regarding acute kidney injuries for chloride‐restrictive intravenous fluid administration against that of chloride‐liberal for patients admitted in the medical intensive care unit: A non‐randomised retrospective (chrachl‐mic) study

“…Tubular chloride reabsorption leads to the renal vasoconstrictive effect and responsible for acute kidney injuries 3 . Also, high tubular chloride reabsorption activates the tubule‐glomerular feedback and reduces the glomerular filtration rate 21 . Chloride‐liberal intravenous fluid (angiotensin II antagonist) induces thromboxane release that is associated with vasoconstriction 3 .…”

“…3 Also, high tubular chloride reabsorption activates the tubule-glomerular feedback and reduces the glomerular filtration rate. 21 Chloride-liberal intravenous fluid (angiotensin II antagonist) induces thromboxane release that is associated with * Significantly lower than a chloride-liberal cohort vasoconstriction. 3 The current study reported that several mechanisms through chloride-liberal intravenous fluid may cause acute kidney injuries.…”

DMOG, a Prolyl Hydroxylase Inhibitor, Increases Hemoglobin Levels without Exacerbating Hypertension and Renal Injury in Salt-Sensitive Hypertensive Rats

“…HIF1a induces CD73 (ecto-5-prime-nucleotidase) (Synnestvedt et al, 2002) and increases adenosine signaling. In the kidney, adenosine is a vasoconstrictor involved in tubuloglomerular feedback responses (Schnermann, 2015;Romero and Carretero, 2019). Upregulation of CD73 has been reported to protect the kidney from ischemia-reperfusion injury and diabetic nephropathy (Tak et al, 2014;Sung et al, 2017).…”

Mechanism of herbal medicine on hypertensive nephropathy (Review)

“…Hypertension usually lasts for >10 years before the gradual emergence of nocturia, mild proteinuria and other associated clinical symptoms ( 14 ). This disease is usually preceded by distal tubular dysfunction, followed by glomerular dysfunction ( 15 , 16 ). The patient's renal pathology starts with renal arteriopathy, followed by ischemic renal parenchymal damage ( 11 ).…”