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Urinary system
Published in Aida Lai, Essential Concepts in Anatomy and Pathology for Undergraduate Revision, 2018
Juxtaglomerular apparatus: macula densa cells of DCT – sense fall in GFR → release reningranular cells of afferent arteriole – sense reduction in stretch of afferent arteriole → release reninsympathetic renal nerves – release renin when blood pressure drops
Control of blood vessels: intrinsic control
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
In the kidney, the myogenic response accounts for roughly half of the autoregulation. A specialized, local mechanism called tubuloglomerular feedback accounts for the other half. If glomerular BP increases, increased capillary filtration delivers more fluid and salt into the renal tubule. The Na+Cl- is sensed by macula densa cells in the ascending loop of Henle, which lie adjacent to the glomerulus in a complex called the juxtaglomerular apparatus. Macula densa activation leads, via adenosine and mesangial A1 receptors, to contraction of the adjacent afferent arteriole, reducing glomerular capillary BP to its former level.
Embryology, Anatomy, and Physiology of the Kidneys and Ureters
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Paul Sturch, Sanjeev Madaan, Seshadri Sriprasad
Glomerular filtration is maintained over a range of blood pressures through several mechanisms:Myogenic autoregulationWith increasing arterial pressure, the walls of the afferent arterioles stretch and then contract to regulate flow.Glomerular blood pressure at ~50−60 mmHg.Osmotic autoregulationThe macula densa cells in DCT monitor flow.With increased pressure and flow, granular cells of the juxtaglomerular apparatus release substances (endothelin, TXA2, AT2) → afferent arteriole constriction.Central regulationSympathetic innervation of the afferent arteriole cause:Constriction in response to blood loss.Dilatation in response to hypertension.
Physiological characterization of an arginine vasopressin rat model of preeclampsia
Published in Systems Biology in Reproductive Medicine, 2022
Sapna Ramdin, Thajasvarie Naicker, Virushka Pillay, Sanil D. Singh, Sooraj Baijnath, Blessing N Mkhwanazi, Nalini Govender
Despite the exclusion of proteinuria as a characterizing factor (ACOG 2013), it remains significant in PE diagnosis (Guida et al. 2018; Özkara et al. 2018; Tanacan et al. 2019). We report significantly increased urinary protein: creatinine ratios in the PAVP group compared to the pregnant saline group on GD 8 and 14. It is possible that AVP affects the control of glomerular filtration rate via the macula densa and the tubulo-glomerular feedback mechanism as a result of an increase in intraglomerular pressure. The macula densa cells detects the increased tubular ion content subsequently activating the RAAS, which inhibits the juxtaglomerular release of nitric oxide. This results in arteriolar vasoconstriction and increases glomerular and systemic blood pressure, causing glomerular hyperfiltration and proteinuria. A similar effect was previously demonstrated in diabetic rats (Bankir et al. 2001; Bolignano and Zoccali 2010).
A clinical pharmacist survey of prophylactic strategies used to prevent adverse events of lipid-associated formulations of amphotericin B
Published in Infectious Diseases, 2019
Daniel B. Chastain, Rachele L. Giles, Christopher M. Bland, Carlos Franco-Paredes, Andrés F. Henao-Martínez, Henry N. Young
Afferent renal artery vasoconstriction, proximal tubular cell injury, and renal tubular acidosis have been proposed as mechanisms behind amphotericin B nephrotoxicity. Amphotericin B increases permeability of the macula densa cells leading to inappropriate activation of the tubuloglomerular feedback system inducing arteriolar vasoconstriction resulting in decreased glomerular filtration rate [4]. Volume expansion with saline is believed to decrease both the sensitivity of the tubuloglomerular feedback and release of atrial natriuretic peptide in order to preserve glomerular filtration rate [4]. While data support the use of saline as a nephrotoxicity prevention strategy with amphotericin B deoxycholate, the precise volume of saline necessary and whether this can be extrapolated to LFAB is less clear [4]. Routine administration of intravenous fluid boluses reported in our survey was lower than expected. This could be due the belief that slower release of amphotericin B by LFAB leads to less direct interaction with tubular cells which negates the need for volume expansion. Furthermore, this may also account for the discrepancy regarding intravenous fluid bolus type and volume. Results from our study revealed administration of intravenous fluid boluses were associated with a higher estimated rate of renal dysfunction/acute kidney injury-related LFAB discontinuation; possibly lending support to the inconsistencies observed in respondent’s practice patterns.
Effects of continuous and pulsatile flows generated by ventricular assist devices on renal function and pathology
Published in Expert Review of Medical Devices, 2018
Takuma Miyamoto, Jamshid H. Karimov, Kiyotaka Fukamachi
Under physiologic conditions, the RAA system is activated in response to decreases in blood pressure or salt and extracellular fluid volume [59]. At the organ level, secretion of renin from juxtaglomerular cells is controlled by a number of factors that become active in the direct vicinity of renin-secreting cells [60]. These factors comprise neurotransmitters released from sympathetic nerve endings, which are found at high density around renin-secreting cells, angiotensin II, autacoids released from endothelial or macula densa cells, various hormones, and the intraluminal blood pressure in afferent arterioles. Renin secretion from the kidneys is inversely related to renal perfusion pressure. Renal baroreceptor mechanisms not only regulate acute renin secretion but also the long-term transformation of vascular SMCs into renin producers.