Regional blood flow
Burt B. Hamrell in Cardiovascular Physiology, 2018
Kidney arterioles manifest autoregulation. There is relatively constant renal blood flow (RBF) with arterial mean blood pressure levels of 70 to 170 mm Hg and glomerular filtration rate stays constant over this range. This tendency for stability of renal blood flow contributes to optimizing renal function. In addition to the mechanisms of autoregulation described earlier, in the kidney there is tubuloglomerular feedback. An increase in kidney blood flow and glomerular capillary blood pressure transiently result in more glomerular filtration. More water and Na+ are filtered, travel through the renal tubules, and the increased tubular Na+ is sensed by the macula densa. This leads to vasoconstriction of the afferent arteriole and a return of blood flow and filtration close to their original levels. The combination of tubuloglomerular feedback and stretch activation of vascular smooth muscle maintains stability of renal blood flow and glomerular filtration.
Renal physiology
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
Renal blood flow is about 20% of the total cardiac output and is autoregulated. Renal blood flow determines the GFR; delivers oxygen, nutrients and hormones to cells of nephrons; delivers substrates for urinary excretion; participates in the concentrating function of the kidneys; and modifies proximal reabsorption of water and solutes. Autoregulation is achieved by changes in renal vascular resistance mediated by tubuloglomerular feedback and the myogenic reflex and maintains a constant renal blood flow and GFR despite changes in mean arterial pressure of 75–170 mmHg. Sympathetic stimulation, angiotensin II, prostaglandins, nitric oxide, endothelin, bradykinin and adenosine can override the autoregulatory mechanisms. A constant fraction of filtered sodium and water is reabsorbed from the proximal tubule despite changes in GFR; this is called glomerulotubular balance.
Renal Blood Flow
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The renal blood flow remains relatively constant over a mean arterial blood pressure (MAP) range of 75–170 mmHg (Figure 41.1). This is an intrinsic phenomenon and can be demonstrated in isolated kidneys. The glomerular filtration rate (GFR) is also relatively constant over the same range of mean arterial blood pressure. This autoregulation of renal blood flow is produced by changes in the contraction of afferent arteriole smooth muscle in response to changes in perfusion pressure (the efferent arteriole is not involved). A rise or fall in perfusion pressure leads to a corresponding rise or fall in afferent arteriolar resistance, maintaining stability of renal blood flow and GFR. The autoregulation of renal blood flow is by myogenic and tubuloglomerular feedback mechanisms.
Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging
Published in Temperature, 2021
Christopher L. Chapman, Blair D. Johnson, Mark D. Parker, David Hostler, Riana R. Pryor, Zachary Schlader
There is great interest in accurately quantifying changes in renal blood flow because it is a highly controlled variable that has implications for the regulation of blood pressure and water and electrolytes. Thus, it is also important to note that the kidneys have an intrinsic ability to maintain blood flow at varying arterial pressures (i.e., autoregulate). Renal blood flow autoregulation is mediated by actions of the afferent arterioles and interlobular arteries and their myogenic response to constrict or relax in response to changes in perfusion pressure [173-175]. Approximately, 50% of the total autoregulatory response [176,177] rapidly occurs within 3-10 seconds [178,179], which is contributed to by unloading of the renal baroreceptors and tubuloglomerular feedback provided by the juxtaglomerular apparatus [180,181]. Tubuloglomerular feedback also results in renin release by the afferent arterioles in response to sensation of decreased NaCl delivery to the macula densa in the distal tubule [182], which ultimately ensures a relatively stable renal blood flow and glomerular filtration rate (see Glomerular filtration rate). These neural (discussed previously in Autonomic control of kidney function), hormonal (discussed previously in PHYSIOLOGY AND ASSESSMENT OF BODY WATER REGULATION), and autoregulatory mechanisms offer a complex and highly redundant control of renal blood flow to maintain homeostasis utilizing many systems.
Dapagliflozin for the treatment of type 2 diabetes mellitus – an update
Published in Expert Opinion on Pharmacotherapy, 2021
Martha K Nicholson, Randa Ghazal Asswad, John PH Wilding
The benefits of dapagliflozin have also been shown to extend beyond glycemic control in the treatment of people with diabetes. These include lowering blood pressure, renal protection, and improved cardiac function [23], with mechanisms posited for this improvement including improved cardiac energy metabolism and prevention of adverse cardiac remodeling [24]. In T2DM, SGLT2 function is upregulated with increased reabsorption of glucose and sodium. Subsequently, decreased delivery of sodium distal to the PCT and macula densa eventually results in loss of tubuloglomerular feedback. This key autoregulatory mechanism adjusts the renal blood flow and glomerular filtration rate (GFR) to optimize fluid flow through the renal tubule. It is thought that SGLT2 inhibitors such as dapagliflozin enhance delivery of sodium to the macula densa to restore the tubuloglomerular feedback process, thus reducing intraglomerular pressure, reducing proteinuria, and helping to preserve renal function. Additionally, these renal mechanisms will inevitably have a positive impact on cardiovascular function as a secondary effect.
The effects of acute kidney injury in a multicenter cohort of high-risk surgical patients
Published in Renal Failure, 2021
Henrique Tadashi Katayama, Brenno Cardoso Gomes, Suzana Margareth Ajeje Lobo, Renato Carneiro de Freitas Chaves, Thiago Domingos Corrêa, Murillo Santucci Cesar Assunção, Ary Serpa Neto, Luiz Marcelo Sá Malbouisson, João Manoel Silva-Jr
It is expected that, in many cases, simply restoring the circulating volume does not improve the results and maybe counterproductive [4,5]. Organ edema distorts tissue architecture, impairs oxygen and metabolite diffusion, and obstructs the capillary flow and lymphatic drainage. These effects are particularly pronounced in encapsulated organs, such as the kidney, which cannot accommodate additional volume without significant increases in interstitial pressure and compromised blood flow. Elevated intratubular pressure decreases glomerular filtration and activation of tubuloglomerular feedback, with consequent preglomerular vasoconstriction, which leads to an additional reduction in glomerular filtration [29–31]. Studies have shown that excess fluid is an independent factor for the development of AKI and that in patients with AKI, a more positive fluid balance was correlated with higher mortality [32–35]. Regarding the type of solution used, epidemiologic data suggest that 0.9% saline solution, when compared with balanced salt solutions, such as balanced solutions, may increase the risk of AKI. In addition, there is evidence of harm (increased rates of AKI) with the use of hetastarch solutions, which should generally be avoided [36]. In our study was not detect a negative influence of any type of colloid or crystalloid on the development of AKI.
Related Knowledge Centers
- Adenosine
- Distal Convoluted Tubule
- Macula Densa
- Nephron
- Tubular Fluid
- Kidney
- Glomerular Filtration Rate
- Renal Physiology
- Purinergic Signalling
- Ascending Limb of Loop of Henle