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Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
As the enzyme involved in the rate-limiting step of the RAAS, renin plays an integral part in regulating blood pressure. The kidneys play a key role in regulating the production of renin. Within each nephron of the kidney, there is a point where the incoming arteriole from the body (afferent arteriole) comes into contact with the distal tubule that takes the filtrated blood to collecting ducts and then to the bladder. This area is called the juxtaglomerular apparatus and is where renin is produced and secreted. The location of the apparatus allows it to receive information about the body’s blood pressure need within the afferent arteriole and receive information about the components of the tubule infiltrate. Lastly, the apparatus receives information from the central nervous system via nerve endings within the apparatus, thus allowing the production of renin to be connected to increased sympathetic nervous activity.
The patient with acute renal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The kidney secretes an enzyme called renin from cells in the juxtaglomerulus apparatus, and this plays a significant role in regulating fluid balance and subsequently in controlling blood pressure. Renin is a vasoconstrictor and it leads to the release of other substances with similar properties. The chain of events that it initiates is collectively known as the renin–angiotensin–aldosterone system. Renin leads to the release of angiotensinogen, produced by hepatocytes, and converted in the plasma into angiotensin 1. This is then converted in the lungs into angiotensin 2, a very powerful vasopressor. The latter has two main functions: Vasoconstriction of the afferent arterioles, leading to a reduced glomerular filtration rate.Activation of aldosterone from the adrenal cortex, which leads to the reabsorption of sodium into the extracellular space, with chloride and water following it.
Erythropoietin, Atrial Natriuretic Peptide and Sex Hormones
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The physiological effects of ANP involve the kidney, adrenal cortex and the peripheral vascular system: Renal effects. The main effect of ANP is an increased glomerular filtration rate (GFR). This is brought about by constriction of the efferent arteriole and dilation of the afferent arteriole of the glomerulus, thus increasing the hydrostatic pressure in glomerular capillaries. As a result of the increase in GFR as well as an increase in renal medullary blood flow, increased urinary sodium excretion (natriuresis) occurs. An increase in the delivery of sodium and chloride to the macula densa, as well as an increase in the hydrostatic pressure at the juxtaglomerular apparatus secondary to the afferent arteriolar vasodilation, causes an inhibition of renin secretion.Adrenal secretion of aldosterone. ANP blocks the secretion of aldosterone that is stimulated by angiotensin II, ACTH and cAMP.Peripheral vasculature. Vasorelaxation of the smooth muscles of peripheral blood vessels leads to a decrease in mean systemic arterial blood pressure. This is partly brought about by the suppression of renin release.
Balancing renal Ang-II/Ang-(1–7) by xanthenone; an ACE2 activator; contributes to the attenuation of Ang-II/p38 MAPK/NF-κB p65 and Bax/caspase-3 pathways in amphotericin B-induced nephrotoxicity in rats
Published in Toxicology Mechanisms and Methods, 2023
Amany A. Azouz, Doaa M. Abdel-Rahman, Basim Anwar Shehata Messiha
Repeated administration of amphotericin B in our study also elevated renal content of Ang-II, but reduced Ang-(1–7). It has been demonstrated previously that stimulation of the TGF system via amphotericin B administration induces arteriolar vasoconstriction due to electrolyte imbalance (Aghajani and Soheilirad 2020). Vasoconstriction of the afferent arterioles stimulates the release of renin that elevates Ang-II levels, resulting eventually in renal ischemia and azotemia (Jones and Chesney 2009; Chastain et al. 2019). The RAS participates a crucial role in renal physiology, while disturbance of the RAS contributes to renal injury. RAS dysregulation could lead to glomerular and tubular dysfunction via the effector molecule Ang-II and its receptor (Ang-II receptor type 1) (Al-Kuraishy et al. 2019).
Impact of SGLT2 inhibitors on the kidney in people with type 2 diabetes and severely increased albuminuria
Published in Expert Review of Clinical Pharmacology, 2022
Nasir Shah, Vlado Perkovic, Sradha Kotwal
Hyperglycemia causes RAAS activation. Although the exact mechanism remains unknown, the main end effector of this pathway, angiotensin II, is produced at the tissue level in the kidney, other organs, and in the systemic circulation [77–79]. This local RAAS activation causes formation of ROS, cell growth, apoptosis, inflammation, and fibrosis [80]. Additionally, the systemically released angiotensin II plays a key role in glomerular capillary dysregulation. The efferent glomerular arteriole is significantly more sensitive to vasoconstriction by angiotensin II than the afferent arteriole, which results in a higher intraglomerular capillary pressure and subsequent hyperfiltration [77]. These changes contribute to the progression of DKD and form the basis of why RAAS inhibition has been a fundamental part of managing patients with DKD for more than 2 decades. Multiple randomized controlled trials have shown that RAAS inhibition with ACE inhibitors or ARBs reduce the risk of DKD progression in patients with significant albuminuria [81–84]. Current guidelines suggest RAAS inhibition for all patients with DKD, hypertension, and albuminuria [55–57].
The effect of whole blood viscosity on contrast-induced nephropathy development in patients undergoing percutaneous coronary intervention
Published in Postgraduate Medicine, 2022
Mustafa Kinik, Sencer Çamci, Selma Ari, Hasan Ari, Mehmet Melek, Tahsin Bozat
The relationship between lowness of WBV and CIN can be explained by the tubuloglomerular feedback mechanism in the kidneys. The inability of the glomeruli, which have adapted to the low viscosity environment, to adapt to the sudden increase in viscosity caused by the deformation created by contrast material and contrast on the erythrocytes may cause CIN development [26]. Vasodilation in afferent arterioles and vasoconstriction in efferent arterioles occur to provide the necessary glomerular filtration in a low-viscosity environment. However, in case of a sudden increase in viscosity in the distal tubule, renin- and adenosine-mediated mechanisms cause vasoconstriction in afferent arterioles and the medullary vascular bed, causing a decrease in GFR [26]. This GFR decline is one of the main causes of CIN development. Because of decreased GFR, the removal of the contrast material from the body is delayed, and CIN develops because of this event, causing a vicious circle on the kidneys. Since the WBV values in non-STEMI and STEMI patients were higher than those in elective PCI patients, the tubuloglomerular feedback mechanism adapted to a more viscous environment. Therefore, since the viscosity increase in distal renal tubules in these patients is relatively less, the effectiveness of the feedback mechanism and the GFR decrease are less. The second explanation about the relationship between lowness of WBV and CIN; lower WBV conditions lead to a constricted renal circulation, associated with a condition of decreased NO bioavailability [27]. These may explain that WBV values are not CIN development predictors in these groups.