The PAP-technique and antibodies to myosin were used to demonstrate the prerequisites for vasoconstriction in the juxtaglomerular part of the preglomerular arteriole as compared with its proximal segment in rats and mice. In contrast with the myosin-positive/renin-negative proximal part of the afferent arteriole no myosin-like activity could be demonstrated in its distal, renin-positive part. In accordance, no thick myofilaments were found in fully differentiated juxtaglomerular epithelioid cells replete with mature secretory granules. Stimulation of the renin-angiotensin system was followed by an increase of the renin-positive/myosin-negative portions of the preglomerular arteriole. Marked interspecies and internephron variations in the length of this vessel segment under control and stimulated conditions were observed. The juxtaglomerular part of the preglomerular arteriole close to the macula densa seems therefore to have only limited capabilities for vasoconstriction. This finding may be of importance regarding the tubulo-glomerular feedback, a mechanism allegedly triggered by the so-called 'macula densa-signal'. It is suggested that this non-contractile segment of the afferent arteriole may represent the renal vascular receptor responsible for the increase of renin secretion during pressure reduction. Unlike the afferent arterioles, most of the efferent arterioles showed the highest level of their weak but distinct myosin-like immunoreactivity in the juxtaglomerular region, indicating some efferent juxtaglomerular vasoconstrictive ability.
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http://dx.doi.org/10.1007/BF00216486 | DOI Listing |
J Hypertens
November 2024
Department of Nephrology and Hypertension.
Background And Hypothesis: Obesity aggravates the risk to develop chronic kidney disease in hypertensive patients. Whether pre-obesity already impairs renal function, renal perfusion and intraglomerular hemodynamics in hypertensive patients is unknown.
Methods: Renal hemodynamic profiles were measured using steady state input clearance (infusion of para-amino-hippuric acid and inulin) in 36 patients with primary arterial hypertension stage 1-2 without antihypertensive medication.
J Clin Monit Comput
August 2024
Department of Anesthesia and Intensive Care Medicine, IRCCS Humanitas Research Hospital, via Manzoni 56, Rozzano - Milan, 20089, Italy.
J Clin Med
November 2023
Medical Genetics Division, Fondazione IRCCS Casa Sollievo della Sofferenza, 71013 San Giovanni Rotondo, Italy.
Background: Microvascular disorders represent an uncommon site of tissue hypo-perfusion and damage. Various genetic and acquired causes can be involved. A 65-year-old man was admitted because of refractory angina, which he had had since the age of 30 years, micro-hematuria, and recurrent transitory ischemic attacks from the age of 64.
View Article and Find Full Text PDFMagn Reson Med
December 2022
Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Korea.
Purpose: To propose a two-compartment renal perfusion model for calculating glomerular blood transfer rate ( ) as a new measure of renal function.
Theory: The renal perfusion signal was divided into preglomerular and postglomerular flows according to flow velocity. By analyzing perfusion signals acquired with and without diffusion gradients, we estimated , the blood transfer rate from the afferent arterioles into the glomerulus.
Nephron
September 2022
Department of Intensive Care Medicine, Fiona Stanley Hospital, Perth, Washington, Australia.
Background: In 2004, the term acute kidney injury (AKI) was introduced with the intention of broadening our understanding of rapid declines in renal function and to replace the historical terms of acute renal failure and acute tubular necrosis (ATN). Despite this evolution in terminology, the mechanisms of AKI have stayed largely elusive with the pathophysiological concepts of ATN remaining the mainstay in our understanding of AKI.
Summary: The proximal tubule (PT), having the highest mitochondrial content in the kidney and relying heavily on oxidative phosphorylation to generate ATP, is vulnerable to ischaemic insults and mitochondrial dysfunction.
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