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2015 ; 95
(2
): 405-511
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Renal autoregulation in health and disease
#MMPMID25834230
Carlström M
; Wilcox CS
; Arendshorst WJ
Physiol Rev
2015[Apr]; 95
(2
): 405-511
PMID25834230
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Intrarenal autoregulatory mechanisms maintain renal blood flow (RBF) and
glomerular filtration rate (GFR) independent of renal perfusion pressure (RPP)
over a defined range (80-180 mmHg). Such autoregulation is mediated largely by
the myogenic and the macula densa-tubuloglomerular feedback (MD-TGF) responses
that regulate preglomerular vasomotor tone primarily of the afferent arteriole.
Differences in response times allow separation of these mechanisms in the time
and frequency domains. Mechanotransduction initiating the myogenic response
requires a sensing mechanism activated by stretch of vascular smooth muscle cells
(VSMCs) and coupled to intracellular signaling pathways eliciting plasma membrane
depolarization and a rise in cytosolic free calcium concentration ([Ca(2+)]i).
Proposed mechanosensors include epithelial sodium channels (ENaC), integrins,
and/or transient receptor potential (TRP) channels. Increased [Ca(2+)]i occurs
predominantly by Ca(2+) influx through L-type voltage-operated Ca(2+) channels
(VOCC). Increased [Ca(2+)]i activates inositol trisphosphate receptors (IP3R) and
ryanodine receptors (RyR) to mobilize Ca(2+) from sarcoplasmic reticular stores.
Myogenic vasoconstriction is sustained by increased Ca(2+) sensitivity, mediated
by protein kinase C and Rho/Rho-kinase that favors a positive balance between
myosin light-chain kinase and phosphatase. Increased RPP activates MD-TGF by
transducing a signal of epithelial MD salt reabsorption to adjust afferent
arteriolar vasoconstriction. A combination of vascular and tubular mechanisms,
novel to the kidney, provides for high autoregulatory efficiency that maintains
RBF and GFR, stabilizes sodium excretion, and buffers transmission of RPP to
sensitive glomerular capillaries, thereby protecting against hypertensive
barotrauma. A unique aspect of the myogenic response in the renal vasculature is
modulation of its strength and speed by the MD-TGF and by a connecting tubule
glomerular feedback (CT-GF) mechanism. Reactive oxygen species and nitric oxide
are modulators of myogenic and MD-TGF mechanisms. Attenuated renal autoregulation
contributes to renal damage in many, but not all, models of renal, diabetic, and
hypertensive diseases. This review provides a summary of our current knowledge
regarding underlying mechanisms enabling renal autoregulation in health and
disease and methods used for its study.
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