scholarly journals Macula densa arginine delivery and uptake in the rat regulates glomerular capillary pressure. Effects of salt intake.

1997 ◽  
Vol 100 (9) ◽  
pp. 2235-2242 ◽  
Author(s):  
W J Welch ◽  
C S Wilcox
Keyword(s):  
Capillary Pressure ◽  
Salt Intake ◽  
Macula Densa ◽  
Pressure Effects ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure

scholarly journals Nitric oxide synthase in macula densa regulates glomerular capillary pressure.

1992 ◽  
Vol 89 (24) ◽  
pp. 11993-11997 ◽  
Author(s):  
C. S. Wilcox ◽  
W. J. Welch ◽  
F. Murad ◽  
S. S. Gross ◽  
G. Taylor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Capillary Pressure ◽  
Macula Densa ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Oxide Synthase

Arterial pressure effects on preglomerular microvasculature of juxtamedullary nephrons

1990 ◽  
Vol 258 (1) ◽  
pp. F94-F102 ◽  
Author(s):  
P. K. Carmines ◽  
E. W. Inscho ◽  
R. C. Gensure
Keyword(s):  
Arterial Pressure ◽  
Capillary Pressure ◽  
Branch Point ◽  
Perfusion Pressure ◽  
Pressure Effects ◽  
Arterial Perfusion ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Afferent Arterioles

Videomicroscopic and micropuncture techniques were utilized to determine segmental microvascular responses of in vitro blood-perfused juxtamedullary nephrons to step changes in renal arterial perfusion pressure (PP). At a PP of 104 +/- 2 mmHg, inside diameters of arcuate arteries (ARC), interlobular arteries (ILA), and afferent arterioles (AFF) averaged 68.6 +/- 6.4, 35.7 +/- 1.5, and 20.4 +/- 2.3 microns, respectively. Variations in PP within the range of 70-180 mmHg elicited alterations in microvessel diameters with the following slopes: ARC, -0.15 micron/mmHg; ILA, -0.13 micron/mmHg; and AFF, -0.14 micron/mmHg. In other experiments, intravascular pressures were measured during changes in PP. Glomerular capillary pressure was well regulated (slope = 0.19 +/- 0.03 mmHg/mmHg), and mid-AFF pressure was partially regulated (slope = 0.60 +/- 0.17 mmHg/mmHg); however, pressure measured at the ILA-AFF branch point responded passively to changes in PP (slope = 0.95 +/- 0.06 mmHg/mmHg). These observations reveal that, although the entire preglomerular vasculature of juxtamedullary nephrons is capable of actively responding to changes in PP, afferent arterioles are responsible for the predominant resistance adjustment throughout the normal autoregulatory range.

Abstract 104: Dynamic Autoregulation of Glomerular Capillary Pressure

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Scott C Thomson
Keyword(s):  
Blood Pressure ◽  
Time Series ◽  
Blood Flow ◽  
Capillary Pressure ◽  
Tubuloglomerular Feedback ◽  
Step Response ◽  
Glomerular Capillary ◽  
Arterial Blood ◽  
Glomerular Capillary Pressure ◽  
Step Responses

It is generally accepted that renal blood flow (RBF) autoregulation is mediated by myogenic and tubuloglomerular feedback responses acting on the pre-glomerular resistance. If this is so, then autoregulation of RBF and glomerular capillary pressure (PGC) should change in the same direction throughout an autoregulatory step response. We computed autoregulatory step responses from time series recordings of arterial blood pressure (BP) and RBF (Transonics) blood flow or tubular stop-flow pressure (micropuncture), which is a surrogate for PGC in Wistar-Froemter rats fed for one week on low or high salt diets (n=6-10 ). Autoregulatory step responses were generated from time series by an algorithm that treats BP as a leading indicator of RBF or PGC and uses the projection theorem to solve for the impulse response which is integrated to obtain the step response. Step responses shown in the figure represent the uncompensated changes in RBF and PGC (mean + SEM) following a 1 mmHg BP step. The data clearly reveal that the time courses of RBF and PGC differ such that changes in RBF cannot predict changes in PGC. This implies that the renal hemodynamic response to a blood pressure disturbance is not confined to the pre-glomerular resistance. Furthermore, the participation of post-glomerular resistance in the autoregulatory response is sensitive to dietary salt such that PGC is more sensitive to BP on low salt diet.

scholarly journals Genetic heterogeneity and differences in glomerular hemodynamics between inbred colonies of Munich-Wistar rats.

1992 ◽  
Vol 3 (1) ◽  
pp. 66-72
Author(s):  
F J Fenoy ◽  
E St Lezin ◽  
T W Kurtz ◽  
R J Roman
Keyword(s):  
Capillary Pressure ◽  
Genetic Heterogeneity ◽  
Wistar Rats ◽  
Inbred Strains ◽  
The United States ◽  
Dna Fingerprint ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Renal Micropuncture ◽  
Glomerular Hemodynamics

DNA fingerprint analysis and renal micropuncture studies were performed in Munich-Wistar rats purchased from Harlan Industries and Simonsen Laboratories to determine whether these rats are genetically heterogeneous and exhibit differences in glomerular hemodynamics. RBF and GFR were similar in rats from both colonies. Glomerular capillary pressure was lower in rats from the Harlan colony (46 +/- 2 mm Hg) than in those from the Simonsen colony (56 +/- 2 mm Hg). The low glomerular capillary pressure in the Harlan rats was primarily due to a lower postglomerular vascular resistance. The estimated whole-kidney ultrafiltration coefficient (Kf) was significantly greater in the rats obtained from the Harlan colony than in those obtained from the Simonsen colony (0.12 +/- 0.03 versus 0.05 +/- 0.01 mL/min/g kidney wt/mm Hg). The DNA fingerprints of the Simonsen rats were different from those of the Harlan rats. These results provide evidence of physiologic and genetic heterogeneity between commercially available inbred strains of Munich-Wistar rats in the United States and suggest that comparison of results with Munich-Wistar rats from different sources may be more difficult than previously recognized.

Decreased nephron population resulting from increased ureteral pressure

1964 ◽  
Vol 207 (4) ◽  
pp. 835-839 ◽  
Author(s):  
Richard L. Malvin ◽  
Howard Kutchai ◽  
Fred Ostermann
Keyword(s):  
Blood Pressure ◽  
Hydrostatic Pressure ◽  
Capillary Pressure ◽  
Mean Blood Pressure ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Anesthetized Dogs ◽  
The Mean

The glucose Tm and GFR were determined for each kidney in anesthetized dogs. After three control periods a hydrostatic pressure was applied to one ureter. This resulted in a decrease in GFR over all ranges of ureteral pressures. Tm glucose remained essentially unchanged until the ureteral pressure was elevated to more than 30% of mean blood pressure. At ureteral pressures greater than this, Tm glucose was significantly depressed. The data were used in an attempt to calculate the range and the mean glomerular capillary pressure.

scholarly journals Impaired renal hemodynamics and glomerular hyperfiltration contribute to hypertension-induced renal injury

2020 ◽  
Vol 319 (4) ◽  
pp. F624-F635 ◽  
Author(s):  
Letao Fan ◽  
Wenjun Gao ◽  
Bond V. Nguyen ◽  
Joshua R. Jefferson ◽  
Yedan Liu ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Capillary Pressure ◽  
Renal Injury ◽  
Filtration Rate ◽  
Time Course ◽  
Renal Hemodynamics ◽  
Myogenic Response ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure

Recently, we reported a mutation in γ-adducin (ADD3) was associated with an impaired myogenic response of the afferent arteriole and hypertension-induced chronic kidney disease (CKD) in fawn hooded hypertensive (FHH) rats. However, the mechanisms by which altered renal blood flow (RBF) autoregulation promotes hypertension-induced renal injury remain to be determined. The present study compared the time course of changes in renal hemodynamics and the progression of CKD during the development of DOCA-salt hypertension in FHH 1BN congenic rats [wild-type (WT)] with an intact myogenic response versus FHH 1BN Add3KO ( Add3KO) rats, which have impaired myogenic response. RBF was well autoregulated in WT rats but not in Add3KO rats. Glomerular capillary pressure rose by 6 versus 14 mmHg in WT versus Add3KO rats when blood pressure increased from 100 to 150 mmHg. After 1 wk of hypertension, glomerular filtration rate increased by 38% and glomerular nephrin expression decreased by 20% in Add3KO rats. Neither were altered in WT rats. Proteinuria doubled in WT rats versus a sixfold increase in Add3KO rats. The degree of renal injury was greater in Add3KO than WT rats after 3 wk of hypertension. RBF, glomerular filtration rate, and glomerular capillary pressure were lower by 20%, 28%, and 19% in Add3KO rats than in WT rats, which was associated with glomerular matrix expansion and loss of capillary filtration area. The results indicated that impaired RBF autoregulation and eutrophic remodeling of preglomerular arterioles increase the transmission of pressure to glomeruli, which induces podocyte loss and accelerates the progression of CKD in hypertensive Add3KO rats.

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