Abstract 065: Enhanced Glomerular Capillary Pressure and Tubuloglomerular Feedback (tgf) in Obese Alms1 (alstrom Syndrome 1) Knock Out Rats

Hypertension ◽  
2018 ◽  
Vol 72 (Suppl_1) ◽  
Author(s):  
Sumit R Monu ◽  
Keyona King-Medina ◽  
Pablo Ortiz
Keyword(s):  
Capillary Pressure ◽  
Tubuloglomerular Feedback ◽  
Knock Out ◽  
Alström Syndrome ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Alstrom Syndrome

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.

Tubuloglomerular feedback-mediated decreases in glomerular pressure in Munich-Wistar rats

1984 ◽  
Vol 247 (6) ◽  
pp. F877-F880 ◽  
Author(s):  
P. D. Bell ◽  
M. Reddington ◽  
D. Ploth ◽  
L. G. Navar
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Capillary Pressure ◽  
Wistar Rats ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Arteriolar Resistance

These experiments were performed to evaluate directly measured glomerular capillary pressure and single nephron glomerular filtration rate (SNGFR) tubuloglomerular feedback responses in Munich-Wistar rats during increased distal flow rate achieved by infusing an isotonic electrolyte solution into unblocked late proximal tubules. Arterial pressure averaged 114 +/- 2 mmHg and proximal tubule pressure was 14 +/- 1 mmHg. In eight tubules, control SNGFR based on distal tubular fluid collections averaged 22 +/- 3 nl/min, decreased to 15 +/- 2.3 nl/min when 10-12 nl/min of perfusate was infused into the late proximal tubule, and further decreased to 9 +/- 1.7 nl/min at an infusion of 20-24 nl/min. In 22 tubules, control glomerular capillary pressure was 55 +/- 1.6 mmHg, decreased to 43 +/- 2.5 mmHg with addition of perfusate into a late proximal tubule at a rate of 24 nl/min, and returned to 53 +/- 3.1 mmHg when perfusion was stopped. In eight nephrons, glomerular capillary pressure was shown to be responsive to smaller increments in the late proximal infusion rate and was reduced by 4 +/- 0.5 and 7 +/- 1.1 mmHg at the intermediate rates of 10 and 15 nl/min, respectively. These results demonstrate that glomerular pressure decreases during increased distal delivery even when the tubule is not blocked. They are consistent with the hypothesis that increases in afferent arteriolar resistance are primarily responsible for feedback-mediated reductions in glomerular filtration rate.

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.

Abstract 063: Impaired Myogenic Response of the Af-art Contributes to the Increased Susceptibility to Hypertension and Diabetic Induced Renal Disease in Milan Normotensive Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Ying Ge ◽  
Fan Fan ◽  
Richard J Roman
Keyword(s):  
Capillary Pressure ◽  
Perfusion Pressure ◽  
Sequence Variant ◽  
Myogenic Response ◽  
Glomerular Capillary ◽  
Protein Excretion ◽  
Glomerular Capillary Pressure ◽  
Increased Susceptibility ◽  
Glomerular Capillaries

Previous studies have indicated that Milan normotensive (MNS) rats are more susceptible to the development of hypertension and diabetic induced renal injury than Milan hypertensive (MHS) rats, but the genes and pathways involved are unknown. MNS also develop proteinuria and chronic kidney disease (CKD) as they age, whereas hypertensive MHS do not. We compared the myogenic response of isolated perfused Af-Art and autoregulation of RBF and glomerular capillary pressure in 6-9 week old MNS and MHS rats. The diameter of Af-Art of MNS rats increased from 14.0 ± 0.5 to 14.2 ± 0.6 μm (n=6) when elevation in perfusion pressure from 60 to 120 mmHg. In contrast, the diameter of the Af-Art decreased significantly from 14.3 ± 0.5 to 11.5 ± 0.6 μm (n=6) in MHS rats. In vivo, RBF increased by 26% when RPP was increased from 100 to 140 mmHg in MNS rats but it remained unchanged in MHS rats. Glomerular capillary pressure rose by 11 mmHg in MNS following the elevation in RPP from 100 to 140 mm Hg but not in MHS rats. Protein excretion increased from 8.9 ± 0.7 to 158.2 ± 23.1 mg/day in MNS rats as the increased in age from 3 to 9 months of age but it did not increase in MHS rats. In com-parison to other strains susceptible and resistant to CKD, we noticed that both MNS and Fawn Hooded hypertensive (FHH) rats that do not autoregulate RBF also share the same sequence variant in the Adducin 3 gene. We performed a genetic complementation study to test whether this mutation might be responsible for the impaired myogenic response in MNS. The diameter of the Af-Art isolated from an F1 cross of MNS &FHH rats increased from 17.2 ± 0.9 to 18.5 ± 0.9 μM (n=5) in response to increase in perfusion pressure and RBF was not efficiently autoregulated in these animals. These data indicate a mutation in Adducin 3 which impairs myogenic response of the Af-Art and increased transmission of pressure to the glomerular capillaries may contribute to the development of CKD in MNS rats similar to what is seen in FHH rats.

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