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 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.

Impaired preservation of GFR during hypotension in preexistent renal hypoperfusion

1989 ◽  
Vol 256 (2) ◽  
pp. F314-F320
Author(s):  
T. Yoshioka ◽  
A. Yared ◽  
V. Kon ◽  
I. Ichikawa
Keyword(s):  
Capillary Pressure ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Arteriolar Resistance ◽  
Single Nephron

Autoregulation of renal blood flow and filtration rate was studied using micropuncture technique in Munich-Wistar rats with acute water deprivation (AWD) or congestive heart failure (CHF). In the first set of experiments, reduction of renal perfusion pressure to approximately to 70% of its initial value resulted in uncoupling of glomerular plasma flow rate and single-nephron glomerular filtration rate (GFR) (i.e., disproportionally profound fall in the latter) in AWD and CHF rats, whereas both indices changed little in normal control (NC) rats. The profound decrease in single-nephron GFR in AWD and CHF rats was primarily due to a reduction in glomerular capillary pressure (change from base-line value was -29 +/- 2% in AWD, -27 +/- 1% in CHF, and -8 +/- 2% in NC). This profound fall in glomerular capillary pressure in AWD and CHF rats was associated with a reduction in efferent arteriolar resistance, which contrastingly increased in NC. To investigate the mechanism underlying this unique efferent arteriolar responsiveness in AWD and CHF, the response of renal arterioles to exogenous angiotensin II was examined in separate groups of AWD, CHF, and NC. There was a markedly attenuated efferent arteriolar vasoconstrictive response in AWD and CHF (the change of efferent arteriolar resistance in both groups was some 5% of that in NC). Thus impairment in the ability to preserve GFR in these two conditions is attributed, at least in part, to altered efferent arteriolar response in the face of reduced renal perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Progressive glomerular injury after limited renal infarction in the rat

1988 ◽  
Vol 254 (6) ◽  
pp. F856-F862 ◽  
Author(s):  
T. W. Meyer ◽  
H. G. Rennke
Keyword(s):  
Glomerular Filtration Rate ◽  
Capillary Pressure ◽  
Renal Mass ◽  
Filtration Rate ◽  
Glomerular Sclerosis ◽  
Glomerular Injury ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Group 2 ◽  
Group 1

Wistar Munich rats subjected to partial renal ablation were compared with intact rats. Group 1 rats were subjected to bilateral segmental infarction of 40% of their total renal mass. Group 2 rats underwent uninephrectomy. Group 3 rats underwent sham operation. Micropuncture and morphological studies were performed in each group at 28 wk after operation. In group 1, glomerular capillary pressure was elevated by 7 mmHg and systemic blood pressure was elevated by 31 mmHg despite reduction of nephron number by only 40% and reduction of glomerular filtration rate (GFR) by only 10%. Progressive albuminuria and segmental glomerular sclerosis were associated with elevation of glomerular capillary pressure in this group. In group 2, single-nephron glomerular filtration rate (SNGFR) was higher than in group 1, but systemic and glomerular capillary pressure remained normal. Group 2 rats developed markedly less albuminuria and glomerular sclerosis than group 1 rats despite more pronounced remnant nephron hyperfiltration. These studies support the view that glomerular hypertension is the major hemodynamic derangement contributing to remnant glomerular injury and show that capillary hypertension can initiate remnant glomerular injury even when the majority of the renal mass remains intact.

Effects of blood pH changes on potassium excretion in the dog

1962 ◽  
Vol 202 (4) ◽  
pp. 768-772 ◽  
Author(s):  
Charles Toussaint ◽  
Pierre Vereerstraeten
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Distal Tubule ◽  
Potassium Excretion ◽  
Ph Changes ◽  
Blood Ph ◽  
Ph Level

K+ excretion rate was measured at normal as well as at rising plasma K+ concentration in intact, in K-depleted, and in acetazolamide-treated dogs submitted to acute blood pH changes. The results indicate that, for any given value of glomerular filtration rate, K+ excretion rate is determined by at least three factors: 1) plasma K+ concentration, 2) blood pH level, and 3) presumably, the H+ gradient across the luminal border of the distal tubule. The data further suggest that most of the filtered K+ is reabsorbed by the proximal tubule, even in conditions of high filtered loads.

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.

Micropuncture study of the superficial nephron of Perognathus penicillatus

1981 ◽  
Vol 241 (6) ◽  
pp. F612-F617
Author(s):  
E. J. Braun ◽  
D. R. Roy ◽  
R. L. Jamison
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Distal Tubule ◽  
Urine Osmolality ◽  
Small Rodent ◽  
Micropuncture Study ◽  
Single Nephron ◽  
Average Body

A micropuncture study of Perognathus penicillatus, a small rodent native to the deserts of the southwestern United States was performed to evaluate the function of the superficial nephron. Data are reported for 12 animals of 17 g average body wt. Mean glomerular filtration rate was 475 +/- 73 microliter X min-1 X g kidney wt-1. Urine osmolality averaged 1,154 +/- 197 mosmol/kg H2O. Single nephron glomerular filtration rate averaged 43 nl X min-1 X g kidney wt-1 in the proximal tubule and 48 in the distal tubule, values that are not significantly different. In terms of the filtered load remaining unreabsorbed at the end of the accessible proximal tubule, the average percentages were 46 water, 48 total solute, 45 sodium, 56 phosphorus, 62 potassium, 71 magnesium, and 54 calcium. The concentrations of potassium and magnesium in fluid samples increased significantly along the proximal tubule. Approximately at the midpoint of the distal tubule, fractional delivery of water, 13.1%, was greater than that for total solute, 10%, or sodium, 7%, indicating that the intervening segment of nephron reabsorbed solute and sodium in excess of water. The function of the superficial nephron resembles that of species previously investigated except for potassium reabsorption in the proximal convoluted tubule.

Sign in / Sign up

Export Citation Format

Share Document