Interaction between loop of Henle flow and arterial pressure as determinants of glomerular pressure

1989 ◽  
Vol 256 (3) ◽  
pp. F421-F429 ◽  
Author(s):  
J. Schnermann ◽  
J. P. Briggs
Keyword(s):  
Arterial Pressure ◽  
Pressure Range ◽  
Loop Of Henle ◽  
Half Maximum ◽  
Perfusion Rate ◽  
A Value ◽  
Regulatory Input ◽  
Flow Pressure ◽  
The Relationship ◽  
Stop Flow

Experiments were performed in anesthetized rats to study the relationship between loop of Henle perfusion rate, arterial pressure, and stop-flow pressure (SFP) as an index of glomerular capillary pressure. In one set of experiments we measured the SFP feedback response to changes in loop perfusion at three levels of arterial pressure. The maximum SFP response fell significantly from 13.1 +/- 1.44 to 8.14 +/- 1.72 and 3.13 +/- 0.76 mmHg when arterial pressure was reduced from 118.1 +/- 1.27 to 98.8 +/- 0.51 and 78.8 +/- 1.72 mmHg. In other experiments arterial pressure was altered while loop perfusion rate was fixed at one of three levels. Without loop perfusion SFP changed with a slope of 0.27 +/- 0.04 mmHg/mmHg in the arterial pressure range between 80 and 130 mmHg. During perfusion at the flow rate at which response is half maximum, the slope was significantly reduced to 0.12 +/- 0.04. During perfusion at 45 nl/min, it was 0.03 +/- 0.05, a value not significantly different from zero. During dopamine administration (70 micrograms/kg min) SFP was pressure-dependent even during loop perfusion at 45 nl/min. These results show that arterial pressure determines TGF responsiveness and that the TGF signal determines the range of a regulatory input that is directly dependent on arterial pressure.

Evidence for tubuloglomerular feedback in juxtamedullary nephrons of young rats

1983 ◽  
Vol 244 (4) ◽  
pp. F425-F431 ◽  
Author(s):  
R. Muller-Suur ◽  
H. R. Ulfendahl ◽  
A. E. Persson
Keyword(s):  
Filtration Rate ◽  
Proximal Tubules ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Perfusion Rate ◽  
Flow Rates ◽  
Young Rats ◽  
Flow Pressure ◽  
Tubular Flow ◽  
Stop Flow

To determine whether the filtration rate of juxtamedullary nephrons is regulated by tubuloglomerular feedback (TGF), we developed two micropuncture techniques suitable for the papilla of young rats. One consisted of measuring the tubular flow in descending limbs of Henle loops (VDLH) while the ascending limbs of the loop of Henle (ALH) were perfused at various rates with three different solutions: modified Ringer, artificial Henle loop solution, and Ringer containing 10(-4) M furosemide. SNGFR was also measured in several juxtamedullary nephrons. The other protocol consisted of measuring the tubular stop-flow pressure (PSF) in descending limbs of the loop of Henle upstream to a wax block. Distal to the block Ringer was perfused at various rates through ALH. Our results provide the first evidence of a TGF response in juxtamedullary nephrons. VDLH and SNGFR decreased during Ringer perfusion to 42 +/- 4 and 44 +/- 4% of their values at zero perfusion. The same pattern was observed using Henle loop solution as perfusate, whereas with furosemide VDLH did not change. The maximal decrease in PSF was 14.1 +/- 1.4 mmHg. The perfusion rate necessary to induce a half-maximal PSF decrease was 9.1 +/- 0.9 nl/min. Similar micropuncture techniques were used in proximal tubules of surface nephrons in these rats, which in comparison to the deep nephrons showed smaller feedback responses. The mechanism seems to be active at physiological nephron flow rates in both nephron populations. Thus, TGF can exert its effect on GFR of the whole kidney by acting in both deep and surface nephrons.

Dissociation of tubuloglomerular feedback responses from distal tubular chloride concentration in the rat

1981 ◽  
Vol 240 (2) ◽  
pp. F111-F119 ◽  
Author(s):  
P. D. Bell ◽  
C. B. McLean ◽  
L. G. Navar
Keyword(s):  
Chloride Concentration ◽  
Tubuloglomerular Feedback ◽  
Fluid Solution ◽  
Perfusion Rate ◽  
Receptor System ◽  
Retrograde Perfusion ◽  
Perfusion Studies ◽  
Flow Pressure ◽  
Stop Flow ◽  
Feedback Responses

Previous studies have demonstrated that stop-flow pressure (SFP) feedback responses can occur during orthograde perfusion with solutions having low amounts of sodium or chloride. However, retrograde perfusion studies have suggested a specific role for chloride concentration in mediating feedback responses. These studies were conducted to compare SFP feedback responses during orthograde and retrograde perfusion with an artificial tubular fluid solution (ATF) (Cl- = 135 meq/liter) and a Na+ isethionate solution (Cl- = 6 meq/liter). With ATF, increases in perfusion rate from 10 to 35 nl/min led to decreases in SFP of 11 +/- 1.4 mmHg, increases in distal tubular fluid Cl- of 46 +/- 4.9 meq/liter, and osmolality of 58 +/- 10 mosmol/kg. There were significant inverse relationships between SFP and changes in Cl- and osmolality. With Na+ isethionate, SFP decreased by 8.4 +/- 1.0 mmHg, osmolality increased by 43 +/- 8 mosmol/kg, and Cl- did not change. There was a significant relationship between SFP and osmolality, but not with Cl-. During retrograde perfusion at 15 nl/min, SFP decreased by 12 +/- 1.2 mmHg with ATF and by 12 +/- 1.2 mmHg with Na+ isethionate. These results demonstrate that feedback-mediated decreases in SFP can occur in the absence of concomitant increases in distal Cl- and suggest that the receptor system does not have a unique and specific requirement for chloride.

Enhanced tubuloglomerular feedback during peritubular infusions of angiotensins I and II

1988 ◽  
Vol 255 (3) ◽  
pp. F383-F390 ◽  
Author(s):  
K. D. Mitchell ◽  
L. G. Navar
Keyword(s):  
De Novo ◽  
Feedback Mechanism ◽  
Tubuloglomerular Feedback ◽  
Ang Ii ◽  
Angiotensin I ◽  
Peritubular Capillary ◽  
Perfusion Rate ◽  
Flow Pressure ◽  
Stop Flow ◽  
Feedback Responses

Experiments were performed in pentobarbital sodium-anesthetized rats to determine whether increases in intrarenal generation of angiotensin II (ANG II) can enhance the sensitivity of the tubuloglomerular feedback mechanism. Stop-flow pressure (SFP) feedback responses to step increases in late proximal perfusion rate were obtained during control conditions and during simultaneous peritubular capillary infusion of either angiotensin I (ANG I) or ANG II. Infusion of either 10(-7) M ANG II or 10(-5) M ANG I, at rates (18.3 +/- 0.9 and 14.8 +/- 1.5 nl/min, respectively) that did not affect resting SFP, enhanced the magnitude of SFP feedback responses both at a low proximal perfusion rate of 10 nl/min (2.9 +/- 0.9 vs. 0.3 +/- 0.2 and 4.5 +/- 1.0 vs. 0.1 +/- 0.1 mmHg, respectively) and at proximal perfusion rates (greater than 30 nl/min) that elicited a maximal feedback response (13.1 +/- 1.0 vs. 10.1 +/- 0.7 and 13.5 +/- 1.6 vs. 9.8 +/- 0.8 mmHg, respectively). With a higher ANG I infusion rate (20 nl/min), control SFP measured in the absence of distal volume delivery decreased from 39.2 +/- 0.6 to 12.0 +/- 2.8 mmHg (n = 18). These effects were blocked when the ANG II receptor antagonist, saralasin (10(-5) M, Sar), was added to the infusate. In addition, the magnitude of the maximal SFP feedback response was not altered during infusion of Sar alone or ANG I + Sar. These findings indicate that ANG II, either added or formed de novo beyond the glomerular circulation, can enhance the sensitivity of the tubuloglomerular feedback mechanism.

Absence of estimated glomerular pressure autoregulation during interrupted distal delivery

1975 ◽  
Vol 229 (6) ◽  
pp. 1596-1603 ◽  
Author(s):  
LG Navar ◽  
B Chomdej ◽  
PD Bell
Keyword(s):  
Arterial Pressure ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Feedback System ◽  
Colloid Osmotic Pressure ◽  
Feedback Mechanism ◽  
Arterial Blood ◽  
Flow Pressure ◽  
Stop Flow ◽  
Distal Delivery

Micropuncture studies in dogs have suggested that a distal tubule-to-afferent arteriole feedback system may participate in the autoregulation mechanism at the single-nephron level. To evaluate the effect of interrupted distal delivery on glomerular capillary pressure (GP) and its autoregulation, the proximal tubule was blocked with oil and maximal stop-flow pressure was measured with a micropressure servo-null system. The GP was estimated from the sum of stop-flow pressure and the plasma colloid osmotic pressure (membrane oncometer). In 18 dogs given a mild mannitol load, average +/- SD control arterial pressure was 118 +/- 16 mmHg, proximal tubule pressure was 24 +/- 5 mmHg, and estimated GP averaged 70 +/- 10 mmHg. There was a highly significant relationship between estimated GP and arterial blood pressure. Similar results were obtained in hydropenic dogs. In response to decreases in renal arterial pressure in individual dogs, stop-flow pressure and estimated GP failed to exhibit autoregulation although autoregulation of renal blood flow, GFR, and proximal tubule pressure was observed over an arterial pressure range of 150-95 mmHg. These results indicate that interruption of normal distal delivery by proximal tubule blockage interferes with the ability of the nephron to autoregulate glomerular pressure. They provide further evidence in support of the concept that a distal tubular feedback mechanism participates, at least in part, in the autoregulatory control of glomerular pressure.

Native tubular fluid attenuates ANF-induced inhibition of tubuloglomerular feedback

1990 ◽  
Vol 258 (1) ◽  
pp. F189-F198 ◽  
Author(s):  
D. M. Pollock ◽  
W. J. Arendshorst
Keyword(s):  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Pressure Range ◽  
Tubuloglomerular Feedback ◽  
Fluid Delivery ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Flow Pressure ◽  
Stop Flow

The effect of atrial natriuretic factor [ANF-(1–28); 0.25 microgram.kg-1.min-1] on tubuloglomerular feedback (TGF) and the efficiency of renal blood flow (RBF) autoregulation was determined in anesthetized euvolemic rats. In microperfusion studies, ANF dramatically inhibited (greater than 80%) feedback-mediated decreases in single-nephron glomerular filtration rate (SNGFR) and stop-flow pressure (Psf) when Henle's loop was perfused at 0–48 nl/min with artificial fluid. The sigmoidal relationship between Psf and loop perfusion during control was shifted to a linear relation during ANF; reactivity was almost nonexistent and no inflection point could be discerned. ANF almost completely blocked maximum Psf and SNGFR responses to loop perfusion at rates greater than 24 nl/min. In contrast 30 nl/min loop perfusion with native proximal tubular fluid obtained during ANF infusion restored maximum TGF activity to 70% of control levels. During ANF administration, the paired Psf responses to native and artificial perfusate were significantly different (-5.3 vs. -0.8 mmHg, P less than 0.001), compared with similar responses during control conditions (-7.6 vs. -8.3 mmHg, P greater than 0.1). In free-flow studies, ANF increased proximally and distally measured SNGFR equally. The constancy of the proximal-distal SNGFR difference (10.3 vs. 9.3 nl/min) in the presence of increased distal fluid delivery suggests partial inhibition of TGF during ANF administration. ANF elevated Psf but did not affect basal RBF or the RBF autoregulatory index over an arterial pressure range of 130–70 mmHg. These results indicate that 1) RBF autoregulation is efficiently maintained during ANF infusion when preglomerular vessels are vasodilated and TGF is inhibited by approximately 30%; 2) an endogenous factor(s) in native proximal tubular fluid may attenuate ANF-induced inhibition of TGF; and 3) microperfusion studies using artificial fluid significantly overestimate the net in vivo effect of ANF on TGF.

Filtration rate and stop-flow pressure feedback responses to nephron perfusion in the dog

1978 ◽  
Vol 234 (2) ◽  
pp. F154-F165 ◽  
Author(s):  
P. D. Bell ◽  
C. Thomas ◽  
R. H. Williams ◽  
L. G. Navar
Keyword(s):  
Filtration Rate ◽  
Feedback System ◽  
Electrolyte Solutions ◽  
Feedback Mechanism ◽  
Perfusion Rate ◽  
Glomerular Function ◽  
Pressure Feedback ◽  
Flow Pressure ◽  
Distal Perfusion ◽  
Stop Flow

Experiments were performed to evaluate the influence of the distal tubular feedback mechanism on glomerular function in the dog. Single nephron glomerular filtration rate (SNGFR) and stop-flow pressure (SFP) were measured from early segments of proximal tubules during alterations in distal perfusion rate (via a late proximal puncture site) and perfusate composition. Perfusion rate (PR) was varied from 16 to 68 nl/min with a microperfusion pump. The intermediate segment of the nephron was blocked with a solid wax cast, thus preventing retrograde influences of the microperfusion procedure. During perfusion with an ultrafiltrate of plasma and an artificial tubular fluid solution (ATF), SNGFR decreased from 63 +/- 2.6 (SE) nl/min at a PR of 16 nl/min to 20 +/- 2.4 nl/min at a PR of 63 +/- 2.6 nl/min. At a PR of 16 nl/min, SFP was 48 +/- 1.3 mmHg with ultrafiltrate and ATF. Increases in PR to 68 nl/min led to a reduction in SFP to 26 +/- 1.5 mmHg. SFP was also measured during changes in PR with various electrolyte solutions of decreasing complexity. Elimination or substitution of Na+, K+, Cl-, HCO3-, and Ca2+ did not significantly alter the magnitude of the feedback response to increases in PR to 68 nl/min. These results confirm the existence of a feedback system in the dog capable of adjusting glomerular function in response to changes in distal perfusion rate. The results based on the various perfusion solutions fail to indicate a unique requirement for any specific component.

Effect of P-450 omega-hydroxylase metabolites of arachidonic acid on tubuloglomerular feedback

1994 ◽  
Vol 266 (6) ◽  
pp. F934-F941 ◽  
Author(s):  
A. P. Zou ◽  
J. D. Imig ◽  
P. R. Ortiz de Montellano ◽  
Z. Sui ◽  
J. R. Falck ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Rate Dependent ◽  
Nephron Segment ◽  
Flow Pressure ◽  
Renal Vascular ◽  
Stop Flow ◽  
Renal Vascular Tone

The role of endogenous P-450 metabolites of arachidonic acid (AA) on the tubuloglomerular feedback (TGF) response was examined. Under control conditions stop-flow pressure (SFP) fell by 17.0 +/- 2.1 mmHg when the perfusion rate of the loop of Henle was increased from 0 to 50 nl/min. Addition of AA (50 microM) to the perfusate lowered basal SFP by 11.4 +/- 1.1 mmHg and potentiated the TGF response. This effect was blocked by addition of a P-450 inhibitor, 17-octadecynoic acid (17-ODYA) (10 microM), to the perfusate. Perfusion of the loop of Henle with 17-ODYA elevated basal SFP by 3.7 +/- 0.3 mmHg and reduced the TGF response by 80%. After blockade of endogenous P-450 activity with 17-ODYA, addition of 20-hydroxyeicosatetraenoic acid (20-HETE, 10 microM) to the perfusate produced a flow rate-dependent fall in SFP. The effect of 20-HETE was not altered by pretreating the animal with meclofenamate (2 mg/kg iv) or by perfusing the nephron segment with furosemide (50 microM). These results indicate that endogenous P-450 metabolites of AA, particularly 20-HETE, may play a role in TGF and the regulation of renal vascular tone.

Enhanced tubuloglomerular feedback activity in rats developing spontaneous hypertension

1984 ◽  
Vol 247 (4) ◽  
pp. F672-F679 ◽  
Author(s):  
J. R. Dilley ◽  
W. J. Arendshorst
Keyword(s):  
Arterial Pressure ◽  
Strain Differences ◽  
Tubuloglomerular Feedback ◽  
Adult Rats ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Flow Through ◽  
Flow Pressure ◽  
Wistar Kyoto ◽  
Stop Flow

Tubular microperfusion was used to evaluate tubuloglomerular feedback (TGF)-mediated changes in single nephron glomerular filtration rate (SNGFR) and stop-flow pressure (SFP) in euvolemic 6- and 11- to 14-wk-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Young SHR compared with WKY had an elevated mean arterial pressure (107 vs. 90 mmHg, P less than 0.001) and a lower proximally measured SNGFR (14 vs. 17 nl/min, P less than 0.001) with no loop perfusion. Perfusion at 32 nl/min produced a greater decrease in SNGFR of SHR (6 vs. 2 nl/min, P less than 0.001). Although basal SFPs were identical (39 mmHg), loop perfusion elicited a greater maximal decline in SFP (-10 vs. -4 mmHg, P less than 0.001) and reactivity of SFP (-1.2 vs. -0.5 mmHg X min X nl-1, P less than 0.001) in young SHR; a lower rate produced a half-maximal decrease in SFP (7 vs. 10 nl/min, P less than 0.02). In adult rats, SNGFRs with no flow through Henle's loop were the same (27 and 28 nl/min) and perfusion at 32 nl/min produced similar decrements in SNGFR (-13 vs. -11 nl/min). The maximal change in SFP was greater in adult SHR (-12 vs. -10 mmHg, P less than 0.02), but there were no strain differences in maximal SFP reactivity (-1.8 vs. -1.3 mmHg X min X nl-1) and the rate eliciting half-maximal SFP changes (12 vs. 12 nl/min). Reduction of arterial pressure to the normotensive range did not alter responses in either age group of SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of isoprostane on tubuloglomerular feedback: roles of TP receptors, NOS, and salt intake

2005 ◽  
Vol 288 (4) ◽  
pp. F757-F762 ◽  
Author(s):  
William J. Welch
Keyword(s):  
Salt Intake ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Dietary Salt ◽  
Low Salt ◽  
Luminal Perfusion ◽  
Tp Receptors ◽  
Flow Pressure ◽  
Stop Flow ◽  
Stimulation Of

A thromboxane prostanoid receptor (TP-R) agonist U-46,619 enhances tubuloglomerular feedback (TGF). Glomerular expression of TP-R and enhancement of TGF by U-46,619 increase with salt intake. We investigated the hypothesis that 8-isoprostaglandin F2α (8-Iso) activates TGF via TP-R. The maximal TGF response in rats was assessed from the fall in proximal stop flow pressure (PSF; an index of glomerular capillary pressure) during loop of Henle (LH) microperfusion of artificial tubular fluid (ATF) at 40 nl/min. Microperfusion of 8-Iso (10−4 M) into the efferent arteriole (EA) enhanced TGF responses by 20 ± 3% ( P < 0.01). TGF response to 8-Iso was independent of dietary salt [ΔTGF%, low salt (LS): 21 ± 5%; normal salt (NS): 17 ± 4%; high salt (HS): 29 ± 8%, not significant (ns)], unlike the salt-dependent effect of U-46,619 (ΔTGF%, LS: 41 ± 5%; NS: 52 ± 4%; HS: 112 ± 21%). Ifetroban, the TP-R antagonist, abolished TGF responses to 8-Iso and U-46,619 at all levels of salt intake. During luminal perfusion of N-monomethyl-l-arginine (l-NMA), the effect of 8-Iso on TGF was enhanced in NS and HS but not in LS (LS: 22 ± 6 vs. LS + l-NMA: 28 ± 6%, ns; NS: 18 ± 4 vs. NS + l-NMA: 40 ± 4, P < 0.01; HS: 27 ± 3 vs. HS + l-NMA: 65 ± 6, P < 0.01). However, U-46,619 did not further increase TGF after l-NMA in all salt groups (LS: 43 ± 7 vs. LS + l-NMA: 51 ± 6, ns; NS: 52 ± 7 vs. NS + l-NMA: 48 ± 8, ns; HS: 114 ± 21 vs. HS + l-NMA: 74 ± 22, ns). In conclusion, activation of TP receptors by U-46,619 and 8-Iso-PGF2α enhances TGF. In addition, the effect of U-46,619 was salt dependent, whereas the effect of 8-Iso-PGF2α was salt independent. However, stimulation of NO by 8-isoprostanes masks its salt-sensitive effect on TGF.

Feedback responses during sequential inhibition of angiotensin and thromboxane

1990 ◽  
Vol 258 (3) ◽  
pp. F457-F466 ◽  
Author(s):  
W. J. Welch ◽  
C. S. Wilcox
Keyword(s):  
Enzyme Inhibitor ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Ang Ii ◽  
Synthesis Inhibitor ◽  
In Series ◽  
Flow Pressure ◽  
Induced Changes ◽  
Sequential Inhibition ◽  
Stop Flow

Since thromboxane (Tx) can mediate the actions of angiotensin II (ANG II), we investigated interaction between these systems on the tubuloglomerular feedback (TGF) response. TGF was assessed from proximal stop-flow pressure (PSF) during orthograde perfusion of the loop of Henle (LH) between 0 and 40 nl/min. In the basal state, TGF was 11.3 +/- 0.8 mmHg. In series 1 experiments, it was unaltered by vehicle (+0.3 +/- 0.9 mmHg, n = 9, NS), was reduced by an ANG II antagonist, saralasin (-2.4 +/- 1.1 mmHg, n = 8, P less than 0.0005), and by a TxA2 antagonist SQ 29,548 (-4.8 +/- 0.6 mmHg, n = 11, P less than 0.0001). Both drugs together produced an additive blunting of TGF of -6.9 +/- 0.7 mmHg. In series 2 experiments, TGF was again unchanged by vehicle (+0.2 +/- 0.6 mmHg). It was reduced by -4.4 +/- 0.2 mmHg (P less than 0.0001) by an angiotensin-converting enzyme inhibitor CGS-14,824A (50 mg/kg, n = 5) and by -4.0 +/- 0.4 mmHg (P less than 0.001) by a Tx synthesis inhibitor CGS-13,080 (50 mg/kg, n = 7). Although both drugs together produced a further blunting of the response of -6.1 +/- 0.4 mmHg, this was significantly (P less than 0.001) less than additive. In both series, a response (averaging 3.5 +/- 0.3 mmHg) persisted in all rats given combined antagonists or inhibitors. In conclusion, both ANG II and TxA2 can modulate TGF-induced changes in PSF independently, and the response probably requires other system(s) in addition to ANG II and TxA2.

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