Kidney Function during Decreased Perfusion Pressure Due to Aortic Clamping and Hemorrhagic Hypotension: A Single Nephron Study in Dog Kidney

Heller, J; Horáček, Vladislav

doi:10.1159/000172928

Cited by 10 publications

(10 citation statements)

References 16 publications

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“…The two decades of experience in micropuncturing the dog kidney are probably the reason why our results now, despite the principal similarity, are superior (with regard to the scatter of data) to our earlier experiments (Heller & Horacek, 1984). Thus, although the Kf value showed 'a surprising tendency to rise' (Shirley & Walter, 1995) in our earlier paper, this nonsignificant tendency is not present now.…”

Section: Discussioncontrasting

confidence: 54%

“…We have shown previously (Heller & Horacek, 1984) that this vasoconstriction during mild HH is more pronounced in the efferent than in the afferent arteriole; this difference disappears as HH progresses. These findings of ours were recently criticized (Shirley &Walter, 1995) for using an indirect approach based on a number of challengeable assumptions.…”

Section: Introductionmentioning

confidence: 73%

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Glomerular haemodynamics during renal artery clamping and haemorrhage in the dog

Heller

Horáček²

1997

Experimental Physiology

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SUMMARYThe influence of a gradual decline in renal perfusion pressure (RPP) due either to renal artery clamping (C) or to haemorrhagic hypotension (HH) was studied using micropuncture techniques in anaesthetized dogs. The decrease in renal blood flow (RBF) was more profound and set in earlier during HH than during C, where perfect autoregulation was observed down to a mean arterial blood pressure of 85 mmHg. Glomerular filtration rate (GFR) was also only slightly decreased during C with no change in filtration fraction (FF); again, a much greater decrease in GFR with an increase in FF was seen in HH. The excretion of water, electrolytes and urea were also more decreased during HHAan during C.-Simlar--hanges were seen at the single nephron (SN) level. Opposite changes were observed in arteriolar resistances: during C a decrease in total arteriolar resistance (RT) amounting to -22 % at a RPP of 84 mmHg and -13 % at 60 mmHg was seen, due exclusively to a drop in afferent resistance (RA), but during HH there was a significant increase in RT by +36 % at a RPP of 110 mmHg, +39 % at 85 mmHg and +68 % at 60 mmHg. This increase was mainly due to an increase in efferent resistance (RE) rather than in RA: +42 vs. +31 %, respectively, at 1 10 mmHg and +67 vs. +19 %, respectively, at 85 mmHg. It was not until a RPP of 60 mmHg was reached that this difference between RE and RA disappeared, being +67 % for RE and +69 % for RA. The ultrafiltration coefficient, Kf, did not change during C and only decreased slightly with the biggest drop in RPP during HH (2-84 /sl mmHg-1 min-1 during HH vs.4.19 #1 mmHg-' min-' before HH). The SNGFR/GFR ratio remained unchanged during C but declined with decreasing RPP during HH, which probably indicates a 'redistribution' of RBF to the deeper regions of the renal cortex. In conclusion, major differences in renal function were observed between C and HH whose cause is unknown.

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Section: Discussioncontrasting

confidence: 54%

Section: Introductionmentioning

confidence: 73%

Glomerular haemodynamics during renal artery clamping and haemorrhage in the dog

Heller

Horáček²

1997

Experimental Physiology

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“…Another factor contributing to the limited proximal tubular response 628 might be a fall in colloid osmotic pressure in peritubular capillaries: plasma protein concentration is reduced following haemorrhage as a result of the rapid entry of interstitial fluid into the vascular compartment (Bealer, 1986;Shirley et al 1991). However, although direct evidence exists for a reduced colloid osmotic pressure in efferent arterioles following haemorrhage (Heller & Horacek, 1984), the same study also reported a fall in peritubular capillary hydrostatic pressure. The net change in peritubular physical factors is therefore likely to be small.…”

Section: Resultsmentioning

confidence: 98%

“…In the one detailed study of glomerular dynamics that has been performed (in dogs), Heller & Horacek (1984) found that stepwise haemorrhage-induced reductions in blood pressure caused stepwise reductions in glomerular capillary pressure, although there was a surprising tendency for the calculated ultrafiltration coefficient to rise. Computed values for both afferent and efferent arteriolar resistances increased after haemorrhage, but these calculations were very indirect and based on a number of challengeable assumptions; they therefore provide little clue to the mechanisms involved.…”

Section: Resultsmentioning

confidence: 99%

A micropuncture study of the renal response to haemorrhage in rats: assessment of the role of vasopressin

Shirley¹,

Walter²

1995

Experimental Physiology

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SUMMARYThe acute effects of haemorrhage (15 ml (kg body wt)-') on renal function at whole-kidney and single-nephron levels were studied in Inactin-anaesthetized rats. In order to assess the role of vasopressin in mediating the haemodynamic effects, responses in untreated Long-Evans rats were compared with those in Brattleboro rats (which lack circulating vasopressin) and in Long-Evans rats treated with a V1 receptor antagonist. In time-control animals, there were no significant changes in mean arterial pressure (MAP), excretion rates, glomerular filtration rate (GFR), superficial-nephron GFR (SNGFR) or fluid reabsorption in the superficial proximal tubules during the course of the experiment. Following haemorrhage, the immediate reduction in MAP was followed in each group by partial recovery for 30 min; thereafter, MAP was stable. In untreated Long-Evans rats, haemorrhage was followed by a 26 % reduction in GFR (P < 0-001, measured 60-150 min post-haemorrhage) and a larger reduction (45 %, P < 0.001) in SNGFR, so that the SNGFR/GFR ratio fell significantly ((27.9 + 1.9) x 10-6, control period; (20.2 + 2-2) x 10-6, post-haemorrhage, P <0.01). Slightly greater reductions in GFR and SNGFR were seen in Brattleboro rats and V, antagonist-treated Long-Evans rats, which corresponded to slightly greater haemorrhage-induced reductions in blood pressure in these groups; the falls in the SNGFR/GFR ratio were similar to that in untreated Long-Evans rats. In all three groups of bled rats, fractional reabsorption by the proximal convoluted tubule increased slightly 30-60 min after haemorrhage, but during the subsequent period (60-150 min) returned to values indistinguishable from those during the control period. The results suggest that the renal haemodynamic changes that follow moderate haemorrhage include a preferential reduction in the GFR of superficial nephrons. Vasopressin appears to play no role in this response. Increases in fractional reabsorption in the proximal tubules are seen only during the immediate post-haemorrhage period.

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“…These were described in detail previously [17,18]. Briefly, femoral vessels and both ureters were cannulated for BP monitoring, i.v.…”

Section: Experimental Techniquesmentioning

confidence: 99%

Effect of Intrarenal Infusion of Angiotensin–(1–7) in the Dog

Heller

Kramer

Malý

et al. 2000

Kidney Blood Press Res

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Angiotensin–(1–7), (Ang–(1–7)), a metabolite of Ang II and /or Ang I, was infused into the renal artery (i.r.a) of anesthetized dogs in order to demonstrate its possible direct renal action. The dose administered, 15 Ìg/kg BW/min in isotonic saline (0.072 ml/kg BW/min) throughout the experiment, did not influence the systemic arterial pressure and water and sodium excretion from the contralateral noninfused kidney. Renal blood flow (RBF) was measured by an electromagnetic flowmeter, glomerular filtration rate (GFR) by (exogenous) creatinine clearance. In other groups of animals, either EXP 3174, an AT–1 receptor antagonist alone (30 Ìg/kg BW/ min) or together with Ang–(1–7) (15 Ìg/kg BW/min), were infused. In the last group, the AT–2 receptor antagonist PD 123319, 10 Ìg/kg BW/min, was added to the infusion of Ang–(1–7). A small but significant decrease of RBF from 4.51±0.32 to 3.8±0.29 ml/g BW/min occurred after Ang–(1–7); this decrease was very similar when PD 123319 was added. However, an increase to 4.98±0.34 ml/g BW/min was seen after the addition of EXP 3174 to the i.r.a. infusion of Ang–(1–7); this increase was similar to the increase observed after EXP 3174 alone (5.21±0.33; p<0.02 in both cases). A very small but significant increase in GFR was seen after Ang–(1–7) + EXP 3174 or after the AT–1 blocker alone (0.64±0.049 and 0.62±0.05 vs. 0.6±0.05 ml/g BW/min in the Time Control Group, p<0.01 and 0.05, respectively). Water, sodium and urea excretion rates were increased in all groups infused with Ang–(1–7); after the combination of Ang–(1–7) + EXP 3174, all increases were higher than after every substance alone; however, statistical significance (p<0.05) was reached in sodium excretion values only. Potassium excretion rates were increased just in those groups in which EXP 3174 was present in the infusion fluid. In summary, Ang–(1–7) i.r.a. infusion in the dog is followed by increases in water, sodium and urea (but not potassium) excretion rates, highly probably of tubular origin. This effect is not completely blocked by the AT–1 – and not at all by the AT–2 receptor antagonist – thus indirectly suggesting another receptor could play a role. A small decrease in RBF disappears after EXP 3174, thus indicating an AT–1 receptor action.

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Kidney Function during Decreased Perfusion Pressure Due to Aortic Clamping and Hemorrhagic Hypotension: A Single Nephron Study in Dog Kidney

Cited by 10 publications

References 16 publications

Glomerular haemodynamics during renal artery clamping and haemorrhage in the dog

Glomerular haemodynamics during renal artery clamping and haemorrhage in the dog

A micropuncture study of the renal response to haemorrhage in rats: assessment of the role of vasopressin

Effect of Intrarenal Infusion of Angiotensin–(1–7) in the Dog

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