Glomerular ultrafiltration in rabbits with superficial glomeruli

Denton, Kate M.; Anderson, Warwick P.

doi:10.1007/bf00371101

Cited by 18 publications

(33 citation statements)

References 27 publications

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“…The rabbits were from a colony in which 50 % of the rabbits have glomeruli visible on the surface of the kidney. The glomerular characteristics have been recently reported (Denton & Anderson, 1990, 1991a. These rabbits originated from a larger colony of multicoloured English crossbred rabbits, which have been used extensively in various physiological studies (e.g.…”

Section: Animalsmentioning

confidence: 99%

“…Single (Denton & Anderson, 1990, 1991a for glomerular ultrafiltration at the afferent (PUfa) and efferent (Pufe) ends of the glomerular capillaries were calculated as previously described (Denton & Anderson, 1991a) and the mean ultrafiltration pressure (P0f) was calculated using the formula of Deen, Robertson & Brenner (1972). This formula can only be used if there is net positive pressure at the end of the glomerular capillaries (Deen et al 1972), which is so in these rabbits (Denton & Anderson, 1991a).…”

Section: Measurementsmentioning

confidence: 99%

“…This formula can only be used if there is net positive pressure at the end of the glomerular capillaries (Deen et al 1972), which is so in these rabbits (Denton & Anderson, 1991a). Tubular oncotic pressure was assumed to be zero (Mitruka & Rawnsley, 1977) and efferent arteriolar protein concentration estimated as previously described (Denton & Anderson, 1991a). The glomerular ultrafiltration coefficientwas calculated as:…”

Section: Measurementsmentioning

confidence: 99%

“…In the study presented here, we have used a unique strain of rabbits with superficial glomeruli (Denton & Anderson, 1991a) to test whether this species responds to NO inhibition in a similar manner to rats by measuring the effects on preand postglomerular resistance and on function in this species. The glomerular and renal vascular physiology of these rabbits have been described recently (Denton & Anderson, 1991a) and they represent a useful second laboratory species in which renal micropuncture techniques can be used to study intrarenal haemodynamic, glomerular and tubular physiology.…”

mentioning

confidence: 99%

“…The glomerular and renal vascular physiology of these rabbits have been described recently (Denton & Anderson, 1991a) and they represent a useful second laboratory species in which renal micropuncture techniques can be used to study intrarenal haemodynamic, glomerular and tubular physiology. The only readily available laboratory species with superficial glomeruli has been the Munich-Wistar rat, and Zatz & De Nucci (1991) have reported that blockade of NO production produced both pre-and postglomerular constriction, and markedly reduced the glomerular ultrafiltration coefficient in these animals.…”

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confidence: 99%

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Intrarenal haemodynamic and glomerular responses to inhibition of nitric oxide formation in rabbits.

Denton

Anderson

1994

The Journal of Physiology

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1. The renal effects of inhibiting nitric oxide (NO) formation using N-nitro-L-arginine (NOLA, 20 mg kg1) were examined using micropuncture techniques in pentobarbitoneanaesthetized rabbits.2. Renal vascular resistance doubled from 2-7 + 0 5 to 5 0 + 11 mmHg ml' min' after NOLA (P < 0-01), with similar percentage increases in both pre-(149 + 38 %, P < 0-01) and postglomerular (158 + 42 %, P < 0-01) resistance.3. Glomerular capillary pressure rose from 33 +1 to 40 +1 mmHg after NOLA (P < 0-01) but despite this, glomerular filtration rate (GFR) and single nephron glomerular filtration rate did not significantly change.4. Blood pressure increased 18 + 1 mmHg (P < 0'001) within 10 min of NOLA administration and remained near this level for the next 90 min. 5. The glomerular ultrafiltration coefficient (Kf) decreased significantly from 0-085 + 0-022 to 0'035 + 0-006 nl s' mmHg1 (P < 0 05).6. Urine flow and sodium excretion increased markedly (26 + 9 to 337 ± 102 #1 min' and 5 + 2 to 342 + 12 ,umol min' respectively, (P < 0-001)) and sodium fractional excretion rose from 1.0 + 0 3 to 8-0 + 2-2 % (P < 0-01).7. Thus, administration of NOLA to rabbits caused vasoconstriction of both pre-and postglomerular vessels, diuresis and natriuresis without significant change in GFR, and a reduction in Kf. The results suggest that NO may play an important role in the regulation of renal haemodynamics and glomerular function.

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Section: Animalsmentioning

confidence: 99%

Section: Measurementsmentioning

confidence: 99%

Section: Measurementsmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Intrarenal haemodynamic and glomerular responses to inhibition of nitric oxide formation in rabbits.

Denton

Anderson

1994

The Journal of Physiology

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Renal Vascular Structure and Rarefaction

Chade¹

2013

Comprehensive Physiology

107

102

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An intact microcirculation is vital for diffusion of oxygen and nutrients and for removal of toxins of every organ and system in the human body. The functional and/or anatomical loss of microvessels is known as rarefaction, which can compromise the normal organ function and have been suggested as a possible starting point of several diseases. The purpose of this overview is to discuss the potential underlying mechanisms leading to renal microvascular rarefaction, and the potential consequences on renal function and on the progression of renal damage. Although the kidney is a special organ that receives much more blood than its metabolic needs, experimental and clinical evidence indicates that renal microvascular rarefaction is associated to prevalent cardiovascular diseases such as diabetes, hypertension, and atherosclerosis, either as cause or consequence. On the other hand, emerging experimental evidence using progenitor cells or angiogenic cytokines supports the feasibility of therapeutic interventions capable of modifying the progressive nature of microvascular rarefaction in the kidney. This overview will also attempt to discuss the potential renoprotective mechanisms of the therapeutic targeting of the renal microcirculation.

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