Renal interstitial pressure and sodium excretion during renal vein constriction

Studies were performed on anesthetized dogs to determine the relationship of interstitial pressure to sodium excretion during renal vein constriction in the presence and absence of volume expansion. Renal interstitial pressure was measured from implanted capsules during basal renal venous pressure and increased pressures of 10, 20, 30, and 40 mmHg. A positive relationship between renal venous pressure and interstitial pressure was demonstrated in hydropenia and in volume expansion, with markedly higher interstitial pressures obtained in volume expansion. A positive correlation was demonstrated between fractional sodium excretion and renal interstitial pressure in hydropenia as compared to a significant negative correlation in volume expansion. Negative correlations were demonstrated in volume expansion between renal interstitial pressure and glomerular filtration rate and renal blood flow as compared to no significant change in these parameters in hydropenia. Accordingly, a positive correlation was demonstrated between renal interstitial pressure and sodium excretion in hydropenia but not in volume expansion. Volume expansion was characterized by higher interstitial pressure and decreased sodium excretion in association with decreased renal blood flow and glomerular filtration rate.

Download Full-text

Supersensitivity to norepinephrine in chronically denervated kidneys: evidence for a postsynaptic effect

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-351 ◽

1987 ◽

Vol 65 (11) ◽

pp. 2219-2224 ◽

Cited By ~ 5

Author(s):

J. Krayacich ◽

R. L. Kline ◽

P. F. Mercer

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Filtration Rate ◽

Fractional Excretion ◽

Urine Flow ◽

Fractional Excretion Of Sodium ◽

Infusion Of Norepinephrine

Denervation supersensitivity in chronically denervated kidneys increases renal responsiveness to increased plasma levels of norepinephrine. To determine whether this effect is caused by presynaptic (i.e., loss of uptake) or postsynaptic changes, we studied the effect of continuous infusion of norepinephrine (330 ng/min, i.v.) and methoxamine (4 μg/min, i.v.), an α1 adrenergic agonist that is not taken up by nerve terminals, on renal function of innervated and denervated kidneys. Ganglionic blockade was used to eliminate reflex adjustments in the innervated kidney and mean arterial pressure was maintained at preganglionic blockade levels by an infusion of arginine vasopressin. With renal perfusion pressure controlled there was a significantly greater decrease in renal blood flow (−67 ± 9 vs. −33 ± 8%), glomerular filtration rate (−60 ± 9 vs. −7 ± 20%), urine flow (−61 ± 7 vs. −24 ± 11%), sodium excretion (−51 ± 15 vs. −32 ± 21%), and fractional excretion of sodium (−50 ± 9 vs. −25 ± 15%) from the denervated kidneys compared with the innervated kidneys during the infusion of norepinephrine. During the infusion of methoxamine there was a significantly greater decrease from the denervated compared with the innervated kidneys in renal blood flow (−54 ± 10 vs. −30 ± 14%), glomerular filtration rate (−51 ± 11 vs. −19 ± 17%), urine flow (−55 ± 10 vs. −39 ± 10%), sodium excretion (−70 ± 9 vs. −59 ± 11%), and fractional excretion of sodium (−53 ± 10 vs. −41 ± 10%). These results suggest that vascular and tubular supersensitivity to norepinephrine in chronically denervated kidneys is due to postsynaptic changes involving α1-adrenergic receptors.

Download Full-text

Effect of a kinin antagonist on renal function and haemodynamics during alterations in sodium balance in conscious normotensive rats

Clinical Science ◽

10.1042/cs0780165 ◽

1990 ◽

Vol 78 (2) ◽

pp. 165-168 ◽

Cited By ~ 6

Author(s):

Paolo Madeddu ◽

Nicola Glorioso ◽

Aldo Soro ◽

Paolo Manunta ◽

Chiara Troffa ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Filtration Rate ◽

Sodium Intake ◽

Urinary Sodium Excretion

1. To evaluate whether sodium intake can modulate the action of endogenous kinins on renal function and haemodynamics, a receptor antagonist of bradykinin was infused in conscious normotensive rats maintained on either a normal or a low sodium diet. 2. The antagonist inhibited the hypotensive effect of exogenously administered bradykinin. It did not change the vasodepressor effect of acetylcholine, dopamine or prostaglandin E2. 3. The antagonist did not affect mean blood pressure, glomerular filtration rate, renal blood flow or urinary sodium excretion, in rats on sodium restriction. It did not change mean blood pressure, glomerular filtration rate or urinary sodium excretion, but decreased renal blood flow, in rats on a normal sodium intake. 4. The kallikrein–kinin system has a role in the regulation of renal blood flow in rats on a normal sodium diet.

Download Full-text

Effect of secretin on renal blood flow, interstitial pressure, and sodium excretion

AJP Renal Physiology ◽

10.1152/ajprenal.1977.232.2.f147 ◽

1977 ◽

Vol 232 (2) ◽

pp. F147-F151 ◽

Cited By ~ 4

Author(s):

G. R. Marchand ◽

C. E. Ott ◽

F. C. Lang ◽

R. F. Greger ◽

F. G. Knox

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Glomerular Filtration Rate ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Filtration Rate ◽

Similar Increase ◽

Interstitial Pressure ◽

Polyethylene Matrix ◽

The Relationship

Most renal vasodilators are natriuretic. However, secretin increases renal blood flow (RBF) markedly but produces only a very slight increase in sodium excretion (UNaV). To investigate this observation further, the relationship between vasodilatation, interstitial pressure (IP), and UNaV was studied in dogs. Intrarenal infusion of secretin increased RBF (delta=107+/-19 ml/min). The IP, as measured from chronically implanted polyethylene matrix capsules, was not significantly changed (delta=-0.3+/-0.5 mmHg). UNaV was slightly, although significantly, increased (delta=19+/-4 mueq/min). Following a similar increase in RBF with an intrarenal infusion of acetylcholine (ACh), IP and UNaV increased markedly (delta=8.2+/-0.8 mmHg and 174+/-23 mueq/min, respectively). Neither secretin nor ACh) altered glomerular filtration rate or blood pressure. Both secretin and ACh produced comparable increases in peritubule capillary(delta=5+/-1 and 7.5+/-1.4 mmHg, respectively) and free-flow tubule pressure (delta=7+/-2 and 9.5+/-1.4 mmHg, respectively). In summary, the usual relationship between vasodilatation and IP was dissociated during secretin infusion, whereas the relationship between IP and natriuresis was not dissociated.

Download Full-text

Tubuloglomerular feedback during elevated renal venous pressure

AJP Renal Physiology ◽

10.1152/ajprenal.1985.249.4.f524 ◽

1985 ◽

Vol 249 (4) ◽

pp. F524-F531 ◽

Cited By ~ 5

Author(s):

U. Boberg ◽

A. E. Persson

Keyword(s):

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Volume Expansion ◽

Filtration Rate ◽

Venous Pressure ◽

Tubuloglomerular Feedback ◽

Interstitial Pressure ◽

Single Nephron ◽

Flow Pressure ◽

Stop Flow

Interstitial hydrostatic and oncotic pressures are believed to influence the sensitivity of the tubuloglomerular feedback (TGF) control. To further investigate this hypothesis, three groups of experiments with elevated renal venous pressure (Prv) were conducted. We investigated 1) the stop-flow pressure (Psf) feedback response; 2) urine flow rate, glomerular filtration rate (GFR), subcapsular interstitial hydrostatic pressure (Psc), and interstitial oncotic pressure (pi int); and 3) the proximal-distal single nephron glomerular filtration rate (SNGFR). The results showed that the Psf feedback response was unaffected by Prv elevation. Psc increased from 0.5 to 3.5 mmHg and pi int increased from 2.1 to 5.8 mmHg; thus, no change in net interstitial pressure (Psc - pi int) was found during elevated Prv. There was a significant proximal-distal SNGFR difference during both control and elevated Prv (8.0 and 6.3 nl/min, respectively). A 20% reduction in total GFR and SNGFR was observed at increased Prv. In separate experiments using the same protocol, a 5% body wt/h volume expansion with saline was induced before Prv was elevated. During volume expansion, TGF sensitivity declined and net interstitial pressure increased, both of which were normalized by increasing Prv. The results show that the TGF sensitivity is normal during elevated Prv to 20 mmHg and that the increase in Psc during this condition is counter-balanced by an increase in pi int. In addition, the decrease in GFR and SNGFR during increased Prv cannot be explained by a change in TGF activity. However, these findings indicate that both interstitial hydrostatic and oncotic pressures may influence the resetting of the TGF sensitivity.

Download Full-text

Glomerular filtration rate, effective renal plasma flow and renal blood flow in adult chacma baboons (Papio ursinus)

Comparative Biochemistry and Physiology Part A Molecular & Integrative Physiology ◽

10.1016/s1095-6433(99)90309-4 ◽

1999 ◽

Vol 124 ◽

pp. S78

Author(s):

JP Evans ◽

GP Candy ◽

MG Veller ◽

JD Esser

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Plasma Flow ◽

Filtration Rate ◽

Renal Plasma Flow ◽

Effective Renal Plasma Flow ◽

Papio Ursinus ◽

Chacma Baboons

Download Full-text

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

Clinical Science ◽

10.1042/cs0740063 ◽

1988 ◽

Vol 74 (1) ◽

pp. 63-69 ◽

Cited By ~ 35

Author(s):

S. B. Harrap ◽

A. E. Doyle

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Filtration Rate ◽

Spontaneously Hypertensive Rat ◽

Plasma Renin ◽

Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Download Full-text