Effect of variation in dietary NaCl intake on the intrarenal distribution of plasma flow in the rat

Blantz, Roland C.; Wallin, J. D.; Rector, Floyd C.; Seldin, Donald W.

doi:10.1172/jci107101

Cited by 12 publications

(8 citation statements)

References 16 publications

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“…However, it is consistent with a number of studies in conscious animals (11,12) and in man (10), in which renal blood flow was found to be unaffected by sodium depletion. It is possible, in part, that the conflicting results are related to the different methods used by the investigators to measuire renal blood flow.…”

Section: Discussionsupporting

confidence: 91%

“…Similarly, inhibition of prostaglandin synthesis enhaniees the renial iselmeiiit mediated by angiotensin II a1nad the symiipathetic nerves during hemorrhagic hypotension in clogs (9). Furthermore, it is of interest that the renial 1)lood0 flow is not invaribly reduced by sodium depletion despite activation of the renin angiotensin system (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

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Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Oliver¹,

Pinto²,

Sciacca³

et al. 1980

J. Clin. Invest.

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A B S T R A C T To determine whether vasoactive renal hormones modulate renal blood flow during alterations of sodium balance, simultaneous measurements of arterial and renal venous concentrations of norepinephrine and prostaglandin E2 (PGE2) and of plasma renin activity, as well as renal blood flow and systemic hemodynamics were carried out in 24 sodiumdepleted and 28 sodium-replete anesthetized dogs. The mean arterial blood pressure of the sodium depleted dogs was not significantly different from that of the animals fed a normal sodium diet, but cardiac outptut was significantly lower (3.07±0.18 vs. 3.77±0.17 liters/mim, mean±SEM; P < 0.01). Despite the higher total peripheral vascular resistance in the sodiumdepleted dogs (46.1±2.9 vs. 37.0±2.1 arbitrary resistance U; P < 0.02), the renal blood flow and renal vascular resistance were not significantly different in the two groups. The arterial plasma renin activity and concentration of norepinephrine were higher in the sodium-depleted animals than in the controls; the arterial concentration of PGE2 was e(ual in both groups. The renal venous plasma renin activity was higher in the sodium-depleted dogs. Similarly, the renal venous norepinephrine concentration was higher in the sodium-depleted dogs than in the controls (457±44 vs. 196±25 pg/ml; P <0.01); renal venous PGE2 concentration was also higher in the sodium depleted dogs (92±22 vs. 48±11 pg/ml; P < 0.01). Administration of indomethacin to five sodium-replete dogs had no effect on renal blood flow. In five sodium-depleted dogs indomethacin lowered renal blood flow from 243±19 to 189+30 ml/min (P < 0.05) and PGE2 in renal venous blood from 71±14 to 15±2 pg/ml (P < 0.02). The results indicate that moderate chronic sodium depletion, in addition to enhancing the activity of the renin-angiotensin system, also increases the activity of the renal adrenergic nervous system and increases renal PGE2 synthesis. In sodiumReceived for publication 19 February 1980 and in revised form 4 June 1980. 748 depleted dogs, inhibition of prostaglandin synthesis was associated with a significant decrease in renal blood flow. The results suggest that the renal blood flow is maintained during moderate sodiulm depletion by an effect of the prostaglandins to oppose the vasoconstrictor effects of angiotensin II and the rencal sympathetic nervous system.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Oliver¹,

Pinto²,

Sciacca³

et al. 1980

J. Clin. Invest.

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“…A basic electrolyte-deficient liquid diet was used. The diet contained approximately 2 g of protein, carbohydrate, fat, amino acid supplements, trace elements, and full vitamin requirements per daily portion; 10 Na + and K + were then added to 2-liter quantities of this diet. Each animal was provided 40 ml of a semisolid diet containing 2 mEq Na + , 2 mEq K + .…”

Section: Balance Studiesmentioning

confidence: 99%

Glomerular hemodynamics in moderate Goldblatt hypertension in the rat.

Steiner¹,

Tucker²,

Gushwa³

et al. 1982

Hypertension

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SUMMARY Glomerular bemodynamics were studied by mJcropuncture technique in the undipped kidney in rats in which modest two kidney Goldblatt hypertension was maintained for 4 weeks and in normotensive controls. Both groups ingested less than 2 mEq Na + /day. In hypertensive rats at micropuncture, mean hydrostatic pressure was elevated both systemically (128 ± 5 vs 113 ± 3 mm Hg,p < 0.05) and within glomerular capillaries (55 ± 2 vs 48 ± 1 mm Hg,p < 0.05), resulting in an Increase in the transglomerular hydrostatic pressure gradient (40 ± 2 TS 33 ± 1 mm Hg, p < 0.05). The glomerular capillary permeability coefficient, however, was decreased in the hypertensive rats (0.063 ± 0.017 vs 0.115 ± 0.011 nl/s/g kw/mm Hg, p < 0.05), resulting in no change in nephron filtration rate (38.9 ± 2.3 TS 39.9 ± 2.5 nl/min/g kw). Nephron plasma flow also remained unchanged (154 ± 10 vs 140 ± 7 ml/mln/g kw). In separate studies in this model of hypertension, saralasin infusion demonstrated a peripheral effect of circulating angiotensin II which was increased over controls. Kidney mass and GFR were not different between clipped and undipped kidneys. No consistent abnormalities were observed by light or electron microscopy either in glomeruli or in vessels in the undipped kidney. This study demonstrates that glomerular bemodynamics may be altered early In the course of modest hypertension in this model without altering blood flow or fUtration rate. The deaease in glomerular capillary area and/or permeability (LpA) in the hypertensive rats could be either a result of the increased effect of circulating angiotensin II or the direct effect of glomerular capillary hypertension. 1 "* In much of this work, marked chronic systemic hypertension has produced significant secondary focal glomerular damage, coexisting with focal "superfunctioning" glomeruli. Thus, experimental findings in these models may be influenced by the process of compensatory glomerular hypertrophy. We therefore attempted the present micropuncture study, which examines glomerular pressures, flows, resistances, and permeabilities in the undipped kidney 4 weeks after moderate systemic hypertension was es- 51tablished in the Goldblatt hypertensive MunichWistar rat. This study was undertaken 4 weeks after hypertension was established to minimize the effects of both focal glomerular obsolescence and other structural changes in the glomeruli studied, e.g., segmental sclerosis and/or glomerular hypertrophy. In this way we sought to define the initial glomerular adaptations to systemic hypertension in a model exhibiting the moderate increases in blood pressure which are most frequently encountered in clinical populations. MethodsMale Munich-Wistar rats were used; they weighed 180 to 200 g (80-90 days old) at the start of the experiment. This strain of rat, raised and housed in an isolated colony at the Veterans Administration Medical Center, San Diego, California, characteristically provides from three to eight surface glomeruli accessible to micropuncture. Three groups of rats w...

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“…This is the conclusion which has also been reached by a number of workers studying different levels of sodium excretion in various animal preparations, using more direct methods to measure the intrarenal blood flow distribution (e.g. Blantz, Wallin and Rector, 1972;Stein et al, 1971).…”

Section: With Normal Renal Perfusionmentioning

confidence: 59%

Renal retention of sodium in cirrhosis and fulminant hepatic failure

Wilkinson¹,

Алам²,

Moodie³

et al. 1975

Postgraduate Medical Journal

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Summary Abnormal renal retention of sodium is a characteristic finding in both cirrhosis and fulminant hepatic failure. In cirrhosis the pathogenesis varies according to the level of renal perfusion. When this is normal, hyperaldosteronism is probably the most important factor and this results from an increased release of renin by the kidney. The stimulus to the latter may be a shunting of blood from the outer cortical to juxtamedullary nephrons, although there is no direct relationship between the changes in intrarenal blood flow distribution and sodium excretion. The patients with hyperaldosteronism fail to escape from its sodium retaining effects because of impaired production of natriuretic hormone, which in turn is the result of a failure to expand the ‘effective’ extracellular fluid volume, because of ascites formation. In fulminant hepatic failure the site in the nephron of abnormal sodium retention appears to be predominantly the proximal tubule, but its cause is obscure.

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Effect of variation in dietary NaCl intake on the intrarenal distribution of plasma flow in the rat

Cited by 12 publications

References 16 publications

Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Glomerular hemodynamics in moderate Goldblatt hypertension in the rat.

Renal retention of sodium in cirrhosis and fulminant hepatic failure

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