Influence of sodium deprivation and loading on the plasma‐renin in man

Brown, Jerry M.; Davies, D. L.; Lever, A. F.; Robertson, J. I. S.

doi:10.1113/jphysiol.1964.sp007464

Cited by 124 publications

(49 citation statements)

References 46 publications

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“…S., the amount of sodium excreted was 2-3 meq/day less than the measured amount of sodium ingested ( Fig. 1; Table IV), a characteristic occurrence in normal subjects during dietary restriction of sodium (23)(24)(25)(26).…”

Section: Resultsmentioning

confidence: 99%

Impaired renal conservation of sodium and chloride during sustained correction of systemic acidosis in patients with type 1, classic renal tubular acidosis.

Sebastián¹,

McSherry²,

Morris³

1976

J. Clin. Invest.

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A B S T R A C T in 10 patients with classic renal tubular acidosis in whom correction of acidosis was sustained with orally administered potassium bicarbonate, renal conservation of sodium was evaluated when dietary intake of sodium was restricted to 9-13 meq/day. In five patients, renal conservation of sodium was impaired by at least one criterion of impairment. In the remaining patients, renal conservation of sodium appeared to be relatively well-maintained, but an impairment could not be excluded. In each of six patients studied during induced water diuresis, including two in whom renal conservation of sodium was not unequivocally impaired, the minimal urinary concentrations of sodium were inappropriately high and the urinary excretion rates of sodium were flow-dependent. These results provide direct evidence that an abnormality in renal transport of sodium can occur in classic renal tubular acidosis, and compel a reconsideration of the pathophysiology of disordered renal transport of sodium in this disorder. The results indicate that in at least some patients with classic renal tubular acidosis impaired renal conservation of sodium is not exclusively a reversible consequence of the renal acidification defect. These findings raise the question whether renal transport of sodium is unimpaired in any patients with classic renal tubular acidosis. In the presently studied patients, the impairment in renal conservation of sodium appeared to be in part the consequence of an impaired ability of the vasopressinresponsive segments of the distal nephron to generate and maintain appropriately steep transepithelial sodium concentration gradients. INTRODUCTIONIn patients with classic renal tubular acidosis (type 1, "distal" RTA)V, irrespective of the presence or absence of nephrocalcinosis, correction of systemic acidosis with alkali therapy can result in a reduction of the urinary excretion rate of potassium, sodium, and aldosterone (1-9); when correction of acidosis is sustained and dietary intake of sodium and potassium is not restricted, the external balance of potassium and sodium can become sufficiently positive to correct hypokalemia and secondary hyperaldosteronism (4, 5). It has been inferred from these observations that the impairment in renal conservation of potassium and sodium demonstrable in untreated, acidotic patients with classic RTA is fully corrected when acidosis is corrected with alkali therapy (5). This inference constitutes the basis for the widely accepted conclusion that in classic RTA impaired renal conservation of potassium and sodium is exclusively a reversible consequence of the renal acidification defect (5, 10-13). But the validity of this inference can be questioned, since it cannot be ascertained from the results of published studies whether renal conservation of potassium and sodium is unimpaired when dietary intake of these ions is restricted and correction of acidosis is sustained (1)(2)(3)(4)(5)(6)(7)(8)(9) In the present investigation of children and adult patients with classic RTA, w...

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Section: Resultsmentioning

confidence: 99%

Impaired renal conservation of sodium and chloride during sustained correction of systemic acidosis in patients with type 1, classic renal tubular acidosis.

Sebastián¹,

McSherry²,

Morris³

1976

J. Clin. Invest.

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“…Preliminary studies in the nephrectomized rat (N = 3) had shown that this dose of inhibitor reduced the angiotensin I pressor response initially to 17%; after 60 minutes the response was still only 1 Generously supplied by Dr. R. A. Vukovick of the Squibb Institute.…”

Section: Methodsmentioning

confidence: 99%

“…A reciprocal relationship between plasma renin activity and sodium balance has been well documented (1,2). Thus, sodium depletion stimulates renin secretion, and sodium loading suppresses renin release.…”

mentioning

confidence: 99%

Prior receptor occupancy as a determinant of the pressor activity of infused angiotensin II in the rat.

Thurston¹,

Laragh²

1975

Circulation Research

131

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The pressor responsiveness to angiotensin II and norepinephrine was examined in rats before and during blockade of converting enzyme activity with the nonapeptide SQ 20881. Responses to angiotensin II were impaired by sodium deprivation but enhanced by sodium loading or bilateral nephrectomy. During the period of converting enzyme blockade, a twofold increase in the angiotensin II pressor response was observed in the salt-restricted rats, whereas only a small change occurred in the salt-loaded rats. Infusion of the inhibitor produced a profound fall in the blood pressure of the salt-depleted rats with a relatively minor fall in the sodium-loaded rats. Norepinephrine pressor responses were slightly potentiated in the salt-restricted rats after administration of SQ 20881, but no change occurred in the salt-loaded or the nephrectomized rats. These observations support the view that the decrease in angiotensin II pressor activity during salt deprivation is the result of a prior occupancy of receptor sites by endogenous hormone. Therefore, a change in the number or the affinity of receptors consequent to changes in sodium balance need not be postulated to explain the phenomenon. KEY WORDS pressor responsesodium depletion and loading blood pressure norepinephrine coverting enzyme blockade bilateral nephrectomy• Most studies of the renin-angiotensin system depend on measurements of the circulating levels of renin and angiotensin II. A reciprocal relationship between plasma renin activity and sodium balance has been well documented (1, 2). Thus, sodium depletion stimulates renin secretion, and sodium loading suppresses renin release. However, under circumstances of body fluid volume depletion, during which increased renin levels are found, pressor reactivity to exogenous angiotensin becomes markedly impaired (3-7). Conversely, when sodium is given in excess, especially if a mineralocorticoid is also administered, the pressor response to angiotensin infusion is enhanced (6). Thus, angiotensin pressor reactivity appears to correlate directly with sodium balance but in-

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“…Katsuyoshi Kudoh 1) , Chikashi Shibata 2) , Yuji Funayama 3) , Kouhei Fukushima 4) , Kenichi Takahashi 5) , Munenori Nagao 1) , Sho Haneda 5) , Kazuhiro Watanabe 1) , Takeshi Naitoh 1) and Michiaki Unno 1)…”

Section: Oral Rehydration Solution Normalizes Plasma Renin and Aldostmentioning

confidence: 99%

“…Dehydration and sodium deprivation induce hypersecretion of renin from the juxtaglomerular apparatus in the kidney [4][5][6] . Renin finally increases the secretion of aldosterone and the antidiuretic hormone vasopressin via the angiotensin pathway.…”

Section: Introductionmentioning

confidence: 99%

Oral rehydration solution normalizes plasma renin and aldosterone levels in patients with ulcerative colitis after proctocolectomy

Kudoh

Shibata²,

Funayama

et al. 2017

J Anus Rectum Colon

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Abstract:Objectives: The possible effects and benefits of oral rehydration solution (ORS) on chronic dehydration after total proctocolectomy. Methods: To evaluate the effect of ORS on the renin-angiotensin system after remnant proctocolectomy in patients with ulcerative colitis (UC), we selected 20 patients after remnant proctocolectomy, ileal J pouch-anal anastomosis, and construction of a diverting ileostomy for UC. Patients were randomly divided into two groups, A (n=9) or B (n=11), 2 weeks after the surgery. In group A, ORS (1000 mL/day) was given for the first 7 days and mineral water (1000 mL/day) for the next 7 days. In group B, mineral water (1000 mL/day) was given for the first 7 days and ORS (1000 mL/day) for next 7 days. Plasma levels of renin, aldosterone and excretion of sodium in urine were evaluated at days 0, 7, and 14. We defined day 0 as the day of beginning this study. Results: Mean plasma renin levels on day 0 were six to eight times greater than the upper normal limit. In group A, ORS lowered plasma renin levels. In group B, plasma levels of renin and aldosterone after ORS were lower than those at days 0 and 7. Conclusions: ORS corrected increased plasma levels of renin and aldosterone to within the normal range in patients after proctocolectomy.

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Influence of sodium deprivation and loading on the plasma‐renin in man

Abstract: The mechanisms controlling the secretion of aldosterone are incompletely understood

Cited by 124 publications

References 46 publications

Impaired renal conservation of sodium and chloride during sustained correction of systemic acidosis in patients with type 1, classic renal tubular acidosis.

Impaired renal conservation of sodium and chloride during sustained correction of systemic acidosis in patients with type 1, classic renal tubular acidosis.

Prior receptor occupancy as a determinant of the pressor activity of infused angiotensin II in the rat.

Oral rehydration solution normalizes plasma renin and aldosterone levels in patients with ulcerative colitis after proctocolectomy

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