Increased plasma level of renin in experimental secondary hyperaldosteronism

Higgins, James T.; Davis, James O.; Urquhart, John; Olichney, Michael J.

doi:10.1152/ajplegacy.1964.207.4.814

Cited by 19 publications

(14 citation statements)

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“…Plasma renin activity and renin substrate concentration. In another group of 14 pregnant dogs, plasma renin activity was elevated in comparison with that of a group of 12 normal dogs studied at the same time and under the same conditions (Fig. 2).…”

Section: Introductionmentioning

confidence: 70%

“…Plasma renin activity was frequently elevated and the increase for the group was statistically significant; it seems unlikely that the occasional normal value observed was related to the level of sodium intake since this was constant. Also, our earlier studies (12,19) have been done at this level of sodium intake and there was no evidence that it depresses plasma renin activity. Consequently, the findings in dogs and the observations on women suggest that plasma renin activity varies from a normal level to an elevated one during pregnancy.…”

Section: Introductionmentioning

confidence: 88%

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Mechanisms regulating the renal excretion of sodium during pregnancy

Robb¹,

Davis²,

Johnson³

et al. 1970

J. Clin. Invest.

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A B S T R A C T Observations were made on the relation of the renin-angiotensin-aldosterone system and renal hemodynamic function to sodium balance in 43 pregnant dogs. Daily balance studies revealed that about 30-40% of ingested sodium was retained during the last half of pregnancy; during the same period, potassium balance was also positive but to a lesser extent. For groups of pregnant dogs, plasma renin activity (n = 14) and aldosterone secretion (n = 19) were significantly higher than normal; however, in some animals one or both functions were normal even though sodium retention was present. In contrast, plasma renin substrate concentration was consistently elevated during pregnancy in seven dogs. In a group of nine dogs in which both aldosterone secretion and plasma renin activity were measured, aldosterone secretion was elevated in the three dogs with the highest values for plasma renin activity; in two of the remaining six animals aldosterone secretion was elevated but plasma renin activity was normal or only slightly increased. The sequestration of sodium and water into the uterine contents was defined quantitatively in this study but evidence was lacking to support the idea that such changes led to renin release. The glomerular filtration rate (GFR) was significantly elevated throughout pregnancy but a significant decrease from the high level of mid-pregnancy occurred during the last half of pregnancy; this decrease in GFR probably contributed to the sodium retention. Administration of a large dose of deoxycorticosterone acetate (DOCA) to dogs in late pregnancy produced marked sodium retention but "escape" from the sodium-retaining steroid occurred. The data demonstrate that although increased activity of the renin-angiotensin-aldosterone system was frequently present during pregnancy, a normal rate of aldosterone secretion occurred. This finding and the observed "es-

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Section: Introductionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 88%

Mechanisms regulating the renal excretion of sodium during pregnancy

Robb¹,

Davis²,

Johnson³

et al. 1970

J. Clin. Invest.

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“…When dog renin was added to dog plasma, 94 to 109% was recovered. Evidence for the specificity of the modified Helmer procedure has been presented previously (18,19). Plasma renin substrate was measured by a method described elsewhere (19).…”

Section: Methodsmentioning

confidence: 96%

“…Each tube contained 0.1 M of disodium ethylenediaminetetraacetate (EDTA) for each 20 ml of whole blood; EDTA served as an anticoagulant and as an inhibitor of angiotensinase activity. Plasma renin was measured by a modified Helmer method adapted for dog blood (18,19); all values are expressed in nanograms of angiotensin II formed during a 4-hour incubation period. When synthetic angiotensin iSupplied by Upl'ohn and Company.…”

Section: Methodsmentioning

confidence: 99%

Plasma Renin in Chronic Experimental Heart Failure and during Renal Sodium "Escape" from Mineralocorticoids

Johnston

Davis

Robb

et al. 1968

Circulation Research

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A striking increase in the plasma renin level occurred in dogs with low output right heart failure secondary to tricuspid insufficiency and pulmonic stenosis and in three of five animals with high output failure produced by a large arteriovenous fistula. When dogs with a small arteriovenous fistula were given daily injections of DOCA, the renal sodium "escape" phenomenon occurred. In these animals, the level of plasma renin was suppressed during DOCA administration both during the initial period of sodium retention and also later when sodium balance was normal or negative. In contrast, when dogs with a larger arteriovenous fistula but without evidence of cardiac failure were given DOCA, they retained sodium and developed signs of congestive heart failure. However, in these animals with congestion and ascites, in contrast to-the dogs that developed spontaneous high output failure, the plasma renin was low. Renin-substrate was unaltered in all of the experimental situations studied except for the decrease observed in dogs with low output right heart failure, la these animals, it seems likely that decreased renin-substrate was secondary to hepatic congestion and liver damage. The renin-angiotensin system does not seem to be related to the "escape" phenomenon, and renin does not appear to be the factor that makes the kidney unusually responsive to mineralocorticoids. Thus, in experimental heart failure the reninangiotensin system was activated, but in the congestive syndrome produced by DOCA the plasma renin level was suppressed. ADDITIONAL KEY WORDSrenin-angiotensin system arteriovenous fistula desoxycorticosterone sodium balance renin-substrate tricuspid insufficiency and pulmonic stenosis high output failure conscious dogs• Hypersecretion of aldosterone is common in edematous states (1-12). Many patients with congestive heart failure have increased secretion and excretion of aldosterone (1, 3-7), but patients with edema also have normal rates of secretion, of this hormone (8-10). Experimental heart failure in dogs is regularly accompanied by an increase in aldosteroneFrom the Departments of Physiology and Surgery, University of Missouri School of Medicine, Columbia, Missouri 6520X.This investigation was supported in part by U. S. Public Health Service Research Grant HE 10612-01 from the National Heart Institute.Dr. Johnston is Research Fellow, National Heart Foundation of Australia.Accepted for publication December 10, 1967. secretion and a high plasma level of aldosterone (2,11,12). The increase in plasma aldosterone in heart failure also results from a decrease in the metabolic clearance of aldosterone by the Ever (4, 9, 13). The present study relates the participation of the reninangiotensin system in experimental heart failure to sodium balance and to the known hypersecfetion of aldosterone. This investigation is also concerned with the role of the renin-angiotensin system in the "escape" phenomenon (14-15). Normal humans or animals given large quantities of a mineralocorticoid retain sodium for only ...

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“…Samples of renal venous blood were prepared for bioassay by the method of Helmer (22). The pressor response of the rat to angiotensin formed during incubation of the plasma was measured as an index of renin activity as described by Higgins, Davis, Urguhart, and Olichney (23).…”

Section: Methodsmentioning

confidence: 99%

The effect of altered sodium concentration in the distal nephron segments on renin release

Cooke¹,

Brown²,

Zacherle³

et al. 1970

J. Clin. Invest.

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A B S T R A C T Ethacrynic acid, a potent inhibitor of sodium reabsorption in the ascending limb of Henle's loop, produces a sharp rise in renal venous renin activity within 5 min after intravenous administration in anesthetized dogs. This response persists when volume depletion is prevented by returning urinary outflow to the femoral vein. Comparable studies with chlorothiazide, a diuretic with little or no effect on the medullary portion of the ascending limb of the loop of Henle, failed to produce a significant increase in renal venous renin activity.When administered during ureteral occlusion, ethacrynic acid produced no change in renal venous renin activity until ureteral occlusion was released and flow restored. Following release of the ureters, a prompt rise in renal venous renin was again observed within 5 min of release. Control studies of ureteral occlusion yielded a fall in renal venous renin activity following release of the ureter without administration of ethacrynic acid. These studies identify a prompt stimulatory effect of ethacrynic acid on renin release that is unrelated to volume depletion but dependent upon the presence of tubular urine flow. Although further definition of the site and characteristics of the distal tubular mechanism for stimulation of renin release requires more direct study, the data presented here indicate that changes in sodium concentration in distal tubular fluid serve as a stimulus for renin release.

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Increased plasma level of renin in experimental secondary hyperaldosteronism

Cited by 19 publications

References 0 publications

Mechanisms regulating the renal excretion of sodium during pregnancy

Mechanisms regulating the renal excretion of sodium during pregnancy

Plasma Renin in Chronic Experimental Heart Failure and during Renal Sodium "Escape" from Mineralocorticoids

The effect of altered sodium concentration in the distal nephron segments on renin release

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