Concept of natriuretic hormone.

Wardener, H. E. de; Clarkson, E. M.

doi:10.1152/physrev.1985.65.3.658

Cited by 290 publications

(110 citation statements)

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“…In accordance with the concept of a natriuretic hormone (30,31), we can speculate that lower MBG levels during the first few days of NaCl loading in some subjects can add to the deficit (acquired or inherited) in sodium excretion, with commensurate increases in total blood volume, and, as a result, in greater elevation in BP. Furthermore, a lack of MBG production following NaCl loading could result in a relatively high renotubular sodium pump activity.…”

Section: Discussionsupporting

confidence: 81%

“…The vasoactive effects of SPI have been repeatedly documented with respect to NaCl-dependence of BP (6,18,30). Chronic NaCl loading in salt-sensitive rodent models with abnormal renal function results in sustained, elevated levels of MBG that mediate sustained NaCl-dependent increases in arterial pressure (10).…”

Section: Discussionmentioning

confidence: 99%

“…It has been postulated for some time that endogenous substances [sodium pump inhibitors (SPI)] are stimulated by increased Na intake and increase natriuresis by inhibiting renal tubular Na pumps to prevent renal reabsorption of filtered Na (6,18,30). However, such substances were not purified adequately in early studies, and their assays were nonspecific (17).…”

mentioning

confidence: 99%

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Endogenous sodium pump inhibitors and age-associated increases in salt sensitivity of blood pressure in normotensives

Anderson¹,

Федорова²,

Morrell³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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AY, Lakatta EG. Endogenous sodium pump inhibitors and age-associated increases in salt sensitivity of blood pressure in normotensives. Am J Physiol Regul Integr Comp Physiol 294: R1248-R1254, 2008. First published February 20, 2008 doi:10.1152/ajpregu.00782.2007.-Factors that mediate increases in salt sensitivity of blood pressure with age remain to be clarified. The present study investigated 1) the effects of high-NaCl intake on two Na pump inhibitors, endogenous ouabain (EO) and marinobufagenin (MBG), in middle-aged and older normotensive Caucasian women; and 2) whether individual differences in EO and MBG are linked to variations in sodium excretion or salt sensitivity. A change from 6 days of a lower (0.7 mmol ⅐ kg Ϫ1 ⅐ day Ϫ1 )-to 6 days of a higher (4 mmol ⅐ kg Ϫ1 ⅐ day Ϫ1 )-NaCl diet elicited a sustained increase in MBG excretion that directly correlated with an increase in the fractional Na excretion and was inversely related to age and to an age-dependent increase in salt sensitivity. In contrast, EO excretion increased only transiently in response to NaCl loading and did not vary with age or correlate with fractional Na excretion or salt sensitivity. A positive correlation of both plasma and urine levels of EO and MBG during salt loading may indicate a casual link between two Na pump inhibitors in response to NaCl loading, as observed in animal models. A linear mixed-effects model demonstrated that age, dietary NaCl, renal MBG excretion, and body mass index were each independently associated with systolic blood pressure. Thus, a sustained increase in MBG in response to acutely elevated dietary NaCl is inversely linked to salt sensitivity in normotensive middle-aged and older women, and a relative failure of MBG elaboration by these older persons may be involved in the increased salt sensitivity with advancing age. marinobufagenin; ouabain; hypertension NUMEROUS STUDIES HAVE REPORTED that the magnitude of the systolic blood pressure (SBP) response to acute changes in dietary NaCl intake, i.e., salt sensitivity of blood pressure, increases with advancing age (16,20,27,(32)(33)(34)(35). Specific determinants of the greater blood pressure response of older persons to dietary NaCl, however, remain to be identified.NaCl ingestion results in an increase in plasma volume and natriuresis. It has been postulated for some time that endogenous substances [sodium pump inhibitors (SPI)] are stimulated by increased Na intake and increase natriuresis by inhibiting renal tubular Na pumps to prevent renal reabsorption of filtered Na (6,18,30). However, such substances were not purified adequately in early studies, and their assays were nonspecific (17).More recently, SPI assays have improved and become more specific (3,14), and studies in various animal models and in humans have documented an increased elaboration of SPI in response to NaCl loading. This research has focused largely on two SPI: an endogenous ouabain (EO) and a bufadienoide, marinobufagenin (MBG). Differences in the kinetics and tissue actions of thes...

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

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Endogenous sodium pump inhibitors and age-associated increases in salt sensitivity of blood pressure in normotensives

Anderson¹,

Федорова²,

Morrell³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This difference in fluid inhibitors of Na / ,K / -ATPase involved in the regulation of celludistribution, although also in gray matter, may be caused by lar sodium transport. 35,36 The consistent increase in the concendifferences between the galactosamine and ischemic models.…”

Section: Modified Aftermentioning

confidence: 89%

Regional cerebral edema and chloride space in galactosamine-induced liver failure in rats

Gove¹

1997

Hepatology

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toxic edema, in which inhibition of ouabain-sensitive sodium The pathogenesis of cerebral edema, which is a major transport is characteristic, a net increase in intracellular wacomplication of fulminant hepatic failure, is poorly unter occurs, reflecting impaired cellular osmo-regulation. 5 Cerderstood. In previous studies, increased regional brain tain common mechanisms appear to be involved in both these water content was observed in rats at an early stage of forms of edema, making distinction between them less clear. 6 acute liver failure caused by galactosamine. At a laterIn a postmortem study of the ultrastructure of brain capillarstage when the animals had developed deep coma, brain ies of patients dying from fulminant hepatic failure, marked water content was reduced, possibly as a result of generintracellular swelling of perivascular astrocytes was observed alized dehydration. In the present investigation, we consistent with a mainly cytotoxic mechanism, but increases have determined brain water content at a late stage of in the number of vesicles and vacuoles in endothelial cells liver failure, 48 hours after galactosamine, in animals were also seen, suggesting a vasogenic component. 7 Conflictthat had been maintained in fluid balance by continuous ing results on this were obtained in earlier animal studies, 6 intraperitoneal infusion of glucose solution. In these aniand it has been suggested that an initial cytotoxic injury mals, brain water content, determined from the ratio of evolves into vasogenic edema. 8,9 Some of these studies have wet to dry weight, showed a greater increase than that been criticized as describing a phenomenon that occurs in observed previously at the early stage (hindbrain region essentially moribund animals. 10,11 [cerebellum, pons, and brain stem] increased by 4.2%;In previous studies using rats with galactosamine-induced forebrain region increased by 1.4% compared with conliver failure, we found a small increase (0.5%) in hindbrain trols). Regional analysis of brain water, using a tissue-(cerebellum, pons, and brain stem) water content at an early specific gravity method, showed a significant increase stage of liver failure, 43 hours after galactosamine. 12 This was in cerebellar gray matter water content. Analysis of chloin agreement with the observations of Groflin and Tholen, 13 ride space showed the extra fluid to be mainly extracelusing the same model, in which the water contents of cerebellular in the hindbrain region, but not in the forebrain lum and brain stem were increased when the rats were mildly region. Ultrastructural examination of capillaries in encephalopathic. However, in both these studies at later gray matter from cerebellum and cerebrum showed no stages of acute liver failure when the rats progressed to deep evidence of gross disruption of the tight junctions. Swellcoma (immobility and/or gross ataxia), fore-and hindbrain ing of the astroglial foot processes was observed in the water contents were reduced in comparison with animals studcerebellar gray m...

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“…The factor responsible for this phenomenon (the so-called 'third factor') was a topic of great interest in the 1960s and 1970s. 9 Cort and Lichardus 27 and Buckalew and colleagues 28 demonstrated that volume expansion is associated with increased levels of a circulating substance that inhibits active sodium transport in vitro. Extremely important contributions to measuring and understanding the implications of this 'third factor' were made by Schrier and co-workers 29-31 and by Kramer and Gonick.…”

Section: Historical Perspectivementioning

confidence: 99%

Endogenous digitalis: pathophysiologic roles and therapeutic applications

2008

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SUMMARYEndogenous digitalis-like factors, also called cardiotonic steroids, have been thought for nearly half a century to have important roles in health and disease. The endogenous cardiotonic steroids ouabain and marinobufagenin have been identified in humans, and an effector mechanism has been delineated by which these hormones signal through the sodium/potassium-transporting ATPase. These findings have increased interest in this field substantially. Although cardiotonic steroids were first considered important in the regulation of renal sodium transport and arterial pressure, subsequent work has implicated these hormones in the control of cell growth, apoptosis and fibrosis, among other processes. This Review focuses on the role of endogenous cardiotonic steroids in the pathophysiology of essential hypertension, congestive heart failure, end-stage renal disease and pre-eclampsia. We also discuss potential therapeutic strategies that have emerged as a result of the increased understanding of the regulation and actions of cardiotonic steroids.

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Concept of natriuretic hormone.

Cited by 290 publications

References 0 publications

Endogenous sodium pump inhibitors and age-associated increases in salt sensitivity of blood pressure in normotensives

Endogenous sodium pump inhibitors and age-associated increases in salt sensitivity of blood pressure in normotensives

Regional cerebral edema and chloride space in galactosamine-induced liver failure in rats

Endogenous digitalis: pathophysiologic roles and therapeutic applications

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