Effects of Dietary Sodium and of Acute Saline Infusion on the Interrelationship between Dopamine Excretion and Adrenergic Activity in Man

Alexander, R. Wayne; Gill, John R.; Yamabe, Hirohiko; Lovenberg, Walter; Keiser, Harry R.

doi:10.1172/jci107743

Cited by 265 publications

(110 citation statements)

References 28 publications

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“…When sodium metabolism, plasma and urinary NE, and urinary DA during normal, low, and high sodium intakes were compared in these two subsets and in a group of normal subjects, additional differences between the two subsets as well as differences from normal were found. The SS patients retained more sodium than normal and plasma or urinary NE did not decrease when they were given a high sodium intake; mean urinary DA was normal but did not increase, as it does in normal subjects, 12 when sodium intake was increased (see Figures 1, 2, and 5). The SR patients excreted sodium normally and plasma and urinary NE decreased by 30 and 37%, respectively, when they were given a high sodium intake; mean urinary DA was high and did not increase further when sodium intake was increased (see Figures 1,2, and 5).…”

Section: Discussionmentioning

confidence: 81%

“…If the values for mean urinary DA in both the SR and SS subjects represented maximal achievable compensatory responses to enhanced tubular sodium reabsorption, this may explain why urinary DA was not increased above normal in SS subjects and why it showed only a slight increase or none at all in the two subsets when sodium intake was increased. The notion that DA may be an important determinant of sodium excretion in the hypertensive subjects, as it appears to be in normal subjects, 12 and that differences in renal formation of DA by the two subsets may be responsible for differences in sodium excretion is supported by the finding that cumulative sodium retention was inversely correlated with mean urinary DA in SR and SS subjects (see Figure 3). …”

Section: Discussionmentioning

confidence: 92%

“…124 Although cumulative sodium retention tended to be greater in SS than in SR subjects, espe- daily when differences in blood pressure and glomerular filtration rate were minimal (see Figure 4), the difference between the two groups was not significant, as it has been in previous studies. 12 '' The excessive sodium retention that appears to characterize SS hypertensive patients may also explain why some patients with idiopathic hypertension have high levels of circulating atrial natriuretic peptide. 19 The cause of the impaired sodium excretion observed in the SS hypertensive patients in this and other studies is unknown, but it may be attributable, in part, to an increase in reabsorption of sodium by the proximal tubule.…”

Section: Discussionmentioning

confidence: 99%

“…Urinary dopamine (DA) was also measured to assess the possibility that DA, which appears to play a role in normal sodium metabolism and adrenergic function, 12 ' 13 may also be a determinant of the physiological responses of SS and SR patients.…”

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confidence: 99%

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Plasma and urinary catecholamines in salt-sensitive idiopathic hypertension.

et al. 1988

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SUMMARY Nineteen patients with normal renin idiopathic hypertension were arbitrarily classified as salt-sensitive or salt-resistant depending on whether their mean arterial pressure did or did not increase by 8% or more when sodium intake was increased. The responses of the two subsets and of five normal subjects to sodium intakes of 9, 109, and 249 mEq/day given for 7 days were as follows: The salt-sensitive subjects retained more sodium than normal and plasma or urinary norepinephrine did not decrease when they were given a high sodium intake; urinary dopamine was normal but did not increase normally when sodium intake was increased. The salt-resistant subjects excreted sodium normally and plasma and urinary norepinephrine was decreased by 30 and 37%, respectively, when they were given a high sodium intake; urinary dopamine was supernormal and did not increase further when sodium intake was increased. Cumulative sodium retention during the high sodium intake was directly related to the percentage of change in plasma norepinephrine in the hypertensive subjects, suggesting that renal adrenergic activity was a factor in the impaired sodium excretion in the salt-sensitive patients. Cumulative sodium retention and the percentage of change hi plasma norepinephrine were inversely related to urinary dopamine in the hypertensive subjects, suggesting that increased formation of dopamine in renal and neural tissue in the salt-resistant subjects may have been responsible for the differences between the subsets hi renal and adrenergic responses to a high sodium intake. Supernormal sodium retention and a failure to suppress adrenergic activity may explain, hi part, the phenomenon of salt sensitivity of blood pressure in salt-sensitive patients and may also be factors in the pathogenesis of hypertension in this subset. (Hypertension 11: 312-319, 1988) KEY WORDS • plasma norepinephrine • urinary dopamine • blood pressure P ATIENTS with hypertension have been arbitrarily defined as salt-sensitive (SS) or saltresistant (SR) based on the response of blood pressure to manipulations of dietary sodium intake or of body fluid volume.1 " 5 Categorization of patients with idiopathic hypertension by these criteria suggests that 25 to 51 % may be SS. '• 6 Studies that compared SS and SR patients suggest that the difference between

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Plasma and urinary catecholamines in salt-sensitive idiopathic hypertension.

et al. 1988

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“…Dopamine is subsequently eliminated either by urine excretion or methylation and deamination. Dopamine concentrations are 1000-fold higher in kidneys (nmol/L range) than in plasma (pM range) [124,125] , and increase even more after sodium loading [126,127] . As described below, dopamine modulates the renal Na + transport through an autocrine or paracrine pathway [128] .…”

Section: Prostanoid Receptorsmentioning

confidence: 98%

New insights into sodium transport regulation in the distal nephron: Role of G-protein coupled receptors

Morla

Edwards

Crambert

2016

WJBC

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The renal handling of Na + balance is a major determinant of the blood pressure (BP) level. The inability of the kidney to excrete the daily load of Na + represents the primary cause of chronic hypertension. Among the different segments that constitute the nephron, those present in the distal part (i.e ., the cortical thick ascending limb, the distal convoluted tubule, the connecting and collecting tubules) play a central role in the fine-tuning of renal Na + excretion and are the target of many different regulatory processes that modulate Na + retention more or less efficiently. G-protein coupled receptors (GPCRs) are crucially involved in this regulation and could represent efficient pharmacological targets to control BP levels. In this review, we describe both classical and novel GPCR-dependent regulatory systems that have been shown to modulate renal Na + absorption in the distal nephron. In addition to the multiplicity of the GPCR that regulate Na + excretion, this review also highlights the complexity of these different pathways, and the connections between them.

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