Plasma and Urine Dopamine in Man Given Sodium Chloride in the Diet

Oates, N. S.; Ball, Stephen G.; Perkins, C. M.; Lee, M. R.

doi:10.1042/cs0560261

Cited by 90 publications

(35 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…If this occurs in the renal tubules, where there is a high level of aromatic amino acid decarboxylase activity, the DOPA could not be derived from circulating tyrosine since tyrosine hydroxylase is not present in these cells (Nagatsu, 1973). As has been previously reported, the dopamine in plasma can account for only a small proportion of the dopamine excreted in urine (Oates, Ball, Perkins & Lee, 1979). When, however, the apparent clearance of plasma DOPA by renal decarboxylation was calculated on the assumption that urine free dopamine is mainly derived from plasma DOPA, this was found to be a little over 100 ml/min.…”

Section: Discussionmentioning

confidence: 73%

See 1 more Smart Citation

A specific radioenzymatic assay for dihydroxyphenylalanine (DOPA). Plasma dopa may be the precursor of urine free dopamine.

Brown¹,

Dollery²

1981

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 A sensitive radioenzymatic assay was developed, in which DOPA is enzymatically decarboxylated to dopamine and the latter converted to [:H]-methoxytryamine in the presence of [:3H]-S-adenosyl-Lmethionine and catechol-o-methyltransferase. 2 The assay was specific for DOPA, and was sensitive to 50 pg/ml.3 Endogen6us DOPA was found to be present in the plasma of eight human volunteers at a concentration of 10.46 + 2.42 nmol/l. 4 Simultaneous urine collections in the same subjects showed a free dopamine excretion of 68.88 ± 17.70 nmol/h. There was a significant correlation (P < 0.01) between plasma DOPA concentration and urine free dopamine excretion (r = 0.84). 5 After the oral administration of 250 mg levodopa, plasma DOPA and urine dopamine both increased by a similar proportion (98 ± 8.4-fold, and 93.4 ± 6.9-fold respectively). These compare with an increase in plasma dopamine of only 26 ± 15-fold (P<0.01).6 Following the oral dose of DOPA, the increase in plasma DOPA, but not plasma dopamine, could account for the increase in urine dopamine. The calculated clearance of plasma DOPA by renal decarboxylation to dopamine was 114 + 20 ml/min. 7 This is not significantly different from the apparent clearance of endogenous DOPA by renal decarboxylation to dopamine, and suggests that there is adequate renal decarboxylase activity for DOPA to be the precursor for renal dopamine formation.

show abstract

Section: Discussionmentioning

confidence: 73%

“…Sodium intake is also known to influence dopamine excretion (Alexander et al, 1974;Faucheux, Buu & Kuchel, 1977;Oates et al, 1979); it will be of interest to investigate whether these two factors operate independently, or whether changes in sodium intake may modulate dopamine excretion via changes in plasma DOPA concentration.…”

Section: Discussionmentioning

confidence: 99%

A specific radioenzymatic assay for dihydroxyphenylalanine (DOPA). Plasma dopa may be the precursor of urine free dopamine.

Brown¹,

Dollery²

1981

Brit J Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…29 -31 For example, we have shown that almost 60% of the natriuresis seen during acute volume expansion (5% of body weight) is accompanied by an increase in urinary dopamine excretion and could be antagonized by SCH 23390 30 and attenuated by carbidopa, an inhibitor of dopa decarboxylase which converts L-dopa into dopamine. 31 The increased sodium excretion seen in animals placed on a high sodium diet is accompanied by an increase in urinary dopamine excretion. 32,33 These results suggest that endogenously formed kidney dopamine plays a pivotal role in maintaining body sodium homeostasis during increases in sodium intake.…”

Section: Physiological Role Of Dopamine In the Kidneymentioning

confidence: 99%

Renal Dopamine Receptor Function in Hypertension

1998

View full text Add to dashboard Cite

Abstract-Dopamine plays an important role in the regulation of renal sodium excretion. The synthesis of dopamine and the presence of dopamine receptor subtypes (D 1A , D 1B as D 1 -like and D 2 , and D 3 as D 2 -like) have been shown within the kidney. The activation of D 1 -like receptors located on the proximal tubules causes inhibition of tubular sodium reabsorption by inhibiting Na,H-exchanger and Na,K-ATPase activity. The D 1 -like receptors are linked to the multiple cellular signaling systems (namely, adenylyl cyclase, phospholipase C, and phospholipase A 2 ) in the different regions of the nephron. Defective renal dopamine production and/or dopamine receptor function have been reported in human primary hypertension as well as in genetic models of animal hypertension. There may be a primary defect in D 1 -like receptors and an altered signaling system in the proximal tubules that lead to reduced dopamine-mediated effects on renal sodium excretion in hypertension. Recently, it has been shown in animal models that the disruption of either D 1A or D 3 receptors at the gene level causes hypertension in mice. Dopamine and dopamine receptor agonists also provide therapeutic potential in treatment of various cardiovascular pathological conditions, including hypertension. However, because of the poor bioavailability of the currently available compounds, the use of D 1 -like agonists is limited to the management of patients with severe hypertension when a rapid reduction of blood pressure is clinically indicated and in acute management of patients with heart failure. In conclusion, there is convincing evidence that dopamine and dopamine receptors play an important role in regulation of renal function, suggesting that a defective dopamine receptor/signaling system may contribute to the development and maintenance of hypertension. Further studies need to be directed toward establishing a direct correlation between defective dopamine receptor gene in the kidney and development of hypertension. Subsequently, it may be possible to use a therapeutic approach to correct the defect in dopamine receptor gene causing the hypertension. (Hypertension. 1998;32:187-197.)Key Words: dopamine Ⅲ receptors, dopamine Ⅲ kidney tubules, proximal Ⅲ kidney Ⅲ hypertension, renal D opamine is known to play an important role in the control of renal sodium excretion. Specific receptors for dopamine have been identified in various regions of the nephron, and it is reported that dopamine is synthesized within the renal proximal tubules. Endogenously produced dopamine, as well as exogenously administered dopamine, exerts pronounced effects on renal function. There are reports suggesting that a defect in renal dopamine receptor function and/or dopamine production may play a role in the pathogenesis of hypertension. For example, reduced urinary dopamine/ sodium excretion is reported in some forms of human primary hypertension. [1][2][3] It is reported that a defect in dopamine receptor-G protein coupling and alterations in the signaling component...

show abstract

“…8 This is based on the observation that an increase in dietary sodium intake is accompanied by an increase in sodium and dopamine excretion. 9 However, a cause and effect relation between these two events has not been firmly established.…”

mentioning

confidence: 99%

Role of kidney dopamine in the natriuretic response to volume expansion in rats.

1989

View full text Add to dashboard Cite

It has been postulated that endogenously produced dopamine (DA) may play a role in the regulation of renal sodium excretion. In the present study, experiments were designed to test the hypothesis that acute volume expansion with isotonic sodium chloride stimulates the production of DA within the kidney, which in turn acts on specific DA, receptors to promote sodium excretion. In pentobarbital-anesthetized rats, acute volume expansion over a period of 1 hour evoked a pronounced increase in urine output and urinary sodium excretion. These diuretic and natriuretic effects were not accompanied by any significant changes in blood pressure or heart rate. However, there was a significant elevation in central venous pressure and a transient rise in glomerular filtration rate. The natriuretic and diuretic response was accompanied by a significant increase in urinary DA excretion, and this effect was clearly dissociated from the rise in glomerular filtration rate. In a separate group of rats, the effects of acute volume expansion were studied in the presence of selective DA, receptor antagonist SCH-23390 (50 figlkg i.v. bolus; 10 /xg/kg/min). During DA, receptor blockade, there was a marked attenuation in the diuretic and natriuretic response throughout the period of volume expansion, when compared with that in the control group. The changes in central venous pressure and glomerular filtration rate were identical in the two groups. In another group of rats, the renal effects of exogenously administered DA were studied. DA (0.5 /ug/kg/min) produced significant increases in urine output and urinary sodium excretion, without causing any alterations in blood pressure or glomerular filtration rate, suggesting a tubular site of action. SCH-23390, in a dose that had previously attenuated the natriuretic response to volume expansion, blocked the diuretic response and attenuated the natriuretic response to DA. The DA, receptor antagonist produced no significant hemodynamic and renal effects by itself in normally hydrated animals. These results suggest that endogenously produced DA contributes, at least in part, to the natriuretic and diuretic response to acute volume expansion by activation of DA, receptors located on renal tubules. (Hypertension 1989;13:828-834) D opamine (DA) has the ability to produce a variety of cardiovascular and renal effects by acting on specific DA receptors. 1 The renal effects of DA include increases in glomerular filtration rate and renal blood flow as well as diuresis and natriuresis.2 DA receptors of both the DA, and DA 2 subtype have been identified in the nephron using radioligand binding techniques.3 -5 In addition, DA has been shown to produce an inhibition of Na + ,K + -ATPase in the proximal tubule, a potential mechanism to explain its natriuretic effect.

show abstract

Plasma and Urine Dopamine in Man Given Sodium Chloride in the Diet

Cited by 90 publications

References 15 publications

A specific radioenzymatic assay for dihydroxyphenylalanine (DOPA). Plasma dopa may be the precursor of urine free dopamine.

A specific radioenzymatic assay for dihydroxyphenylalanine (DOPA). Plasma dopa may be the precursor of urine free dopamine.

Renal Dopamine Receptor Function in Hypertension

Role of kidney dopamine in the natriuretic response to volume expansion in rats.

Contact Info

Product

Resources

About