Sequential changes in catecholamine plasma levels during isotonic volume expansion in dogs

Carrière, S; Lalumière, Gaston; Daigneault, Andrée; Champlain, Jacques de

doi:10.1152/ajprenal.1978.235.2.f119

Cited by 7 publications

(4 citation statements)

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“…and Carrier? et al 4 observed a prompt fall in the sum of the NE and E levels in plasma measured as total catecholamines after volume expansion. We have found E levels to be 41% of the NE levels in arterial blood during the control period, and therefore a fall in E levels alone could produce a significant change if total catecholamines were quantitated.…”

Section: Discussionmentioning

confidence: 98%

Renal modulation of urinary catecholamine excretion during volume expansion in the dog.

Boren

Henry²,

Selkurt³

et al. 1980

Hypertension

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The role of the kidney in handling the biologically acthe, nnconjugated endogenous catecholamines epinephrine (E), noreptnephrine (NE), dopamlne (DA), and the O-methylated metabolite of NE, normetanephrine (NM), was studied in the anesthetized dog before and after Toloroe expansion with iaotonk saline by measuring renal arterial deUrery, urinary excretion rate, and renal Tenons return of these materials. Net turnover in the renal metabolic compartment was estimated by comparing arterial delivery to urinary excretion and renal Tenons return. The kidney extracted E and produced NE, DA, and NM before and after Tolume expansion. After Tolume expansion a significant decrease in the extraction of E, an Increase in the production of DA, and no change in the production of NE or NM was seen. Clearance of catecbolamlnes and NM through the kidneys appeared to increase with Tolume expansion. The clearance of DA exceeded the clearance of creatinine (Cr) after volume expansion, while the clearance of NM exceeded that of Cr before and after volume expansion, indicating that urinary DA and NM are derived, in part, from processes other than glomerular filtration. These observations suggest an important role for the kidney in the modulation of the excretion of catecholamines and metabolites. This role must be considered before the urinary excretion rate of N, E, DA, and NM can be related to generalized sympathetic function. The observed increases in renal DA production after saline infusion suggest a possible natriuretic function of intrarenal DA. (Hypertension 2: 383-389, 1980)

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Section: Discussionmentioning

confidence: 98%

Renal modulation of urinary catecholamine excretion during volume expansion in the dog.

Boren

Henry²,

Selkurt³

et al. 1980

Hypertension

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show abstract

“…Obviously, our data do not rule out the possibility that adrenergic mecha nisms do come into play when a heavy saline load is given. This would induce a marked expansion ofintravascular volume which, as shown in experimental animals, could pos sibly lead to reflex sympathetic withdrawal through adequate stimulation of cardiopul monary volume receptors [5][6][7]18].…”

Section: Discussionmentioning

confidence: 99%

“…Volume expansion after salt loading is a well-known suppressor of renin secretion [1,3], Experi mental evidence suggests that saline sup pression of renin secretion is primarily due to the sodium (chloride) that crosses the macula densa, rather than to the increase in intravascular volume perse [3,4], However, volume expansion may also reduce the ac tivity of the adrenergic nervous system [5][6][7] and no evidence has been available as to whether intra-or extrarenal neurally me diated mechanisms participate in saline in hibition of renin secretion in humans. To examine the role of neural and humoral adrenergic mechanisms, in this study the renal arterial and venous plasma concentra tions of noradrenaline (NA) and adrenaline (A) and the plasma renin activity (PRA)…”

Section: Introductionmentioning

confidence: 99%

Effects of Light Saline Loading on Renal Renin and Catecholamine Release in Hypertensive Humans

Cannella

Picotti

Cesura

et al. 1983

Kidney Blood Press Res

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In 8 essential hypertensive patients infusion of 7.5 ml kg^-1 b.w. of isotonic saline over 20 min decreased plasma renin activity but did not affect plasma adrenaline or noradrenaline concentrations in suprarenal aortic, renal venous and caval blood. Mean blood pressures and heart rates were unchanged throughout the saline infusion period, whereas the hematocrit was significantly decreased. These data suggest that inhibition of renin secretion after slight volume expansion with saline in hypertensive humans occurs without parallel inhibition of either renal neurosympathetic drive or humoral adrenergic tone to the kidney through circulating catecholamines.

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“…Acute ECFV expan sion with i.v. saline infusion, a condition in which the renal sympathetic tone is consider ably suppressed [22], was shown to be accom panied by increased urinary DA excretion [5][6][7][8][9][10], As the plasma levels of DA remain unde tectable [22] or decrease [10] under these con ditions, the production of endogenous DA within the kidney must have increased [23]. In PCT cells, L-amino acid decarboxylase converts L-DOPA to DA [24,25], This locally formed DA is thought to inhibit Na-KATPase activity [26,27] in PCT cells [28,29] by involving DA-1 and/or DA-2 receptors [30] and to participate in proximal tubular fluid and Na absorption [31].…”

Section: Discussionmentioning

confidence: 99%

Metoclopramide Does Not Affect Renal Function and Atrial Natriuretic Peptide Release in Response to Acute Saline Loading in Conscious Rats

Nati¹,

Campean²,

Kramer³

1994

Pharmacology

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It was previously shown in man that metoclopramide (MCP), a dopamine (DA)-2 receptor blocker, attenuates the natriuresis of water immersion. In the present study, we therefore investigated the effects of MCP on renal function and atrial natriuretic peptide (ANP) release in conscious rats. Under basal conditions MCP did not affect glomerular filtration rate (GFR)(7.4 ± 1.7 ml/min/kg without and 7.8 ± 0.6 ml/min/kg with MCP), urinary fractional excretion of Na (FE_Na) (0.3 ± 0.1% without and 0.3 ± 0.1% with MCP) and K (FE_K) (20.6 ± 1.4% without and 28.0 ± 6.2% with MCP) or plasma ANP (37 ± 5 pmol/l without and 31 ± 6 pmol/l with MCP). During acute saline loading equal to a 10% rise in body weight, which significantly (p < 0.05) increased GFR, MCP again had no effects on GFR (8.8 ± 1.8 ml/min/kg with vs. 9.7 ± 2.5 ml/ min/kg without MCP), FE_Na (24.5 ± 6.9% with vs. 20.4 ± 5.1% without MCP), FE_K (52.5 ± 6.9% with vs. 52.5 ± 9.5% without MCP) and plasma ANP (89 ± 8 pmol/l with vs. 91 ± 9 pmol/l without MCP). These results indicate that DA does not modulate renal function or ANP release via DA-2 receptors under basal conditions nor in response to acute saline loading in conscious rats.

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Sequential changes in catecholamine plasma levels during isotonic volume expansion in dogs

Cited by 7 publications

References 0 publications

Renal modulation of urinary catecholamine excretion during volume expansion in the dog.

Renal modulation of urinary catecholamine excretion during volume expansion in the dog.

Effects of Light Saline Loading on Renal Renin and Catecholamine Release in Hypertensive Humans

Metoclopramide Does Not Affect Renal Function and Atrial Natriuretic Peptide Release in Response to Acute Saline Loading in Conscious Rats

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