Plasma and urinary catecholamines in salt-sensitive idiopathic hypertension.

Gill, Jr Jr; Güllner, G; Lake, C. Raymond; Lakatua, D. J.; Lan, Gordon

doi:10.1161/01.hyp.11.4.312

Cited by 115 publications

(58 citation statements)

References 30 publications

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“…27 Failure to appropriately suppress neural activity may also contribute to salt-sensitive hypertension in humans. 28 In the present study, we suggest that stimulation of sympathetic nervous system activity by dietary sucrose renders the normotensive rat salt sensitive. In the spontaneously hypertensive rat, high dietary intakes of both sucrose and NaCl increase both neural activity and blood pressure to a greater extent than provision of either sucrose or NaCl alone.…”

Section: -12mentioning

confidence: 50%

Sucrose does not raise blood pressure in rats maintained on a low salt intake.

1993

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Diets high in sucrose or fructose have been shown by others to induce a modest elevation of blood pressure in rats. The present experiments were conducted to determine whether the sucrose-induced increase of blood pressure is dependent on the intake of sodium chloride. Four groups of Sprague-Dawley rats were studied: 1) a group maintained on a low salt diet and distilled water (0.45% sodium chloride, no added sucrose), 2) a low salt-high sucrose group (0.45% sodium chloride diet and 7% sucrose in distilled water), 3) a high salt group (4% sodium chloride diet and distilled water), and 4) a high salt-high sucrose group on a diet adjusted dairy to maintain the same high intakes of sodium chloride and sucrose as those of groups 2 and 3. Systolic blood pressures were measured by tail-cuff plethysmography during weeks 1-3 of treatment, and direct mean arterial blood pressures were recorded in conscious animals during week 4. Animals on the high salt diet gained weight more slowly than those on the low salt intake. On the low sodium chloride intake, blood pressures were not affected by high dietary sucrose (group 1 versus 2). In contrast, on the high sodium chloride intake, blood pressures were 10-14 mm Hg higher in sucrosedrinking animals than in water-drinking animals (group 3 versus 4). The increments in blood pressures of the high sodium chloride-high sucrose group were not accompanied by greater increments in body weight compared with the animals on the high sodium chloride intake alone. Sucrose-fed animals exhibited an increase in basal plasma norepinephrine concentrations and increased responsiveness of both norepinephrine and epinephrine to stress (mild electrical foot shock), regardless of the sodium chloride intake. Thus, in the Sprague-Dawley rat, sucrose elevates blood pressure only when adequate salt is present in the diet We hypothesize that a high sucrose intake may activate the sympathetic nervous system but that this activation is effective in elevating blood pressure only when there is a concomitant high intake of sodium chloride. (Hypertension 1993^1:779-785) KEY WORDS • insulin • catecholamines • sympathetic nervous system • hypertension, sodium-dependent S imple carbohydrate feeding (sucrose, glucose, or fructose) increases blood pressure in several normotensive strains of rats, including the Sprague-Dawley rat, the Wistar-Kyoto rat, and the Dahl salt-resistant rat.1 -8 Sucrose feeding also potentiates the development of hypertension in the spontaneously hypertensive rat and in a rat model of adrenal regeneration hypertension.9 " 11 Sucrose-induced increases of blood pressure have been attributed to increased sympathetic nervous system activity. In earlier studies, Hall and Hall 912 reported that addition of sucrose to a 1% NaCl drinking solution augmented the development of both adrenal regeneration hypertension and hypertension after unilateral nephrectomy, and this augmentation was attributed to increased salt consumption in sucrose-drinking rats. More recent evidence, based on indirect blood p...

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Section: -12mentioning

confidence: 50%

Sucrose does not raise blood pressure in rats maintained on a low salt intake.

1993

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“…In rats with deoxycorticosterone acetate (DOCA)-salt hypertension, a model of salt-dependent hypertension, the increased sympathetic activity in the kidney might contribute, through sodium retention, 6 -7 to the development of hypertension. Accordingly, we and recently GUI et al 10 have hypothesized that the persistence of autonomic "drive" in the SS patients might play an important role in the impaired renal function for sodium excretion and the resultant increases in cardiac output and blood pressure with…”

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confidence: 80%

“…27 A bolus of indocyanine green (50 mg) was rapidly injected into an antecubital vein and a 2 ml sample of blood was drawn at 4,6,8,10,12,14,16,18,20, and 22 minutes after the injection. Indocyanine green concentrations in the serum were estimated with a Beckman DU-2 spectrophotometer (Beckman Instruments, Inc., Irvine, Calif.) at a wavelength of 805 nm.…”

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confidence: 99%

Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

1990

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Twenty-two patients with normal plasma renln and essential hypertension were classified as "salt-sensitive" (SS) (n=9) or "non-salt-sensitive" (NSS) (n=13) from an increase in mean blood pressure with changes in sodium intake from 25 to 250 meq/day. With the high sodium diet, the SS patients gained more weight (/?<0.05), retained more sodium (/><0.05), and had a greater increase in cardiac output (/?<0.05). Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, whereas the NSS patients had a significant decrease in systemic vascular resistance. Thus, the greater increase in blood pressure with sodium loads in SS patients can be attributed not only to an increase in cardiac output, possibly resulting from greater sodium retention, but also to inappropriately elevated systemic vascular resistance. Concomitant with a greater increase in cardiac output, the SS patients had a greater increase in forearm blood flow with sodium loading than the NSS patients (p<0.02). In contrast, blood flow to the kidney and the liver was not significantly changed in either group; renal (p<0.05) and hepatic (/><0.01) vascular resistance increased significantly in SS patients but remained unchanged in NSS patients. Thus, evidence presented suggests that the greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogenous distribution of local flow and resistance in SS patients; renal and hepatic blood flow remains essentially unchanged and skeletal muscle blood flow receives almost all of the increase in cardiac output Moreover, systemic vascular resistance changes did not reflect the resistance of individual beds because vasoconstriction appeared in the kidney and the splanchnic area but was masked by prominent vasodilation in the skeletal muscle. Because this hemodynamic pattern is similar to the pattern evoked during defense reaction, it is suggested that sympathetic overactivity on a selective basis might be involved in the impaired renal function for sodium excretion and the increase in blood pressure with sodium loads in SS patients. (Hypertension 1990,16:235-244)

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“…The physiological role of renal dopamine has recently gained further relevance with the observations that in somq hypertensive patients, namely those with sodium sensitive hypertension, an inherited or acquired defect in the renal handling of dopamine may be of some pathophysiological importance (Gill et al, 1988; Lee et al, 1990;Williams et al+ 1990). Neither dopamine nor its precursor L-DOPA appear; however, particularly suitable for the correction of the hypothetical deficit of renal dopaminergic mechanisms in hypertension, mainly because of their extrarenal actions (Lee, 1988).…”

Section: Introductionmentioning

confidence: 99%

The renal handling of dopamine originating from l‐DOPA and γ‐glutamyl‐l‐DOPA

Pestana¹,

Soares‐da‐Silva²

1994

British J Pharmacology

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1 The formation and outflow of dopamine and its deaminated metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) was studied in cortical fragments of the rat kidney loaded with L-P-3,4-dihydroxyphenylalanine (L-DOPA) or y-glutamyl-L-DOPA (GluDOPA). Dopamine and DOPAC in the tissues and in the effluent were assayed by means of h.p.l.c. with electrochemical detection. 2 In rats given 30 mg kg-' L-DOPA, tissue and outflow levels of both dopamine and DOPAC were 3 fold those observed with a lower dose of L-DOPA (10 mg kg-'). In rats given GluDOPA (16.7 mg kg-') levels of dopamine in renal tissues and in perifusate samples were found to be higher than those obtained with an equimolar dose of L-DOPA (10 mg kg-'); however, no significant difference was observed for DOPAC. The outflow of both dopamine and DOPAC in kidney slices of rats injected with L-DOPA (10 and 30mg kg-') or GluDOPA (16.7 mg kg') was found to decline monophasically with similar slopes of decline. The rate constants of loss (k, min-') of DOPAC (10mg kg-' L-DOPA, k = 0.0070; 30 mg kg-' L-DOPA, k = 0.0087; 16.7 mg kg-' GluDOPA, k = 0.0080) were 2 to 3 fold those of dopamine (10 mg kg-' L-DOPA, k = 0.0027; 30 mg kg-' L-DOPA, k = 0.0034; 16.7 mg kgGluDOPA, k = 0.0030). With both precursors the DOPAC/dopamine ratio in perifusate samples were 2.0 fold those in the tissues. 3 Tissue and outflow levels of dopamine after incubation of renal tissues with L-DOPA, 50 and 100 JM were found to be lower than those observed with GluDOPA (50 and 100 fM). DOPAC/dopamine ratios in tissues and perifusate samples of experiments performed with L-DOPA were significantly higher (P<0.01) than those observed with GluDOPA. The outflow of both dopamine and DOPAC in renal slices incubated with L-DOPA (50 and 100 gM) were found to decline with time, but presented a biphasic shape. DOPAC/dopamine ratios in perifusate samples were 3 fold that in the tissues with both precursors.4 In conclusion, the present results show that both L-DOPA and GluDOPA give origin to substantial amounts of dopamine and the newly-formed amine undergoes considerable deamination to DOPAC. However, dopamine originating from GluDOPA was less deaminated than that resulting from L-DOPA; it appears that this different behaviour may concern aspects related to the formation of the amine and also those related to its deamination and disposition, namely the processes involved in the access of newly-formed dopamine to MAO.

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Plasma and urinary catecholamines in salt-sensitive idiopathic hypertension.

Cited by 115 publications

References 30 publications

Sucrose does not raise blood pressure in rats maintained on a low salt intake.

Sucrose does not raise blood pressure in rats maintained on a low salt intake.

Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

The renal handling of dopamine originating from l‐DOPA and γ‐glutamyl‐l‐DOPA

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