Manipulation of mobile phase parameters for the HPLC separation of endogenous monoamines in rat brain tissue

Kontur, Paul J.; Dawson, Ralph; Monjan, Andrew

doi:10.1016/0165-0270(84)90003-7

Cited by 95 publications

(36 citation statements)

References 32 publications

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“…At death, the heart, kidneys, adrenal glands, and uterus were removed, cleaned of extraneous tissue, and weighed on a torsion balance. The adrenal glands were placed immediately in a freezer at -8 0 °C until analysis for catecholamine content by HPLC with electrochemical detection [15].…”

Section: Experiments 2: Effect O F Chronic Dietarytreatment With L-trymentioning

confidence: 99%

Effect of Chronic Dietary Treatment with L-Tryptophan on the Development of Renal Hypertension in Rats

Fregly¹,

Lockley²,

Cade³

1988

Pharmacology

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Chronic dietary administration of L-tryptophan (2.5 and 5.0 g/100 g food) to rats provided significant protection against the development of hypertension induced by bilateral encapsulation of the kidneys with latex envelopes. Lower doses of tryptophan (0.5 and 1.0 g/100 g food) attenuated the rate of elevation of blood pressure, but failed to maintain systolic blood pressures at levels significantly below that of untreated renal hypertensive controls. The body weight of the rats was not affected significantly by treatment with any dose of tryptophan used. Chronic treatment with tryptophan also protected against the reduced urinary concentrating ability during a 24-hour dehydration that characteristically accompanies renal encapsulation. A modest (5–8%) effect of treatment to reduce cardiac hypertrophy was also observed. The mechanism of the antihypertensive effect of tryptophan is not revealed by these studies although they rule out the possibilities that reduction in sodium intake and/or reduction in body weight may be important factors.

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Section: Experiments 2: Effect O F Chronic Dietarytreatment With L-trymentioning

confidence: 99%

Effect of Chronic Dietary Treatment with L-Tryptophan on the Development of Renal Hypertension in Rats

Fregly¹,

Lockley²,

Cade³

1988

Pharmacology

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“…The extracted samples were assayed using high-performance liquid chromatography and electrochemical detection as previously described. 16 …”

Section: Renal Norepinephrine Determinationmentioning

confidence: 99%

Upregulation of renal alpha 2-adrenergic receptors is not indicative of salt-related increases in blood pressure in spontaneously hypertensive rats.

1990

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The aim of the present study was to determine if elevations in salt intake were coupled to increases in renal a^-adrenergic receptors in SHR that differ in their blood pressure response to high salt diets. Salt-resistant spontaneously hypertensive rats (SHR-R), which do not increase their blood pressure in response to high salt intake, and salt-sensitive spontaneously hypertensive rats (SHR-S), which do exhibit significant elevations in blood pressure on high salt diets (3.15% NaCl), were used. Radioligand binding studies using [3 H]rauwolscine were performed on 6-and 11-week-old SHR-S and Wistar-Kyoto (WKY) rats to determine the effects of age, strain, and salt intake on o^-adrenergic receptor number and affinity. One week of high salt intake significantly increased blood pressure 22% in 6-week-old SHR-S and increased the blood pressure of 11-week-old SHR-S 12% without altering WKY rat controls. This treatment did not significantly increase renal a^-adrenergjc receptors in either SHR-S or WKY rats. SHR-S had significantly higher numbers of renal o^-adrenergic receptors than WKY rats on the high salt diets. One week of high (3.15%) or low (0.05%) salt intake did not significantly alter renal oj-adrenergic receptor number in 11-week-old SHR-S or WKY rats; however, blood pressure was significantly elevated in the SHR-S (175.0±3S versus 196.0±3.0 mm Hg). Two weeks of high salt intake did produce significant 37-48% increases in renal o^-adrenergic receptor numbers in both SHR-S and SHR-R; however, this treatment increased blood pressure significantly only in the SHR-S. The results of these studies show that salt-induced increases in blood pressure in the SHR-S occur previous to significant increases in renal «j-adrenergic receptors that are seen in both SHR-S and SHR-R after 2 weeks of high salt treatment These findings suggest that salt-induced increases in blood pressure are independent of the upregulation of renal o^-adrenergic receptors. (Hypertension 1990;16:49-54)

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“…The tissues were weighed and homogenized in 0.1 mol/l perchloric acid containing 100 mg/1 of NajEDTA and then centri fuged at 10.000 g for 15 min. The supernatants from the brain regions, posterior pituitary, adrenals and heart were filtered through 0.2-pm nylon 66 filters and directly injected onto the column for analysis by HPLC-ECD [ 14], The supernatants from the right kid ney were extracted with alumina and also assayed by HPLC-ECD [14], The amino acid content of the fore brain was determined by HPLC-ECD after derivatization with o-phthalaldehyde.…”

Section: Neurochemical Studiesmentioning

confidence: 99%

“…and commercially available kits were used to measure creatinine, serum urea nitrogen (SUN), protein and glucose. Urinary catecholamines were extracted [13] and determined by HPLC with electrochemical detec tion (HPLC-ECD) [14],…”

Section: Urinary Measurementsmentioning

confidence: 99%

Neural-Renal Interactions in the Hypertension Induced by Papillary Necrosis: Role of Dietary Salt Intake

Dawson

Wallace²

1990

Pharmacology

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The effects of high salt intake (1.0% NaCl in the drinking water) on rats made hypertensive by 2-bromoethylamine hydrobromide (BEA) treatment (200 mg/kg, i.p.) were examined. BEA-induced medullary necrosis resulted in a mild hypertension (146 ± 5 mm Hg) that was exacerbated by 4 weeks of high salt intake (163 ± 6 mmHg). BEA-treated rats had significant salt-induced increases in urinary norepinephrine excretion and hypothalamic and brainstem norepinephrine content, that were not present in BEA-treated rats drinking tap water or control rats drinking saline. BEA treatment in combination with increased salt intake produced a decrease (p < 0.05) in renal dopamine content and adrenal norepinephrine stores relative to BEA treatment alone. BEA treatment also significantly decreased renal norepinephrine stores and dopamine binding sites irrespective of salt intake. Renal α₂-adrenergic receptors and central nervous system stores of dopamine and serotonin were unaffected by BEA treatment. Renal function was well preserved as indicated by normal creatinine, glucose and protein excretion; however, significant (p < 0.05) disruption of the urinary concentrating mechanism was present. These studies suggest that BEA-induced hypertension has a neural component that is exacerbated by high salt intake. The primary defect in BEA hypertension appears to be the lack of circulating antihypertensive lipids that attenuate the ability of salt loads to simulate sympathetic nervous system activity.

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Manipulation of mobile phase parameters for the HPLC separation of endogenous monoamines in rat brain tissue

Cited by 95 publications

References 32 publications

Effect of Chronic Dietary Treatment with L-Tryptophan on the Development of Renal Hypertension in Rats

Effect of Chronic Dietary Treatment with L-Tryptophan on the Development of Renal Hypertension in Rats

Upregulation of renal alpha 2-adrenergic receptors is not indicative of salt-related increases in blood pressure in spontaneously hypertensive rats.

Neural-Renal Interactions in the Hypertension Induced by Papillary Necrosis: Role of Dietary Salt Intake

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