Alterations in Tyrosine Hydroxylase and Monoamine Oxidase Activity in Blood Vessels

Tarver, James; Berkowitz, Barry A.; Spector, Sydney

doi:10.1038/newbio231252a0

Cited by 32 publications

(16 citation statements)

References 10 publications

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“…The cycling protocol (PE 480 thermal cycler, Perkin-Elmer) consisted of an initial denaturation (95°C, 5 minutes) followed by sequential cycles of denaturation (95°C, 1 minute), annealing (60°C, 1 minute), and extension (72°C, 1 minute) followed by a final extension stage (72°C, 7 minutes). The cycle numbers for NGF (30) and GAPDH (23) were chosen to ensure that both reactions were in the exponential phase. The two gene amplifications were carried out in separate reactions and repeated four times for each cDNA sample to limit the tube-to-tube variation of PCR amplification.…”

Section: Pcr Amplificationmentioning

confidence: 99%

Persistent Reduction in Renal Nerve Growth Factor mRNA After Perindopril Treatment of Young Spontaneously Hypertensive Rats

1998

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Abstract-Nerve growth factor (NGF) determines sympathetic innervation of target tissues, and NGF levels are increased in young spontaneously hypertensive rats (SHR). Angiotensin can affect NGF levels, and the persistent reduction in blood pressure after brief angiotensin-converting enzyme inhibition in young SHR may involve long-term changes in NGF and sympathetic innervation. We measured the relative abundance of renal NGF mRNA by reverse transcription-polymerase chain reaction in SHR during and after treatment from 6 to 10 weeks of age with vehicle, perindopril (3 mg/kg per day), the bradykinin B 2 antagonist Hoe 140 (0.5 mg/kg per day), both perindopril and Hoe 140, or angiotensin II (Ang II; 200 ng/kg per minute). Glomerular filtration rates were estimated at 10 and 20 weeks of age. At 10 weeks of age, Ang II caused a significant (PϽ.01) increase and perindopril caused a significant (PϽ.01) decrease in renal NGF mRNA levels. Blockade of the bradykinin B 2 receptor during perindopril treatment attenuated (PϽ.05) the reduction in NGF mRNA levels. Renal NGF mRNA (Pϭ.005) and blood pressure (PϽ.001) remained significantly lower than control 10 weeks after perindopril treatment was stopped. The partial reduction in blood pressure at 20 weeks of age in rats that had received perindopril and Hoe 140 was not associated with any difference in renal NGF mRNA. Perindopril-induced long-term reduction in renal NGF mRNA levels may decrease sympathetic innervation and thereby contribute to the long-term posttreatment blood pressure reduction. (Hypertension. 1998;31:678-683.)

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Section: Pcr Amplificationmentioning

confidence: 99%

Persistent Reduction in Renal Nerve Growth Factor mRNA After Perindopril Treatment of Young Spontaneously Hypertensive Rats

1998

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“…In SHR tissues, age-related differences have been reported in the enzymes implicated in the synthesis (such as tyrosine hydroxylase and dopamine ␤-hydroxylase) and metabolism (such as monoamine oxidase and catechol-o-methyltransferase) of norepinephrine (NE), which has been found to be higher in resistance arteries 5 but normal in the heart in the early phases of hypertension development, with an inverse relationship in adult rats. 6 -9 Neuronal uptake of NE, the active mechanism responsible for removing NE from the synaptic cleft once released from the nerve terminal, 10 has been found to be normal in cardiac and vascular tissue, 11,12 increased in the kidney and skeletal muscle of young SHR, 4 but reduced in the heart 13,14 and kidney 4 and increased in resistance arteries 15,16 of adult SHR.…”

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Norepinephrine Reuptake Is Impaired in Skeletal Muscle of Hypertensive Rats In Vivo

et al. 2001

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Abstract-Certain forms of experimental hypertension are characterized by organ-specific alterations of catecholaminergic pathways. The purpose of this study was to evaluate, in the same awake and freely moving normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) before and after the development of arterial hypertension, the norepinephrine (NE) turnover and, in particular, the neuronal NE reuptake activity that ends its effects once released from nerve terminals, in subcutaneous adipose tissue and in skeletal muscle, whose sympathetic efferents are respectively independent or dependent from baroreflexes. Plasma and tissue interstitial NE and 3,4-dihydroxyphenylethylene glycol (DHPG), its major deaminated metabolite, were measured before and after blockade of NE reuptake by tissue perfusion of desipramine through microdialysis probes. Arterial pressure and plasma NE in SHR were similar to those in WKY at 5 weeks of age but increased at 16 weeks of age. In contrast, plasma DHPG was already higher in young SHR. Basal interstitial NE and DHPG were increased in both tissues of young and old SHR compared with age-matched WKY. Desipramine induced a higher rise of interstitial NE in SHR of both ages, with a lesser increase in the skeletal muscle of old compared with young SHR. These results indicate an increased NE turnover in prehypertensive and hypertensive SHR in both baroreflex-dependent and -independent tissues, not shown by plasma NE levels in young SHR. In the skeletal muscle, where sympathetic efferents are baroreflex dependent, the reduced interstitial NE reuptake contributes to the higher availability of interstitial NE for postsynaptic effects in old SHR. Key Words: muscle, skeletal Ⅲ adipose tissue Ⅲ nervous system, sympathetic Ⅲ norepinephrine Ⅲ rats, inbred SHR A bnormalities of the central neural mechanisms regulating peripheral sympathetic outflow and catecholamine metabolism after the release of the neurotransmitter from the nerve endings have been described in the development of hypertension in humans 1,2 and in spontaneously hypertensive rats (SHR), 3,4 the animal model of essential hypertension most used. In SHR tissues, age-related differences have been reported in the enzymes implicated in the synthesis (such as tyrosine hydroxylase and dopamine ␤-hydroxylase) and metabolism (such as monoamine oxidase and catechol-o-methyltransferase) of norepinephrine (NE), which has been found to be higher in resistance arteries 5 but normal in the heart in the early phases of hypertension development, with an inverse relationship in adult rats. 6 -9 Neuronal uptake of NE, the active mechanism responsible for removing NE from the synaptic cleft once released from the nerve terminal, 10 has been found to be normal in cardiac and vascular tissue, 11,12 increased in the kidney and skeletal muscle of young SHR, 4 but reduced in the heart 13,14 and kidney 4 and increased in resistance arteries 15,16 of adult SHR. Most of these data on NE turnover are obtained from in vitro or ex vivo tissue st...

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“…Normotensive controls were intact, male Wistar rats maintained on a standard laboratory diet and water. Spontaneously hypertensive rats were selected from the available males of uniform age generated by the Hoffmann-La Roche colony described (11,12). Normotensive controls for these spontaneously hypertensive rats were genetically related Wistar-Kyoto male rats, whose breeding stock was obtained from Dr. Carl T. Hansen, Genetics Unit, Animal Production Section, N.I.H., Bethesda, Md.…”

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confidence: 99%

Increased Collagen Synthesis in Blood Vessels of Hypertensive Rats and Its Reversal by Antihypertensive Agents

Ooshima

Fuller

Cardinale

et al. 1974

Proc. Natl. Acad. Sci. U.S.A.

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144

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Collagen synthesis is increased in the aortas, mesenteric arteries, and to a lesser extent, in the hearts of rats either made hypertensive with desoxycorticosterone acetate-salt or that are spontaneously hypertensive. Several markers of collagen biosynthesis were shown to be increased, including prolyl hydroxylase (EC 1.14.11.2; proline, 2-oxoglutarate dioxygenase), prolyl hydroxylaserelated antigen, total collagen content, and the incorporation of [3Hiproline into total protein and into collagen.The antihypertensive agents chlorothiazide and reserpine, when administered before the onset of hypertension in the rats treated with desoxycorticosterone acetate-salt, prevented or diminished the increase in collagen biosynthesis. When reserpine was given after the onset of hypertension, prolyl hydroxylase activity was decreased concomitant with the decrease in blood pressure. Treatment with reserpine is particularly effective in diminishing arterial prolyl hydroxylase activity.

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Alterations in Tyrosine Hydroxylase and Monoamine Oxidase Activity in Blood Vessels

Cited by 32 publications

References 10 publications

Persistent Reduction in Renal Nerve Growth Factor mRNA After Perindopril Treatment of Young Spontaneously Hypertensive Rats

Persistent Reduction in Renal Nerve Growth Factor mRNA After Perindopril Treatment of Young Spontaneously Hypertensive Rats

Norepinephrine Reuptake Is Impaired in Skeletal Muscle of Hypertensive Rats In Vivo

Increased Collagen Synthesis in Blood Vessels of Hypertensive Rats and Its Reversal by Antihypertensive Agents

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