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Biomedical subjects

K W Perry

Publications and source records attributed to K W Perry.

At least 91 records · Page 5Linked to original sources
PubMed1981

Sympathetic noradrenergic innervation of guinea-pig liver: histofluorescence and pharmacological studies.

Norepinephrine concentration was higher in guinea-pig liver than in rat or mouse liver and evidence was obtained that the norepinephrine was present within nerves. In guinea pigs, norepinephrine in liver was depleted by reserpine, 6-hydroxydopamine and metaraminol. The depletion by 6-hydroxydopamine and metaraminol was antagonized by prior treatment with desipramine, an inhibitor of uptake into norepinephrine neurons. Guinea-pig liver concentrated metaraminol to a greater extent than did rat liver; the concentration of metaraminol was lowered by desipramine pretreatment and, within three tissues of the guinea pig (heart greater than liver greater than muscle), paralleled the concentration of endogenous norepinephrine. These findings constitute pharmacological evidence for noradrenergic innervation of guinea-pig liver to a greater extent than in other species. Histofluorescence studies confirmed the existence of norepinephrine-containing nerve terminals in guinea-pig liver. Norepinephrine-containing varicosities were seen adjacent to the hepatic artery, portal vein and bile duct in the portal spaces and adjacent to sinusoid capillaries and hepatocytes in the liver parenchyma. These findings strengthen the evidence for sympathetic innervation of liver and suggest the guinea pig as a useful species in exploring physiological roles of noradrenergic innervation of liver.

Animals↗
PubMed1978

Effect of lergotrile on 3,4-dihydroxyphenylacetic acid (DOPAC) concentration and dopamine turnover in rat brain.

Lergotrile, a dopamine agonist, lowered whole brain DOPAC (3,4-dihydroxyphenylacetic acid) concentration in rats. At low doses down to 0.5 mg/kg of lergotrile mesylate, this effect occurred within 30 min, whereas at higher doses (20 mg/kg) the decline in DOPAC was delayed. The decrease in DOPAC persisted for several hours and presumably resulted from a compensatory decrease in brain dopamine turnover secondary to receptor stimulation by lergotrile. Other indications of decreased brain dopamine turnover after lergotrile included (a) a slower decline in dopamine concentration after synthesis inhibition by alpha-methyltyrosine, (b) a slower decline in alpha-methyl-m-tyramine, a false transmitter that is stored and released by dopamine neurons, and (c) a decreased accumulation of dopamine in response to gamma-butyrolactone, an agent that blocks firing and dopamine release by dopamine neurons. Lergotrile mesylate (20 mg/kg) also increased brain levels of 5-hydroxyindoleacetic acid and of 3-methoxy-4-hydroxyphenylethylene glycol sulfate, metabolites of serotonin and norepinephrine, respectively, and these increases were not antagonized by spiperone, a dopamine receptor antagonist.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Effect of uptake inhibitors on the depletion of brain norepinephrine and serotonin after alpha-methyl-m-tyrosine administration to rats.

The depletion of brain norepinephrine after alpha-methyl-m-tyrosine injection into rats was antagonized by pretreatment with an uptake inhibitor (protriptyline or chlorimipramine) but was not completely prevented. Administration of protriptyline after alpha-methyl-m-tyrosine injection, at a time when norepinephrine had been depleted, partially reversed the depletion. Serotonin depletion after alpha-methyl-m-tyrosine was not altered by pretreatment with fluoxetine, an inhibitor of uptake into serotonin neurons. Apparently part of the norepinephrine (but not serotonin) depletion occurring after alpha-methyl-m-tyrosine injection is due to the action of amine products that enter the norepinephrine neuron via the membrane uptake pump and whose presence within the nerve terminals is maintained by the uptake pump.

Animals↗
PubMed1978

Effect of prazosin on norepinephrine concentration and turnover in rat brain and heart.

Prazosin hydrochloride injected i.p. into rats markedly increased MOPEG sulfate (3-methoxy-4-hydroxy-phenylethylene glycol sulfate) concentration in brain and the rate of MOPEG sulfate accumulation after probenecid. The increase in MOPEG sulfate was dose-related over a 5-40 mg/kg dose range. After a 20 mg/kg dose of prazosin, the increase in MOPEG sulfate was greater than after the same dose of phenoxybenzamine and persisted for up to 24 hr. The rate of metaraminol disappearance from rat brain after alpha-methyl-m-tyrosine injection and the decline in brain norepinephrine after inhibition of its synthesis by alpha-methyltyrosine injection were increased in rats pretreated with prazosin. These findings indicate that prazosin increased brain norepinephrine turnover, probably via compensation to central alpha adrenoceptor blockade. Prazosin increased sertonin and 5-hydroxy-indoleacetic acid concentration and slightly decreased 3,4-dihydroxy-phenylacetic acid in rat brain. Although prazosin had little effect on brain norepinephrine concentration, heart norepinephrine was depleted for up to 16 hr after a 20 mg/kg dose of prazosin, and the depletion at 4 hr was dose-related down to 2 mg/kg of prazosin. These biochemical changes may all result from prazosin's block of alpha adrenergic receptors.

3,4-Dihydroxyphenylacetic Acid↗