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Biomedical subjects

R H Roth

Publications and source records attributed to R H Roth.

At least 397 records · Page 22Linked to original sources
PubMed1971

Evidence that angiotensin enhances transmitter release during sympathetic nerve stimulation.

1. The effects of angiotensin on the contractility of the transmurally stimulated rabbit portal vein and coeliac artery have been studied in conjunction with its effects on the release and uptake of (+/-)-(3)H-noradrenaline.2. Angiotensin contracted both vein and artery; these responses were enhanced by veratrine and reduced by tetradotoxin. At low (non-contractile) concentrations of angiotensin, contractions elicited by electrical stimulation (0.5-4 Hz) had a quicker onset and reached a higher maximal tension than control responses. Higher concentrations of angiotensin increased the degree of potentiation. Contractions to noradrenaline were not enhanced by angiotensin.3. Pretreatment of the coeliac artery, portal vein and perfused rat heart with angiotensin did not reduce the subsequent uptake of labelled noradrenaline in the presence of angiotensin. Simultaneous treatment with angiotensin and (3)H-noradrenaline caused a small, apparent inhibition of uptake into the portal vein.4. When the portal vein was incubated with (3)H-noradrenaline there was a marked accumulation of label within the tissue; over 90% of the radioactivity retained in the tissue was identified as intact noradrenaline. When the vein, or artery, was superfused with amine-free Krebs there was a steady basal release of label; the greater proportion of this label was identified as deaminated metabolites. Electrcal stimulation evoked a frequency dependent release of (3)H above basal levels. The greater proportion of this increased efflux was due to the release of intact (3)H-noradrenaline, with smaller increases in the amount of O-methylated and deaminated metabolites.5. Angiotensin increased the efflux of labelled noradrenaline + normetanephrine, or of total (3)H, during transmural stimulation (0.5-4 Hz) in both the vein and artery, but did not increase the efflux of deaminated products during electrical stimulation. The output of labelled noradrenaline + normetanephrine was usually doubled in the presence of angiotensin (200-500 ng/ml) during electrical stimulation of the portal vein.6. Cocaine (4 mug/ml) potentiated responses to noradrenaline and transmural stimulation, and doubled the output of (3)H or labelled noradrenaline + nor-metanephrine during electrical stimulation. Cocaine did not alter the potentiating effects of angiotensin.7. Angiotensin elicited transitory increases in the basal efflux of (3)H from both the portal vein and coeliac artery. However, this did not account for the marked increase in efflux seen during electrical stimulation. Vasopressin did not potentiate responses to transmural stimulation or significantly influence the efflux of (3)H from the vein or artery.8. Noradrenaline and 5-hydroxytryptamine, but not acetylcholine, markedly increased the efflux of (3)H from the portal vein. This increase in efflux of label is believed to result from an exchange of exogenous noradrenaline and 5-hydroxytryptamine with labelled tissue stores of noradrenaline.9. It is suggested that angiotensin is able to facilitate the release of the sympathetic transmitter and that this is the basis for its action in potentiating the responses to sympathetic stimulation. It is also suggested that the nor-adrenaline releasing action of angiotensin (by excitation of sympathetic nerve endings) has led to confusion in previous investigations of the effects of angiotensin on noradrenaline uptake.

5-Hydroxytryptophan↗
PubMed1970

Acceleration of noradrenaline biosynthesis in the guinea-pig vas deferens by potassium.

1. Increasing the concentration of KCl in Krebs-Henseleit bicarbonate solution enhanced the formation of (14)C-noradrenaline ((14)C-NA) from (14)C-tyrosine in the guinea-pig vas deferens. In 52 mM KCl Krebs-Henseleit solution the specific activity of the newly formed (14)C-NA was double that of controls.2. The rate of synthesis of (14)C-NA from (14)C-tyrosine was constant for up to 2 h in 52 mM KCl Krebs-Henseleit solution and for 4 h in unmodified Krebs-Henseleit solution.3. There was no increase in NA formation in the presence of KCl rich Krebs-Henseleit solution if (14)C-DOPA was used as the starting substrate instead of (14)C-tyrosine.4. The specific activity of (14)C-tyrosine in the high KCl treated vas deferens was 80% of that of control tissues. Thus the enhanced synthesis of (14)C-NA in high KCl Krebs-Henseleit solution did not arise from an increase in the specific activity of precursor.5. The effect of K(+) on NA synthesis was not mimicked by ganglionic stimulants nor blocked by tetrodotoxin.6. Removal of Ca(2+) ions or increasing the concentration of Mg(2+) ions abolished the increase in synthesis of NA seen in high KCl Krebs-Henseleit solution but left the basal rate of NA synthesis in unmodified Krebs-Henseleit solution unaltered.7. The spontaneous release of newly synthesized catecholamines ((14)C-labelled) or tritiated noradrenaline ((3)H-NA) from vasa deferentia was increased in 52 mM KCl Krebs-Henseleit solution. Removal of Ca(2+) ions reduced the increased efflux of newly synthesized amine in high KCl media to that seen in unmodified Krebs-Henseleit solution. The efflux of (3)H-NA was reduced to one-third of its former rate in the absence of Ca(2+).8. High KCl Krebs-Henseleit solution caused a substantial contraction of the vas deferens which was not abolished by tetrodotoxin. Release of (3)H-NA paralleled the contractile response, and was likewise unaffected by tetrodotoxin.9. No evidence was obtained for any alterations in the activity of tyrosine hydroxylase, the rate limiting enzyme in the formation of NA from tyrosine, in homogenates of vas deferens which had been treated with 52 mM KCl Krebs-Henseleit solution.10. These results support the hypothesis that acceleration of NA synthesis occurs when tyrosine hydroxylase is freed from end-product inhibition by the release of noradrenaline, brought about in this case, by high concentrations of KCl.

Animals↗