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How does angiotensin II increase cardiac dopamine-β-hydroxylation?
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AbstractThe potent accelerating effect of angiotensin II (Ang II) on cardiac dopamine β-hydroxylation was studied on slices of rat heart. Ang II did not affect the kinetics of β-hydroxylation but it increased the axonal uptake of dopamine, and, concomitant with the acceleration of biosynthesis, it enhanced the accumulation of dopamine into tissue. Puromycin, in contrast to actinomycin D, antagonized the stimulation of dopamine β-hydroxylation by Ang II, but did not suppress the rise in cardiac dopamine. Therefore, to promote the acceleration of dopamine β-hydroxylation, (i) the rise in tissue dopamine available for conversion appeared to be insufficient, (ii) the formation of new proteins by activation of traduction seemed to constitute the basic mechanism of Ang II action.
Oxford University Press (OUP)
Title: How does angiotensin II increase cardiac dopamine-β-hydroxylation?
Description:
AbstractThe potent accelerating effect of angiotensin II (Ang II) on cardiac dopamine β-hydroxylation was studied on slices of rat heart.
Ang II did not affect the kinetics of β-hydroxylation but it increased the axonal uptake of dopamine, and, concomitant with the acceleration of biosynthesis, it enhanced the accumulation of dopamine into tissue.
Puromycin, in contrast to actinomycin D, antagonized the stimulation of dopamine β-hydroxylation by Ang II, but did not suppress the rise in cardiac dopamine.
Therefore, to promote the acceleration of dopamine β-hydroxylation, (i) the rise in tissue dopamine available for conversion appeared to be insufficient, (ii) the formation of new proteins by activation of traduction seemed to constitute the basic mechanism of Ang II action.
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