The effect of tyrosine on blood pressure and its relation to plasma and brain catecholamine levels in the rat
Bresnahan, Margaret Ryan
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To help clarify the action of acute administration of the amino acid L-tyrosine in lowering blood pressure, L-tyrosine ethylester was infused intravenously into awake (deoxycorticosterone acetate (DOCA)-salt) hypertensive rats, (two-kidney Goldblatt) hypertensive rats, and normotensive rats. The effects were measured on mean arterial blood pressure, heart rate, plasma catecholamine levels, plasma renin activity and catecholamine levels in chosen sections of brain. Tyrosine infusion caused a progressive decline of blood pressure and heart rate in all groups, despite significantly elevated plasma dopamine in all groups and epinephrine in the hypertensive groups. Plasma norepinephrine failed to rise significantly in response to the decrease in blood pressure and in some animals it actually decreased; plasma renin activity remained within the normal range for each model. In the normotensive group tyrosine elevated dopamine and norepinephrine levels in medulla oblongata and norepinephrine in a section of cerebrum posterior to transection at the level of the optic chiasma. In the DOCA-salt group (four weeks) tyrosine elevated dopamine levels in medulla oblongata and in the posterior section of cerebrum. It was concluded that increased transport of tyrosine into the brain produced a progressive decline in blood pressure and heart rate by bringing about a sustained state of parasympathetic dominance, as effective sympathetic compensation did not occur. This may be attributed to increased [alpha]-adrenergic activity in key areas of brain (controlling cardiac inhibitory and vasomotor centers), secondary to increased catecholamine synthesis (and tyramine-stimulated release) in these areas. Tyramine-stimulated release would tend to deplete the neuronal cytoplasmic mobile pool of neurotransmitter and allow release of tyrosine hydroxylase from endproduct feedback inhibition, permitting increased catecholamine synthesis in the presence of continued substrate excess. To assess the relationship of central changes in catecholamine levels to peripheral changes in activity of the sympathetic nervous system (SNS), plasma catecholamine levels (an index of sympathoadrenal medullary activity) were compared (in controls versus DOCA-salt treated rats) during an eight week period of progression of the hypertension, while catecholamine levels in chosen sections of brain were compared at four weeks (when the hypertension is still benign) and at eight weeks (during the malignant phase). During the first four weeks of the hypertension, the period of positive sodium balance, plasma norepinephrine did not rise above baseline, · but from the fifth to the eighth week, when negative sodium balance ensues, a progressive rise of plasma norepinephrine was seen. These data do not support the concept of increased SNS activity throughout the progression of the DOCA-salt hypertension; however, in the early stages, salt retention may somewhat mask a rise in plasma norepinephrine, while salt loss in the latter stages may enhance it. Plasma epinephrine was not significantly different from control levels except at four and six weeks when it was higher in the DOCA-salt group, reflecting hyperactlvity of the adrenal medulla at this time. However, both epinephrine - and dopamine were suppressed at the eighth week, concomitant with the rise of plasma norepinephrine to maximum. There were no significant changes in catecholamine levels in any section of brain at four weeks of the hypertension. However, at eight weeks, the DOCA-salt group exhibited an elevation of central catecholamine levels, including epinephrine in medulla oblongata, which is implicated in centrally increased sympathetic tone.
PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact firstname.lastname@example.org.Thesis (D.Sc.D.)--Boston University, Henry M. Goldman School of Graduate Dentistry (Nutritional Sciences), l980.Bibliography: leaves 102-120.
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