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Biomedical subjects

O Kuchel

Publications and source records attributed to O Kuchel.

222 records · Page 13Linked to original sources
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Regional sources of free and sulfoconjugated catecholamines in hypertension.

To elucidate the sources of free catecholamines (CA) and their sulfates in hyperadrenergic essential hypertensives (EH), their arteriovenous differences were determined radioenzymatically and by sulfatase hydrolysis (with correction for cross-contamination) across several organs and regions in 16 hyperadrenergic essential hypertensive patients. Comparison with arterial concentrations showed that: the adrenal venous outflow contains 240 times more free epinephrine (E), 55 times more free norepinephrine (NE), and 7 times more free dopamine (DA) concentrations, but E, NE, and DA sulfates are not different; free E concentrations are lower in the peripheral venous blood; NE sulfate concentrations are higher in the superior vena cava (p less than 0.05 for all differences noted). The data suggest the following conclusions for hyperadrenergic EH patients: with the exception of NE sulfate added into the superior vena cava region, no other organ or region can be associated with a net DA or NE sulfate release. The proportional adrenal vein concentrations of DA:NE:E are approximately 1:10:50, which are very close to those seen in other studies performed under different degrees of stress. Free E is extracted in peripheral tissues. The DA surges in hyperadrenergic EH patients probably result from the pulsatile, predominantly adrenal, release of free DA.

Arteries↗
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Pseudopheochromocytoma.

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Adrenal Gland Neoplasms↗
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Bromocriptine decreases blood pressure of spontaneously hypertensive rats without affecting the adrenomedullary synthesis of catecholamines.

Because of controversial data on the role of adrenomedullary catecholamines (CA) in the hypertension of spontaneously hypertensive rats (SHR) and in the hypotensive action of bromocriptine, we studied the effect of chronic bromocriptine treatment on blood pressure (BP), adrenal CA synthesis, tissue CA, and urinary excretions of CA and their metabolites in SHR. We found that the hypertension of 12-week-old SHR (systolic BP, 181 +/- 13 mm Hg) was reduced to 123 +/- 8 mm Hg when they received bromocriptine between 4 and 12 weeks of age (2 X 600 micrograms/kg/day, intraperitoneally). Although the urinary epinephrine (E) and the synthesis of adrenal norepinephrine (NE), E, and dopamine (DA), as well as the tissue content of CA in adrenals, heart, and kidney, remained unchanged after bromocriptine treatment, the urinary NE and DA excretions were lower in bromocriptine-treated SHR than in sham-treated SHR (NE, 2.7 +/- 0.3 versus 4.2 +/- 0.3 nmol/24 h in control SHR; DA, 18.7 +/- 1.6 versus 28.2 +/- 2.2 nmol/24 h in control SHR). In SHR, bromocriptine treatment did not affect the previously observed selectively increased adrenal turnover and synthesis of DA or the urinary excretions of normetanephrine (NM), dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3-MT), or homovanillic acid (HVA). The results suggest that the bromocriptine-induced decrease of BP in SHR is not mediated by changes in adrenomedullary CA and that bromocriptine decreases the BP of SHR without affecting the previously observed increased adrenal DA release of SHR. Thus, other central or peripheral dopaminergic agonist actions of bromocriptine bypassing the adrenal medulla must be considered in the hypotensive action of the drug.

Adrenal Medulla↗
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Dopamine negatively modulates its own blood pressure increasing action.

To evaluate the mechanisms of the hypertensive action of dopamine and its dependence on its metabolic patterns we infused a borderline hypertensive dose of free dopamine into healthy subjects. The moderate rise in systolic and diastolic blood pressure with an expected considerable increase of plasma free dopamine concentrations was associated within 30 minutes with an increase in plasma free norepinephrine and huge increases in plasma 3-4-dihydroxyphenylacetic acid, homovanillic acid and dopamine sulfate, the latter mostly between 60 and 180 minutes of infusion when diastolic blood pressure decreased. The overall pre-, per- and postinfusion changes in systolic blood pressure were negatively correlated with corresponding changes of free dopamine and dopamine sulfate. Reproducible patterns of blood pressure responses to the dopamine infusion made possible a subdivision into those who were blood pressure responders (who generated dopamine sulfate with delay) and non responders (who generated dopamine sulfate immediately). The data suggests that the 4 micrograms/kg/min dopamine infusion rate raises blood pressure indirectly via norepinephrine. Free dopamine and dopamine sulfate (the velocity of generation of which may be an inherited trait) are probably negative modulators of this action.

Adult↗