Stanley A. Tan

Neuroendocrine and Stress Hormone Changes During Mirthful Laughter

Positive emotional activities have been suggested as modifiers of neuroendocrine hormones involved in the classical stress response. To detect changes in these components during a mirthful laughter experience, the authors studied 10 healthy male subjects. Five experimental subjects viewed a 60 minute humor video and five control subjects did not. Serial blood samples were measured for corticotropin (ACTH), cortisol, beta-endorphin, 3,4-dihydrophenylacetic acid (dopac)--the major serum neuronal catabolite of dopamine, epinephrine, norepinephrine, growth hormone, and prolactin. Repeated measures analysis of variance showed that cortisol and dopac in the experimental group decreased more rapidly from baseline than the control group (p = 0.011, p = 0.025, respectively). Epinephrine levels in the experimental group were significantly lower than the control at all time points (p = 0.017). Growth hormone levels in the experimental group significantly increased during baseline (p = 0.027) and then decreased with laughter intervention (p less than 0.0005), whereas, the controls did not change over time (p = 0.787). ACTH, beta-endorphin, prolactin, and norepinephrine levels did not significantly increase. The mirthful laughter experience appears to reduce serum levels of cortisol, dopac, epinephrine, and growth hormone. These biochemical changes have implications for the reversal of the neuroendocrine and classical stress hormone response.

Indapamide regresses, but transdermal clonidine does not regress, left ventricular hypertrophy in hypertensive diabetic patients.

This report describes the effects of indapamide versus transdermal clonidine on left ventricular hypertrophy (LVH) in hypertensive diabetic patients. A sample of 24 hypertensive diabetic men, aged 40-68 years, with echocardiographically proven LVH was equally divided in to 2 groups. Group 1 was treated with indapamide 2.5 mg/day, and group C with transdermal clonidine weekly. Left ventricular mass and posterior wall and septal thickness were measured by standard echocardiograms done at baseline and every 6 months. At 24 months, treatment crossover was done. Normotension was maintained throughout the study. With indapamide, LVH regression was measurable at 6 months, and left ventricular mass had returned to normal after 18 months. Transdermal clonidine did not regress LVH, but when the patients were switched to indapamide, LVH did regress. Clonidine maintained normal ventricular dimensions after regression had been induced by indapamide.

Detection of aminoalkylphosphonates with a ninhydrin-molybdate chromogenic system

Abstract Aminoalkylphosphonates can be detected on paper chromatograms by reacting them with ninhydrin, followed by spraying with hypochlorite, molybdate, and Elon-sulfite solutions. The phosphonates appear as blue spots on the chromatogram. Reagent preparation and staining procedure are described. The sensitivity is 0.1 μmole for ciliatine, 0.01 μmole for phosphonoalanine, and 1.0 μmole for N-methylciliatine.

Hyperiodotyrosinemia-Induced Hyperprolactinemia and Hyperaldosteronism

A 21-year-old goitrous hypothyroid Chinese woman had elevated serum iodotyrosines with a monoiodotyrosine level of 85.9 nmol/l (normal 0.49-0.89 nmol/l) and a diiodotyrosine level of 25.3 nmol/l (normal 0.023-0.53 nmol/l). She was amenorrheic with low luteinizing hormone and follicle-stimulating hormone levels at 5.8 and 2.8 U/l, respectively. The hypogonadotropic hypogonadism was due to an elevated prolactin level of 8.8 nmol/l. She also had a low potassium level of 3.2 mmol/l, and a high urinary aldosterone level of 158 nmol/day. The hyperprolactinemia, hypogonadotropic hypogonadism, hyperaldosteronism and hypokalemia subsided with the administration of bromocriptine 5 mg/day. However, bromocriptine accentuated the hyperiodotyrosinemia, and the patient remained hypothyroid. Levothyroxine therapy lowered the monoiodotyrosine and diiodotyrosine levels, ameliorated all her endocrinopathies, started her periods, and shrank the goiter. She probably had a deiodinase defect which permitted the discharge of accumulated iodotyrosines from the thyroid gland. Since iodotyrosines are tyrosine hydroxylase inhibitors, the hyperiodotyrosinemia causes dopamine synthesis inhibition, and induces the hyperprolactinemia and hyperaldosteronism.

Modulation of the renin-aldosterone system by iodotyrosines as tyrosine hydroxylase inhibitors

This study shows that MIT and DIT stimulate aldosterone secretion. This may be due to their tyrosine hydroxylase inhibitory property. Dopamine abolishes the stimulation. Prolonged MIT administration enhances the stimulation of aldosterone secretion and can cause hypokalemia. Volume expansion reverses the hyperaldosteronism. PRA and blood pressure do not change, even after prolonged MIT intake.