Laboratorio de Glándulas Salivales y Saliva

Director:
Prof. Dr. Omar Tumilasci. Profesor Adjunto de Fisiología, Investigador Independiente del CONICET

Colaborador:
Dr. Mariano Ostuni

Investigadores y Docentes:
Lic María Victoria Ramos (Auxiliar Docente)

Personal de Apoyo a la Investigación:
Elida Monardes (Técnica principal de CONICET)

Tesistas:
Jose Gabriel Gontaretti

Líneas de Investigación

Estudios básicos y aplicados sobre fisiopatología de las glándulas salivales y saliva como método de diagnóstico médico

Abstracts
Eur J Oral Sci 1: 492-496; 2003
Modulation by thyroid hormones of rat parotid amylase secretion stimulated by 5-hydroxytryptamine

Ostuni MA, Houssay AB, Tumilasci OR

Dpto de Fisiologia - Facultad de Medicina - Universidad de Buenos Aires

The effects of 5-hydroxytryptamine (5-HT) upon amylase secretion by rat parotid glands were studied in three groups of animals: (a) intact control rats (euthyroid rats); (b) hypothyroid rats obtained by surgical thyroidectomy 2 wk before the experiments; and (c) hyperthyroid rats obtained by the administration of sodium 1-triiodothyronine for 2 wk before the experiments. Hyperthyroid rats showed significantly higher baseline amylase release than control rats. When the glands were stimulated with 5-HT (30 jim), amylase release was significantly lower in the hypothyroid group and higher in the hyperthyroid rats than in control group. Addition of cholinergic, adrenergic or substance P antagonists did not modify 5-HT-stimulated amylase activity. The effects of 5-HT were partly but significantly blocked by the addition of 10 JIM methysergide (HT112/7 receptor blocker) in the three groups of rats. In contrast, 10 ÁM ketanserine (HT, receptor blocker) partly blocked the response to 5-HT only in the hyperthyroid animals. It was concluded that 5-HT induces amylase secretion by rat parotid glands through specific serotoninergic receptors, and that thyroid status modulates the 5-HT effect.


Archives of Oral Biology; 48: 205-212;2003
Modulation by somatostatin of rat submandibular salivary secretion

Ostuni MA, Ferrero AJ, Bereciartu A, Houssay AB, Tumilasci OR

Facultad de Odontologia, Catedra de Biofisica, Universidad de Buenos Aires, M.T. de Alvear 2142 (C1122AAH), Argentina. ostuni@bichat.inserm.fr

Although somatostatin (somatotrophin release inhibitory factor; SRIF) is a well-known inhibitory peptide, there are only a few reports of it acting as a positive modulator. In this work, the action of somatostatin upon rat submandibular protein secretion was studied. In vivo somatostatin infusion (35 microg/(kg h)) raised protein secretion stimulated by adrenergic and peptidergic agents. To rule out possible systemic effects of somatostatin, in vitro experiments were performed. Somatostatin (90 nmol/l) augmented protein release stimulated by noradrenaline (19 micromol/l) and substance P (10 micromol/l), but it did not affect isoprenaline (400 micromol/l)-induced protein release. Phenoxybenzamine (20 micromol/l) reduced the effect of somatostatin on noradrenaline-stimulated protein release. Propranolol (20 micromol/l) increased the noradrenaline-stimulated protein release and this effect was synergistic with the action of somatostatin. The absence of extracellular calcium did not significantly reduce somatostatin enhancement of agonist-induced secretion. Fluorescence measurements of the Ca(2+)-sensitive dye fluo3 showed that cytosolic calcium in acinar cells remained elevated during stimuli when somatostatin was present in the medium. It was concluded that somatostatin modulates rat submandibular protein secretion by prolonging the time that the cytosolic calcium signal remains high after stimulus.