Salmon calcitonin and cGMP production by human kidney: Studies in vivo and in vitro

Gennari, C; Toccafondi, R; Rotella, Carlo Maria; Francini, Guido; Brandi, Maria Luisa; Maioli, Emanuela

doi:10.1007/bf02405045

Cited by 8 publications

(1 citation statement)

References 19 publications

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“…Erneux et al 1977). Such reciprocal changes in cyclic nucleotide levels have been observed for other endocrine systems (Gennari et al 1983). The inhibitory effect of norepinephrine on TSH-induced cAMP accumulation seems to be specific in view of the lack of effect of norepinephrine on the increase of cAMP produced by prostaglandin E2.…”

Section: Discussionmentioning

confidence: 91%

Evidence for α-adrenergic receptors acting through the guanylate cyclase system in human cultured thyroid cells

Brandi

Rotella

Tanini

et al. 1983

Acta Endocrinologica

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In order to investigate the presence of \ g = a \ \ x = r e q -\ adrenergic receptors in human thyroid, we have studied the effect of \g=a\-adrenergicagonists and antagonists on cGMP cellular content of human thyroid cells in primary culture. Epinephrine as well as TSH were not able to modify the cGMP cellular levels, while norepinephrine significantly increased cGMP accumulation already at 10 nM, a dose inactive on cAMP accumulation. A non selective \g=a\-adrenergicantagonist, phentolamine, significantly inhibited cGMP accumulation induced by norepinephrine. Norepinephrine-induced cGMP accumulation was unaffected by prazosin, an \g=a\1-adrenergic antagonist, but was abolished by yohimbine, an \g=a\2-adrenergic antagonist. Phenylephrine, an \g=a\-adrenergicagonist, produced an increase of cellular cGMP levels without modifying cAMP content. In the presence of TSH, the cGMP response to norepinephrine was not modified; however, the increase of cAMP levels was inhibited by norepinephrine at doses inactive on cAMP accumulation, but active on cGMP levels. The present results demonstrate the existence in human thyroid cells of \g=a\2-adrenergic receptors, regulating the guanylate cyclase system. It may be postulated that the counter-regulation exerted by \g=a\-adrenergicagonists on the response to TSH operates on the TSH-dependent adenylate cyclase. Sympathetic nerves have been found to supply the follicle cells in the thyroid of man and several mammals, and sympathetic activation has been shown to enhance thyroid hormone secretion via adrenergic receptors (Melander 1978). Subsequently, existence of ß-adrenergic receptors, acting through the adenylate cyclase system, has been demonstrated in human cultured thyroid cells ). In addition a potentiating effect of a-adrenergic antagonists on TSH action, together with the results of simultaneous stimula¬ tion with norepinephrine and TSH, suggest the presence of a-adrenergic receptors involved in the counter-regulation of TSH action ).In order to confirm the existence of -receptors in thyroid cells and to characterize their action in modulating the response to TSH, we have studied cyclic AMP and GMP levels in human thyroid cultured cells in response to an acute challenge with catecholamines or to an a-adrenergic agonist such as phenylephrine, in the presence and absence of TSH and of -or a2-adrenergic antagonists.The results indicate that an a2-adrenergic receptor modulates the TSH action through a guanylate cyclase system. Materials and Methods

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Section: Discussionmentioning

confidence: 91%

Evidence for α-adrenergic receptors acting through the guanylate cyclase system in human cultured thyroid cells

Brandi

Rotella

Tanini

et al. 1983

Acta Endocrinologica

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Pertussis Toxin Blocks the Inhibitory Effects of Calcitonin on Cyclic AMP Accumulation in Stimulated Cultured Human Monocytes

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Coderre

1987

Journal of Leukocyte Biology

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Surface stimulation of fresh or cultured human mononuclear cells by latex particles causes an increase in the accumulation of cyclic AMP that is inhibited by preincubation with calcitonin (CT). Preincubation of cultured monocytes with 500 ng/ml pertussis toxin totally blocks the inhibitory effects of CT at low concentrations of this hormone. The effects of pertussis toxin are dose-related and eliminated by boiling the toxin. Similar preincubations with cholera toxin have no significant effects on subsequent inhibition of surface-stimulated cyclic AMP by CT. Membranes prepared from cultured human monocytes contain a 41,000-dalton protein that is ADP-ribosylated by pertussis toxin and may be the inhibitory guanine nucleotide regulatory protein (Ni) mediating this inhibition.

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Effect of prostaglandin E2 on adenylate cyclase system in human kidney cell cultures: interactions with parathormone and arginine-vasopressin

Rotella

Brandi

Toccafondi

1983

J Endocrinol Invest

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We have used human kidney cortical and medullary cells in primary culture as an experimental model, in order to study the effect of prostaglandin E2 on the adenylate cyclase-cyclic AMP system at renal level, in comparison with that of parathormone and desamino 1-D-arginine 8-vasopressin. Prostaglandin E2 is a more potent stimulator of cyclic AMP accumulation in cortical cells than in medullary ones, the minimal effective dose being 3 nM in the cortex and 20 microM in the medulla. The maximal response was obtained with 30 microM in cortical cells and with 0.3 mM in medullary ones. The effects of combining submaximal and maximal active doses of the three hormones were always additive when tested on cortical cells. On the contrary, prostaglandin E2, at doses effective on the medullary cells adenylate cyclase system, produced an increase of cyclic AMP accumulation significantly lower than expected when incubated with submaximal and maximal amounts of desamino 1-D-arginine 8-vasopressin. Present data provide evidence for the existence of distinct receptors for parathormone, arginine-vasopressin and prostaglandin E2 at cortical level; the possible role of prostaglandin E2 in the counter-regulation of arginine-vasopressin action on medullary cells in unlikely, in view of the high prostaglandin E2 concentration which is necessary to exert this effect.

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Salmon calcitonin and cGMP production by human kidney: Studies in vivo and in vitro

Cited by 8 publications

References 19 publications

Evidence for α-adrenergic receptors acting through the guanylate cyclase system in human cultured thyroid cells

Evidence for α-adrenergic receptors acting through the guanylate cyclase system in human cultured thyroid cells

Pertussis Toxin Blocks the Inhibitory Effects of Calcitonin on Cyclic AMP Accumulation in Stimulated Cultured Human Monocytes

Effect of prostaglandin E2 on adenylate cyclase system in human kidney cell cultures: interactions with parathormone and arginine-vasopressin

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