Protein secretion induced by isoproterenol or pentoxifylline in lacrimal gland: Ca2+ effects

In exorbital lacrimal glands, pentoxifylline (a methylxanthine) induces labeled protein secretion in a dose-related manner: the half-maximal and maximal stimulations are at 4 and 10 mM, respectively. In the presence of papaverine (10(-5) M), a phosphodiesterase inhibitor, labeled protein discharge is strongly stimulated by isoproterenol, via beta-adrenergic receptors: the maximal response is at 10(-6) M. l-Propranolol specifically inhibits the secretory stimulation to isoproterenol in a dose-related manner: for 5 X 10(-6) M isoproterenol in the presence of 10(-5) M papaverine, the half-maximal and maximal inhibitions are at 3 X 10(-7) and 10(-5) M, respectively. The beta-adrenergic response is mimicked by the adenosine 3',5'-cyclic monophosphate (cAMP) analogue dibutyryl cAMP (DBcAMP) at a 10(-3) M concentration. The time course of labeled protein secretion induced by pentoxifylline, DBcAMP, and isoproterenol shows a latency. In the presence or absence of extracellular calcium, pentoxifylline and isoproterenol immediately increase the cAMP intracellular level. Extracellular calcium omission increases the observed latency and also affects the maximal rate of protein secretion. As opposed to the cholinergic agonist, pentoxifylline has only a slight but sustained effect on 45Ca efflux, whereas isoproterenol has none. These data suggest that labeled protein secretion, such as that of peroxidase, can also be stimulated in rat exorbital lacrimal gland, through beta-adrenergic receptors; in the stimulation evoked by a beta-adrenergic agonist, DBcAMP, or methylxanthine, calcium could play a key role.

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Age-related decrement in hormone-stimulated lipolysis

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1984.247.6.e772 ◽

1984 ◽

Vol 247 (6) ◽

pp. E772-E777 ◽

Cited By ~ 2

Author(s):

B. B. Hoffman ◽

H. Chang ◽

Z. T. Farahbakhsh ◽

G. M. Reaven

Keyword(s):

Adrenergic Receptors ◽

Beta Adrenergic Receptors ◽

Beta Adrenergic ◽

Kinase Activation ◽

Age Related ◽

Protein Kinase Activation ◽

Camp Analogue ◽

Dependent Protein ◽

Old Rats ◽

Adrenergic Receptor Agonist

The ability of hormones to activate responses in a variety of tissues decreases with age. The mechanism(s) responsible for these alterations are unclear. We have confirmed that the ability of a beta-adrenergic receptor agonist to activate lipolysis in isolated rat adipocytes decreases with age. Maximum response to isoproterenol was greater in 2-mo-old rats (600 +/- 30 nmol of glycerol released/10(5) cells per h) than 12-mo-old rats (250 +/- 25 nmol/10(5) cells per h), P less than 0.001. Similarly, ACTH is less effective in activating lipolysis in the adipocytes from the older rats. However, the cAMP analogue 8-(4-chlorophenothio)adenosine 3',5'-monophosphate cyclic activated lipolysis equally in the two groups, suggesting that the deficit in adipocytes from the older rats was proximal to cAMP-dependent protein kinase activation. Both isoproterenol and ACTH were significantly less effective in promoting cAMP accumulation in adipocytes isolated from 12-mo-old rats. There was no difference in phosphodiesterase activity of the adipocytes between the two groups. beta-Adrenergic receptors were measured using the antagonist radioligand [125I]cyanopindolol. The number of beta-adrenergic receptors was actually increased in the adipocytes from 12-mo-old rats (26,000 +/- 2,600 receptors/cell) compared with cells from 2-mo-old rats (7,200 +/- 1,300 receptors/cell). The results suggest that diminished cAMP production is responsible for the diminished lipolytic response in the adipocytes of older rats. The mechanism responsible for this change is uncertain but cannot be explained by a loss in beta-adrenergic receptors.

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T-kinin has endothelium-dependent vasodilator activity in the cat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.3.h1491 ◽

1997 ◽

Vol 272 (3) ◽

pp. H1491-H1498

Author(s):

J. A. Santiago ◽

H. C. Champion ◽

P. J. Kadowitz

Keyword(s):

Nitric Oxide ◽

Adrenergic Receptors ◽

Adrenergic Receptor ◽

Time Course ◽

Phosphodiesterase Inhibitor ◽

Flow Conditions ◽

Tetraethylammonium Chloride ◽

Beta Adrenergic ◽

Vasodilator Activity ◽

Oxide Synthase

Responses to T-kinin, a peptide formed from the acute-phase substrate T-kininogen, were investigated in the hindlimb vascular bed of the cat. Under constant-flow conditions, injections of T-kinin into the perfusion circuit in doses of 0.03-1 nmol induced rapid dose-related decreases in perfusion pressure. Responses to T-kinin were similar in time course and magnitude to responses to bradykinin and kallidin and were inhibited by the kinin B2-receptor antagonist, Hoe-140. Responses to T-kinin were attenuated by an inhibitor of nitric oxide synthase and by tetraethylammonium chloride and were enhanced in duration by the guanosine 3',5'-cyclic monophosphate (cGMP) phosphodiesterase inhibitor zaprinast. Responses to T-kinin were not altered by inhibitors of K+(ATP) channels, by the cyclooxygenase pathway, or by muscarinic or beta-adrenergic-receptor antagonists. These data suggest that vasodilator responses to T-kinin are mediated by kinin B2-receptor-stimulated release of nitric oxide from the endothelium and increased smooth muscle cGMP levels. These results indicate that activation of K+(ATP) channels and muscarinic or beta-adrenergic receptors and the release of vasodilator prostaglandins are not involved in mediating the response to T-kinin in the hindlimb circulation of the cat.

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The Effect in Man of (+)-Propranolol and Racemic Propranolol on Renin Secretion Stimulated by Orthostatic Stress

Clinical Science ◽

10.1042/cs0440291 ◽

1973 ◽

Vol 44 (3) ◽

pp. 291-295 ◽

Cited By ~ 12

Author(s):

J. A. Tobert ◽

J. D. H. Slater ◽

F. Fogelman ◽

S. L. Lightman ◽

A. B. Kurtz ◽

...

Keyword(s):

Plasma Renin Activity ◽

Adrenergic Receptors ◽

Time Course ◽

Plasma Renin ◽

Normal Subjects ◽

Renin Secretion ◽

Renin Activity ◽

Orthostatic Stress ◽

Beta Adrenergic Receptors ◽

Beta Adrenergic

1. The time-course of the rise in plasma renin activity (PRA) in response to an acute postural stimulus was demonstrated in four normal subjects over 90 min. 2. The ability of racemic propranolol to inhibit this rise was confirmed. 3. This inhibition is shown to be due to antagonism of beta-adrenergic receptors rather than to the membrane-stabilizing properties of racemic propranolol.

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