Cyclic adenosine 3′, 5′ monophosphate levels in rat myometrium under the influence of epinephrine, prostaglandins and oxytocin. Correlations with uterus motility

Harbon, Simone; Clauser, Hubert

doi:10.1016/s0006-291x(71)80255-3

Cited by 73 publications

(20 citation statements)

References 6 publications

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“…In other systems, angiotensin-II was reported to decrease cAMP levels, but only when elevated by cAMP agonists (46,47). Angiotensin-II was also reported to bind (48,49) on isolated glomeruli and to cause glomerular contraction (48); the latter effect was also observed in our laboratory.2 Relation of the effects of angiotensin-II on cAMP to the above mentioned phenomena (48,49), or to its effects on single nephron dynamics in vivo (1,3,4), remains to be established.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Cyclic Nucleotides in Isolated Rat Glomeruli

et al. 1978

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A B S T R A C T Because glomerular functions are modulated by numerous humoral agents, probably acting through cyclic nucleotides, the effects of some polypeptide hormones and biogenic amines on cyclic AMP (cAMP) and cyclic 3',5'-guanosine monophosphate (cGMP) were studied in glomeruli isolated from rat renal cortex. Glomeruli and cortical tubules were prepared by a combination of sieving and density-gradient centrifugation. Under basal conditions, the contents of cAMP and cGMP in glomeruli were significantly higher than in tubules and unfractionated renal cortical tissue.Histamine caused a striking increase in cAMP in glomeruli (+A% 675±87) and, to a lesser degree, increased cAMP in tubules (+A% 103+25) or in tissue slices. This stimulation was dose-dependent in the range of 1 ,uM-1 mM histamine. Metiamide (an H2-antagonist), but not pyrilamine (an H,-antagonist) blocked the effect of histamine on cAMP, which indicates that histamine causes its effect via interaction with H2 receptors. Histamine caused less extensive increases in cGMP in both glomeruli and tubules. Carbamylcholine caused a marked increase in cGMP in glomeruli (+A 295±7) and a much lower increase in tubules (+A% 70+20); these effects were blocked by 1334atropine. Parathyroid hormone (1 ug/ml) increased cAMP and, to a much lesser degree, also cGMP in glomeruli. In tubules, parathyroid hormone caused nmuch more extensive increases in cAMP than in glomeruli; no changes, or rather a small decline in cGMP, was observed. Angiotensin-I1 (2 uM) markedly lowered cAMP in glomeruli (-A% -45±8) and in tubules (-A% 33±7) but had no effect on cGMP. Bradykinin (20 ,M) did not consistently influience either cAMP or cGMP in glomeruli or tubules.Present results demonstrate that cAMP and cGMP metabolism in glomeruli are controlled independently by humoral agents known to alter glomerular functions in vivo. Our findings are consistent with the view that histamine and cholinergic agents generated and (or) released locally in glomeruli or in their vicinity may play important roles as mediators of immunopathological injury of glomeruli, and that these effects are mediatecl by cAMP and (or) cGMP through interaction with H2 receptors and muscarinic receptors. Likewise, our results suggest that the effects of angiotensin-II and parathyroid hormone on glomerular dynamics may be mediated by cyclic nucleotides.Thus, we surmise that extrarenal as well as intrarenal humoral agents may play an important role in the pathology and physiology of glomeruli through mediation of either cAMP, cGMP, or both. INTRODUCTIONIt has become increasingly evident in recent years that many extrarenal and intrarenal humoral agents mraymodulate diverse aspects of glomerular function (1). For example, the administration of agents such as para- thyroid hormone (PTH)' (2), angiotensin (3, 4), bradykinin, acetylcholine (5,6), and others (1) causes changes in glomerular microcirculation, hydraulic permeability, or in the ultrafiltration properties of glomerular membrane. Perhaps more importantly,...

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Section: Discussionmentioning

confidence: 99%

Modulation of Cyclic Nucleotides in Isolated Rat Glomeruli

et al. 1978

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“…In the one available report of in vitro studies, PG E1 and E2 caused an increase in uterine adenylate cyclase activity, while PGF2a was inactive (7).…”

Section: Methodsmentioning

confidence: 95%

“…It was further demonstrated that contractions produced by oxytocin, acetylcholine, and calcium were inhibited by fl-adrenergic effectors, theophylline, and dibutyryl-cAMP (3,4) in association with an increase in adenylate cyclase activity (5)(6)(7). Prostaglandins, particularly those of the E series, are potent stimulators of uterine contraction despite the fact that they stimulate uterine adenylate cyclase activity (7,8).…”

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confidence: 99%

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Bhalla

Sanborn

Korenman

1972

Proc. Natl. Acad. Sci. U.S.A.

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Interactions of hormones stimulating and inhibiting uterine contraction were studied in vitro in uteri from oophorectomized rats. The ,3-adrenergic effector, isoproterenol, a potent inhibitor of contraction, produced a dose-related increase of adenylate cyclase and accumulation of adenosine 3' :5'-cyclic monophosphate (cAMP) that was inhibitable by propranolol. Oxytocin, which stimulates contraction, effectively inhibited accumulation of uterine cAMP induced by isoproterenol in the presence or absence of theophylline. Prostaglandins E2 and F2a, each at a maximum effective concentration of 0.5 AMM, also inhibited accumulation of cAMP induced by isoproterenol, consistent with their effect in stimulation of uterine contraction. Prostaglandin E2, but not prostaglandin F2a, stimulated cAMP accumulation in a dose-related manner at concentrations in excess of 0.5 MM. Neither propranolol nor oxytocin inhibited that response. Bovine endometrial adenylate cyclase failed to respond to isoproterenol but was stimulated by prostaglandins El and E2. When myometrial preparations were studied, isoproterenol stimulation and prostaglandin effects were observed as for whole castrate uterus. The competitive physiological actions of ,B-adrenergic effectors on the one hand, and oxytocin and prostaglandins on the other hand, are based on their influences on a myometrial adenylate cyclase. Stimulation of uterine cAMP accumulation by prostaglandin Ea is due to action at a different and unrelated site.Uterine tissue is designed to respond specifically to hormonal influences in order to provide the appropriate environment for implantation, fetal growth and development, and parturition. It appears to be ideal for study of the relationship between steroid-mediated and cAMP-mediated responses. Recently, it was shown that smooth muscle, particularly uterus, has an adenylate cyclase system whose activation by ,B-adrenergic effectors resulted in inhibition of contractility (1-4). It was further demonstrated that contractions produced by oxytocin, acetylcholine, and calcium were inhibited by fl-adrenergic effectors, theophylline, and dibutyryl-cAMP (3, 4) in association with an increase in adenylate cyclase activity (5-7). Prostaglandins, particularly those of the E series, are potent stimulators of uterine contraction despite the fact that they stimulate uterine adenylate cyclase activity (7,8).In these studies, we show that the stimulatory effects of oxytocin and prostaglandins E2

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“…Other workers have found, under various cir cumstances, that relaxation could occur without any increase in c-AMP; e.g., in Ca++-deficient solutions [Andersson et al, 1972], with papaverine [Triner et al, 1970;, etc. Furthermore, prostaglandin E2 increases c-AMP in rat myometrium associated with contraction [Bhalla et al, 1972;H arbon and Clausen, 1971; Vesin and Harbon, 1974], and angiotensin contracts myometrium despite elevated c-AMP levels [Angles d'AuRiAC and M eyer, 1972].…”

Section: Introductionmentioning

confidence: 99%

Relation of c-AMP to Relaxation of Pulmonary Artery

Daniel¹,

Crankshaw²

1974

J Vasc Res

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We tested the hypothesis that an increase in c-AMP was necessary or sufficient for relaxation of rabbit pulmonary artery. Isoproterenol (INA) partially relaxed serotonin (5-HT) induced contractions. Theophylline (TH) alone relaxed contraction more effectively, but after TH, INA produced no greater relaxation. At the height of relaxation (2 min), c-AMP was not increased, but after 5 min the c-AMP was decreased and the artery was recontracted. c-AMP was increased after TH, and more when INA was given after TH. Noradrenaline contracted the arteries and increased c-AMP; both effects were prevented by phentolamine. A series of other relaxants (papaverine, nitroglycerine, D600, Ro-7-2956, diazoxide and dipyridamole) also failed to produce relaxations directly related to c-AMP levels. We concluded that c-AMP increase was not necessary or sufficient for relaxation in artery, and that in pulmonary artery phosphodiesterase activity played an important role in determining tissue levels of c-AMP.

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Cyclic adenosine 3′, 5′ monophosphate levels in rat myometrium under the influence of epinephrine, prostaglandins and oxytocin. Correlations with uterus motility

Cited by 73 publications

References 6 publications

Modulation of Cyclic Nucleotides in Isolated Rat Glomeruli

Modulation of Cyclic Nucleotides in Isolated Rat Glomeruli

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Relation of c-AMP to Relaxation of Pulmonary Artery

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