Relaxation of hormonally stimulated smooth muscular tissues by the 8-bromo derivative of cyclic GMP

Schultz, Karin; Böhme, Eycke; Kreye, V. A. W.; Schultz, Günter

doi:10.1007/bf00515586

Cited by 75 publications

(25 citation statements)

References 34 publications

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“…The 8-bromo derivative of cyclic GMP has been shown to relax noradrenaline-induced contractions of rat and rabbit aorta (Schultz et al, 1979) and an increased tissue content of cyclic GMP has also been correlated with endothelial dependent relaxant responses of rabbit and rat aorta and beef coronary arteries (Holzmann, 1982;Diamond & Chu, 1983;Rapoport & Murad, 1983). However, the maximal increase in cyclic GMP levels associated with acetylcholine mediated relaxations of pre-contracted rat and rabbit aorta and beef coronary artery (about 10 to 30 fold) was far in excess of that induced by B-HT 920.…”

Section: Discussionmentioning

confidence: 99%

Endothelial mediated inhibition of contraction and increase in cyclic GMP levels evoked by the α‐adrenoceptor agonist B‐HT 920 in rat isolated aorta

Miller

Mony

Schini

et al. 1984

British J Pharmacology

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1In the presence of endothelium maximal contractions of rat aorta preparations evoked by B-HT 920 were about 10% of those evoked in the absence of endothelium.2 6-Allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-(4,5-d)azepin dihydrochloride (B-HT 920, 0.1 jLM to 0.1 mM) induced concentration-dependent contractions of rat aorta in the absence of endothelium. Maximal contractions were comparable in magnitude to those induced by noradrenaline.3 In the presence of endothelium but not in its absence B-HT 920 (0.1 mM) stimulated an increase in tissue cyclic GMP levels of about 2 fold. Levels of cyclic AMP were unaffected. Removal of endothelium reduced basal tissue levels of cyclic GMP.4 The guanylate cyclase inhibitor methylene blue (0.5 pM) potentiated B-HT 920-induced contractions in the presence of endothelium and inhibited increases in cyclic GMP. 5 In the presence of endothelium 5,8,11,14-eicosatetraynoic acid (ETYA; 0.1 mM), an inhibitor of both lipoxygenase and cyclo-oxygenase systems, inhibited the B-HT 920-induced increase in cyclic GMP but did not potentiate B-HT 920-induced contractions. ETYA also antagonized B-HT 920-induced contractions in the absence of endothelium. 6 It is concluded that endothelium continuously releases a product or products which influence the smooth muscle. Inhibition of B-HT920-induced contractions in the presence of endothelium is associated with increased tissue levels of cyclic GMP.

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Section: Discussionmentioning

confidence: 99%

Endothelial mediated inhibition of contraction and increase in cyclic GMP levels evoked by the α‐adrenoceptor agonist B‐HT 920 in rat isolated aorta

Miller

Mony

Schini

et al. 1984

British J Pharmacology

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“…Increased levels of cyclic AMP have also been shown to be involved in the mediation of the actions of catecholamines on vertebrate muscle, including smooth muscle (Janis & Diamond, 1979;Schultz, Bohme, Kneye & Schultz, 1979), cardiac muscle (Reuter, 1974;Morad, Sanders & Weiss, 1981) and skeletal muscle (Bowman & Nott, 1974;Gonzalez-Serratos, Hill & Valle-Aguilera, 1981). The exact responses of vertebrate skeletal muscle, however, vary with the proportion of fast and slow muscle fibres in the muscle (see Bowman & Zaimis, 1958;Bowman & Nott, 1969;Bowman, 1982).…”

Section: Time Coursementioning

confidence: 99%

“…The exact responses of vertebrate skeletal muscle, however, vary with the proportion of fast and slow muscle fibres in the muscle (see Bowman & Zaimis, 1958;Bowman & Nott, 1969;Bowman, 1982). Furthermore, the actual mechanisms linking the increased levels of cyclic AMP to the observed physiological responses are still largely a matter of speculation (see Janis & Diamond, 1979;Schultz et al 1979;Bowman, 1982). This further suggests that all agents shown to mimic the physiological responses of biogenic amines on muscle should also be shown to mimic the biochemical responses.…”

Section: Time Coursementioning

confidence: 99%

A modulatory octopaminergic neurone increases cyclic nucleotide levels in locust skeletal muscle.

Evans¹

1984

The Journal of Physiology

100

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SUMMARY 1. Octopamine increases the level of cyclic AMP in a dose-dependent way in the locust extensor tibiae neuromuscular preparation. The response peaks after a 10 min exposure and then declines to a plateau. The effect of octopamine is potentiated in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). The levels of cyclic GMP in the muscle were not affected by octopamine.2. The response is stereospecific for the naturally occurring D(-) isomer of octopamine and is also specific for monophenolic biogenic amines. Studies with a range of synthetic agonists and antagonists reveal that the receptors mediating the response are of the OCTOPAMINE2 class.3. Forskolin, a diterpene activator of adenylate cyclase activity, increases cyclic AMP but not cyclic GMP levels in the extensor muscle. The response has a prolonged time course and is again potentiated by IBMX.4. Stimulation of the octopaminergic neurone to the extensor muscle increases the levels of cyclic AMP but not those of cyclic GMP. The response is blocked by phentolamine, an a-adrenergic blocking agent that also blocks the effects ofoctopamine in this preparation.5. The results are discussed in terms of the parallels between the biochemical and physiological effects of octopamine on this muscle and in terms of the mode of action of the octopamine receptors present.

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“…Increased levels of cyclic GMP have been observed in response to sodium nitroprusside in various tissues including smooth muscle preparations (1)(2)(3)(4). Cyclic GMP analogues have also been shown to cause relaxation or decreased contraction in smooth muscle (1,(5)(6)(7). Furthermore, agents that inhibit nitroprusside activation of guanylate cyclase in broken cell preparations have been shown to inhibit relaxation as well as nitroprusside-induced increased levels of cyclic GMP (6)(7)(8)(9).…”

mentioning

confidence: 99%

Sodium nitroprusside-induced protein phosphorylation in intact rat aorta is mimicked by 8-bromo cyclic GMP

Rapoport

Draznin

Murad

1982

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

105

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The effects of sodium nitroprusside, 8-bromo cyclic GMP, 8-bromoguanosine 5'-monophosphate, 8-bromo cyclic AMP, dibutyryl cyclic AMP, and isoproterenol on incorporation of 32P into proteins in intact rat thoracic aorta were studied. Aortas were incubated in [32P]orthophosphate in order to label endogenous adenosine triphosphate. Agents were then added for various times and the tissues were homogenized and fractionated (100,000 x g for 60 min) into soluble and particulate fractions. Soluble and particulate fractions were subjected to isoelectric focusing followed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and autoradiographs were made. Nitroprusside induced a concentration-dependent increase in incorporation of 32p into nine proteins and a decrease in 32P incorporation into two proteins. Some of these proteins appeared in both the soluble and particulate fractions of homogenates; others appeared only in the soluble fraction. The pattern of 32p incorporation was identical after 2-or 15-min exposure to nitroprusside and was mimicked by exposure to 50-500 p.M 8-bromo cyclic GMP. 8-Bromoguanosine 5'-monophosphate did not alter 32p incorporation. Dibutyryl cyclic AMP at 50 jaM had no effect upon 32p incorporation whereas a higher concentration (0.5 mM) caused increased or decreased 32P incorporation into some, but not all, of the same proteins. 8-Bromo cyclic AMP (5 mM) produced only small changes in 32P incorporation. The pattern of 32P incorporation induced by a relatively high concentration of isoproterenol 0.1 mM was similar but not identical to that seen with 0.5 mM dibutyryl cyclic AMP. The present study indicates that the incorporation of 32p into endogenous proteins of intact rat aorta can be regulated by nitroprusside. These effects can be mimicked by cyclic GMP analogues and only partially by cyclic AMP analogues or isoproterenol. Presumably, these effects of nitroprusside are mediated through a cyclic GMP-dependent process (protein kinase or phosphatase) which may play a role in the relaxant properties of nitroprusside and cyclic GMP.The present study investigates the hypothesis that smooth muscle relaxation induced by sodium nitroprusside may be mediated by cyclic GMP-dependent phosphorylation of endogenous proteins. Increased levels of cyclic GMP have been observed in response to sodium nitroprusside in various tissues including smooth muscle preparations (1-4). Cyclic GMP analogues have also been shown to cause relaxation or decreased contraction in smooth muscle (1, 5-7). Furthermore, agents that inhibit nitroprusside activation of guanylate cyclase in broken cell preparations have been shown to inhibit relaxation as well as nitroprusside-induced increased levels of cyclic GMP (6-9).However, the molecular mechanism by which nitroprusside and cyclic GMP induce relaxation is not known. Protein phosphorylation is thought to be a final common pathway for many biological processes (10). The addition of cyclic GMP to crude particulate fractions ofvarious smooth muscle preparations s...

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Relaxation of hormonally stimulated smooth muscular tissues by the 8-bromo derivative of cyclic GMP

Cited by 75 publications

References 34 publications

Endothelial mediated inhibition of contraction and increase in cyclic GMP levels evoked by the α‐adrenoceptor agonist B‐HT 920 in rat isolated aorta

Endothelial mediated inhibition of contraction and increase in cyclic GMP levels evoked by the α‐adrenoceptor agonist B‐HT 920 in rat isolated aorta

A modulatory octopaminergic neurone increases cyclic nucleotide levels in locust skeletal muscle.

Sodium nitroprusside-induced protein phosphorylation in intact rat aorta is mimicked by 8-bromo cyclic GMP

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