Different types of relationship between β-adrenergic relaxation and activation of cyclic AMP-dependent protein kinase in canine saphenous and portal veins

doi:10.1016/0014-2999(86)90765-X

European Journal of Pharmacology

Volume 128, Issue 3, 9 September 1986, Pages 187-194

https://doi.org/10.1016/0014-2999(86)90765-X Get rights and content

Abstract

We examined the relationships between the relaxation mediated by β-adrenoceptor and either the associated cyclic AMP production or the activation of cyclic AMP-dependent protein kinase (A-PK) in canine saphenous and portal veins. In the saphenous vein constricted with methoxamine, isoproterenol caused concentration-dependent relaxation (maximum relaxation 92.7%), and concomitant increases in cyclic AMP and A-PK activity ratio from (52.8 to 73.5%). The portal vein was only slightly relaxed by isoproterenol (14.7% in the longitudinal strips) after constriction with methoxamine, while cyclic AMP and A-PK activation increased significantly. Isoproterenol markedly activated A-PK of the portal vein after KCl construction (from 52.6 to 74.6%) but the maximum relaxation was only slight (13.3%). The portal vein also showed a smaller relaxation response to either forskolin or dibutyryl cyclic AMP than the saphenous vein. These results indicated that the relationship between the relaxation response to isoproterenol and either cyclic AMP production or A-PK activation was different in the saphenous and portal veins.

References (33)

J.D. Corbin et al.
Regulation of adenosine 3′,5′-monophosphate-dependent protein kinase. Preliminary characterization of the adipose tissue enzyme in crude extracts
J. Biol. Chem.
(1973)
J.S. Hayes et al.
Selective activation on particulate cAMP-dependent protein kinase by isoproterenol and prostaglandin E₁
J. Biol. Chem.
(1980)
M. Honma et al.
An ultrasensitive method for the simultaneous determination of cyclic AMP and small volume samples from blood and tissue
Biochem. Med.
(1977)
N. Ishikawa et al.
Possible embryogenetical differences of the dog venous system in sensitivity to vasoactive substances
Jap. J. Pharmacol.
(1980)
K.D. Meisheri et al.
Effect of extracellular Na on isoproterenol-induced cAMP levels in depolarized uterus
European J. Pharmacol.
(1978)
A.P. Shepherd et al.
The role of cyclic AMP in mesenteric vasodilation
Microvasc. Res.
(1973)
T. Shigei et al.
Functional venous characteristics in relation to embryology
R. Andersson
Role of cyclic AMP and Ca²⁺ in mechanical and metabolic events in isometrically contracting smooth muscle
Acta Physiol. Scand.
(1973)
G.A. Collins et al.
Quantitative aspects of cyclic AMP and relaxation in the rabbit anterior mesenteric portal vein
Can. J. Physiol. Pharmacol.
(1975)
E.W. Dunham et al.
Alteration of vein cyclic 3′ :5′ nucleotide concentrations during changes in contractility

T. Furuta et al.

A regional difference in the responses of the canine venous system to vasorelaxants

Jap. J. Pharmacol.

(1984)

I.M. Glynn et al.

A simple method for the preparation of ³²P-labelled adenosine triphosphate of high specific activity

Biochem. J.

(1964)

F. Honda et al.

Effect of isoprenaline and phenylephrine on the adenosine 3′,5′-monophosphate content and mechanical activity of cold-stored and fresh taenia caecum from the guinea-pig

Br. J. Pharmacol.

(1977)

T. Itoh et al.

Mechanisms of relaxation induced by activation of β-adrenoceptors in smooth muscle cells of the guinea-pig mesenteric artery

J. Physiol.

(1982)

A.W. Jones et al.

cAMP-dependent reduction in membrane fluxes during relaxation of arterial smooth muscle

Am. J. Physiol.

(1984)

G.L. Kramer et al.

Cyclic nucleotides and blood vessel contraction

Cited by (9)

Protein kinase A increases electrical stimulation-induced neuronal nitric oxide release in rat mesenteric artery
2004, European Journal of Pharmacology
The aim of this study was to analyse the possible influence of cyclic AMP–protein kinase A (cAMP–PKA) activation on neuronal nitric oxide (NO) release induced by electrical field stimulation in mesenteric arteries from Wistar Kyoto (WKY) rats. Western blot experiments demonstrated the expression of neuronal NO synthase (nNOS) in mesenteric artery from WKY rats; however, electrical field stimulation alone did not induce detectable NO release. Preincubation with forskolin allowed NO release induced by electrical field stimulation, which was abolished by: the neuronal toxine tetrodotoxin, the nNOS inhibitors 7-nitroindazole or N^ω-propil-l-arginine (NPLA), and the PKA inhibitors N-(2-(p-Bromocinnamylamino) ethyl 5-isoquinolinesulfonamide hydrochloride (H-89) or (9R,10S,12S)-2,3,9,10,11, 12-Hexahydro-10-9-methyl-1-oxo-9,12-epoxy-1H-diindolo(1,2,3-fg:3,2,1k)pyrrolo(3,4-l)(1,6) benzodiazocine-10-carboxylic acid hexyl ester (KT-5720). Preincubation with prostacyclin also allowed the NO release induced by electrical field stimulation which was significantly decreased by: the neuronal toxine tetrodotoxin, the nNOS inhibitors 7-nitroindazole or NPLA, and the PKA inhibitors H-89 or KT-5720. The NOS inhibitor N^ω-nitro-l-arginine methyl ester (l-NAME) did not modify the vasoconstrictor response induced by electrical field stimulation. However, in the presence of forskolin or prostacyclin, l-NAME increased the vasoconstrictor response to electrical field stimulation. These results indicate that forskolin and prostacyclin allow neuronal NO release induced by electrical field stimulation through a mechanism involving cAMP–PKA activation in rat mesenteric arteries.
Effects of SQ 22536, an adenylyl cyclase inhibitor, on isoproterenol-induced cyclic AMP elevation and relaxation in newborn ovine pulmonary veins
2002, European Journal of Pharmacology
The effects of inhibition of adenylyl cyclase on isoproterenol-induced relaxation were determined in isolated pulmonary veins of newborn lambs (7–12 days old). In veins constricted with endothelin-1, isoproterenol at concentrations ≤3×10⁻⁹ M had no effect on the cyclic AMP (cAMP) content but caused up to 56% relaxation. At higher concentrations (≥10⁻⁸ M), isoproterenol elevated cAMP content and caused further relaxation. In veins constricted with endothelin-1 or U46619 (9,11-dideoxy-11, 9-epoxymethanoprostaglandin prostaglandin F2α), the cAMP elevation but not relaxation caused by isoproterenol was abolished by SQ 22536 [9-(tetrahydro-2-furanyl)-9H-purin-6-amine; an adenylyl cyclase inhibitor]. The effects of isoproterenol on vessel tension and cAMP content were inhibited by propranolol. Rp-8-CPT-cAMPS [8-(4-Chlorophenylthio)-adenosine-3′,5′-cyclic monophosphorothioate, Rp-isomer] and Rp-8-Br-PET-cGMPS [β-phenyl-1, N²-etheno-8-bromoguanosine-3′,5′-cyclic monophosphorothioate, Rp-isomer], inhibitors of cAMP- and guanosine-3′,5′-cyclic monophosphate (cGMP)-dependent protein kinases, respectively, attenuated relaxation caused by a cAMP analog but not that by isoproterenol. In the crude membrane preparations of pulmonary veins, an increase in the activity of adenylyl cyclase caused by isoproterenol was abolished by propranolol and SQ 22536. These results suggest that cAMP may not play a critical role in isoproterenol-induced relaxation of pulmonary veins of newborn lambs.
Relaxation response of isolated canine veins to agents that act on the adenylate cyclase-cyclic AMP system: further investigation
1990, European Journal of Pharmacology
The present study was undertaken to clarify whether there is a deficiency in the relaxation mediated by the adenylate cyclase-cyclic AMP (cAMP) system in the portal vein as compared to the saphenous vein. Longitudinal strips of the portal vein and helical preparations of the saphenous vein were used. The relaxation response to various agents was examined under conditions such that the venous preparations were previously contracted by methoxamine in equipotent concentrations (EC₈₀), i.e., 10⁻⁶ M for portal vein and 10⁻⁵ M for saphenous vein. The saphenous vein relaxed fully in response to isoproterenol but the portal vein relaxed only to 29% of the maximum relaxation induced by papaverine 10⁻⁴ M. However, dibutyryl cAMP and 8-bromo-cAMP, membrane permeable derivatives of cAMP, 3-isobutyl-1-methylxanthine and papaverine, phosphodiesterase inhibitors, and forskolin, a direct stimulator of adenylate cyclase, relaxed portal and saphenous veins similarly though with quantitative differences. The results suggest that there is no profound deficiency in the adenylate cyclase-cAMP system but there may be a deficiency in the coupling between surface β-adrenoceptors and adenylate cyclase or there may be a low density of β-adrenoceptors in the portal vein.
Cyclic AMP and mechanisms of vasolidation
1990, Pharmacology and Therapeutics
Cyclic AMP and the mechanism of vasodilation have been reviewed by first discussing the enzymes involved (adenyl cyclase, cyclic nucleotide phosphodiesterases, cyclic AMP-dependent protein kinase) and then agents that increase cAMP in smooth muscle. Two mechanisms of vasodilation are described: (i) effects on contractile proteins; (ii) effects on Ca²⁺ levels. Evidence for compartments of cAMP is also presented.
Studies on the mechanism of 5‐HT<inf>1</inf> receptor‐induced smooth muscle contraction in dog saphenous vein
1992, British Journal of Pharmacology
The mesenteric-portal vein in research
1990, Pharmacological Reviews

View all citing articles on Scopus

View full text

Different types of relationship between β-adrenergic relaxation and activation of cyclic AMP-dependent protein kinase in canine saphenous and portal veins

Abstract

J. Biol. Chem.

J. Biol. Chem.

Biochem. Med.

Jap. J. Pharmacol.

European J. Pharmacol.

Microvasc. Res.

Role of cyclic AMP and Ca2+ in mechanical and metabolic events in isometrically contracting smooth muscle

Acta Physiol. Scand.

Quantitative aspects of cyclic AMP and relaxation in the rabbit anterior mesenteric portal vein

Can. J. Physiol. Pharmacol.

Alteration of vein cyclic 3′ :5′ nucleotide concentrations during changes in contractility

A regional difference in the responses of the canine venous system to vasorelaxants

Jap. J. Pharmacol.

A simple method for the preparation of 32P-labelled adenosine triphosphate of high specific activity

Biochem. J.

Effect of isoprenaline and phenylephrine on the adenosine 3′,5′-monophosphate content and mechanical activity of cold-stored and fresh taenia caecum from the guinea-pig

Br. J. Pharmacol.

Mechanisms of relaxation induced by activation of β-adrenoceptors in smooth muscle cells of the guinea-pig mesenteric artery

J. Physiol.

cAMP-dependent reduction in membrane fluxes during relaxation of arterial smooth muscle

Am. J. Physiol.

Cyclic nucleotides and blood vessel contraction

Role of cyclic AMP and Ca²⁺ in mechanical and metabolic events in isometrically contracting smooth muscle

A simple method for the preparation of ³²P-labelled adenosine triphosphate of high specific activity