POTENTIATION OF BETA-ADRENERGIC UTERINE RELAXATION WITH ALPHA-ADRENOCEPTOR BLOCKING DRUGS

Abstracts ◽  
1977 ◽  
pp. 314
Author(s):  
V. Saano ◽  
M.M. Airaksinen
Keyword(s):  
Beta Adrenergic ◽  
Alpha Adrenoceptor ◽  
Uterine Relaxation

Effects of beta-adrenergic agonists on splanchnic vascular volume and cardiac output

1991 ◽  
Vol 261 (5) ◽  
pp. H1499-H1507 ◽  
Author(s):  
P. I. Chang ◽  
D. L. Rutlen
Keyword(s):  
Cardiac Output ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Splenic Volume ◽  
Alpha Adrenoceptor ◽  
Beta Adrenergic Agonists ◽  
Anesthetized Dogs ◽  
Beta 2 ◽  
Beta Adrenergic Agonist ◽  
Adrenergic Effects

The effect of beta-adrenergic agonists on splanchnic intravascular volume (SIV), measured with radionuclide imaging, and the subsequent influence of such volume changes on cardiac output (CO) were examined in 40 anesthetized dogs. Isoproterenol (6 micrograms/min) caused a decrease in total SIV of 12 +/- 1% (P less than 0.001). The decrease was due entirely to a decrease in splenic volume of 24 +/- 3% (P less than 0.001), since volume increased in the remainder of the splanchnic vasculature [hepatic and mesenteric volume increased 12 +/- 2% (P less than 0.001) and 11 +/- 3% (P less than 0.02), respectively]. CO increased from 1,724 +/- 187 to 3,138 +/- 321 ml/min (P less than 0.001); after subsequent splenectomy, isoproterenol caused a similar increment. Isoproterenol-associated SIV changes were not altered by carotid denervation and vagotomy or by beta 1-adrenergic inhibition with metoprolol but were abolished by nonselective beta-adrenergic inhibition with propranolol. With a larger dose of metoprolol and smaller dose of isoproterenol to minimize beta 1-adrenergic effects, the isoproterenol-associated CO increment was attenuated (P less than 0.01) by splenectomy. With the beta 2-agonist terbutaline (41 micrograms/min) after metoprolol, total SIV decreased 15 +/- 4% (P less than 0.001). After subsequent alpha-adrenergic inhibition with phenoxybenzamine, terbutaline caused no change in SIV and an attenuated (P less than 0.05) increase in CO. Thus beta-adrenergic agonist administration causes a decrease in total SIV due entirely to a decrease in splenic volume. The SIV decrement is dependent on beta 2- and alpha-adrenoceptor stimulation and appears to enhance CO only if beta 1-adrenergic effects are minimized.

Adrenergic receptor-mediated regulation of cultured rabbit airway smooth muscle cell proliferation

1994 ◽  
Vol 267 (3) ◽  
pp. L291-L299 ◽  
Author(s):  
J. P. Noveral ◽  
M. M. Grunstein
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Adenylate Cyclase ◽  
Cell Count ◽  
Airway Smooth Muscle ◽  
Adrenergic Receptors ◽  
Camp Accumulation ◽  
Beta Adrenergic ◽  
Alpha Adrenoceptor ◽  
Dose Dependent

To evaluate the potential role of adrenergic receptors in regulating airway smooth muscle (ASM) cell proliferation, the mitogenic effects and mechanisms of action of selective alpha- and beta-adrenoceptor activation were investigated in cultured rabbit ASM cells. The alpha 1-adrenoceptor agonists, phenylephrine and methoxamine, elicited significant dose-dependent (10(-10)-10(-4) M) stimulation of ASM cell mitogenesis, with mean +/- SE peak increases in ASM cell count amounting to 17.0 +/- 3.5 and 44.0 +/- 6.8% above unstimulated (control) levels, respectively. Similarly, the alpha 2-adrenoceptor agonist clonidine (10(-8)-10(-4)) also induced ASM cell proliferation, with a 41.1 +/- 5.5% peak increase in cell count above control. The promitogenic responses to alpha-adrenoceptor activation were blocked by pertussis toxin (PT; 100 ng/ml), which ADP-ribosylates G protein negatively coupled to adenylate cyclase activation. In additional studies, we found that 1) treatment with agents inducing intracellular adenosine 3',5'-cyclic monophosphate (cAMP) accumulation including the beta-adrenergic agonist, isoproterenol, the cAMP analogue, 8-(4-chlorophenylthio)-cAMP and forskolin, all produced significant dose-dependent inhibition of serum-stimulated ASM cell growth; 2) alpha-adrenoceptor activation inhibited isoproterenol-induced cAMP accumulation; and 3) the anti-proliferative effects of isoproterenol and PT were additive. Collectively, the above findings provide new evidence that adrenergic receptors exert an opposing duality of action in regulating ASM cell proliferation, wherein receptors which are negatively coupled (i.e., alpha-adrenergic) and those which are positively coupled (i.e., beta-adrenergic) to activation of the adenylate cyclase/cAMP signal-transduction pathway are promitogenic and growth inhibitory to ASM cells, respectively.

Relaxation of bovine mesenteric lymphatics in response to transmural stimulation

1981 ◽  
Vol 240 (4) ◽  
pp. H498-H504
Author(s):  
T. Ohhashi ◽  
I. C. Roddie
Keyword(s):  
Short Duration ◽  
Sympathetic Nerves ◽  
Beta Adrenergic ◽  
Transmural Stimulation ◽  
Alpha Adrenoceptor ◽  
Basal Tone ◽  
Spontaneous Contractions ◽  
Short Type

The responses of isolated quiescent segments of bovine mesenteric lymphatics to 10-s trains of pulses (50 V for 0.3 ms at 2 Hz) administered transmurally have been studied using various drugs. Each train of pulses consistently produced a brief contraction that was completely blocked by tetrodotoxin, alpha-adrenoceptor antagonists, bretylium, and guanethidine. Cocaine potentiated the contractions. Tyramine caused an increase in the basal tone, some spontaneous contractions, and an inhibition of contraction. The contraction was sometimes followed by a relaxation that could be of short duration or long lasting. Both types of relaxation were abolished by tetrodotoxin. Propranolol reduced both types of relaxation, causing more suppression of the short type. Bretylium completely blocked the short type of relaxation and slightly reduced the long-lasting type. Hexamethonium and atropine had no effect on any of the responses. These findings suggest that the contraction resulting from transmural stimulation is due to the action of excitatory postganglionic sympathetic nerves. It is concluded that both types of relaxation occur mainly in response to beta-adrenergic inhibitory stimulation. The possibility of nonadrenergic inhibitory innervation in bovine mesenteric lymphatics is also discussed.

CATECHOLAMINE ANTAGONISM TO OXYTOCIN-INDUCED MILK-EJECTION

1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr
Keyword(s):  
Receptor Blockade ◽  
Milk Ejection ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Alpha Receptors ◽  
Adrenergic Blockers ◽  
Beta Receptor Blockade ◽  
Second Pain ◽  
Stimulation Of

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.

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