Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Phenylephrine  (6)
  • Rabbit papillary muscle  (5)
  • Adenosine  (3)
  • β-Adrenoceptors  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Phorbol ester does not mimic, but antagonizes the alpha-adrenoceptor-mediated positive inotropic effect in the rabbit papillary muscle (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 169-176 
    Details
    ISSN: 1432-1912
    Keywords: Phorbol ester ; Protein kinase C ; alphaAdrenoceptors ; beta-Adrenoceptors ; Positive inotropic effects ; Phenylephrine ; [3H]prazosin binding ; [3H]CGP-12177 binding ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) was used to examine the hypothesis that phosphoinositide turnover is involved in the regulation of myocardial contractility mediated by stimulation of alpha-adrenoceptors in the mammalian cardiac muscle. Exposure of the isolated rabbit papillary muscle electrically driven at a rate of 1 Hz at a temperature of 37°C to TPA in concentrations of 10–1000 nmol/l for 30 min did not affect the basal force of contraction. The concentration-response curve for the positive inotropic effect of (−)-phenylephrine mediated by stimulation of alpha-adrenoceptors in the presence of (±)-bupranolol (100 nmol/1) was shifted to the right and downward by TPA in concentrations of 30–1000 nmol/l, while the effect of (−)-phenylephrine mediated by stimulation of beta-adrenoceptors in the presence of prazosin (100 nmol/l) was not decreased, but slightly enhanced by exposure of the muscle to relatively low concentrations of TPA (10–100 nmol/l). Incubation of the membrane fraction isolated from the rabbit ventricular muscle with TPA in vitro under the same condition as employed in the physiological experiments decreased the specific binding of [3H]prazosin but not that of [3H]CGP-12177, while the non-tumor promoting phorbol ester, αPDD, was ineffective. These results indicate that activation of protein kinase C by TPA does not mimic the positive inotropic effect of catecholamines mediated by activation of myocardial alpha-adrenoceptors. on the other hand, the specific interaction of alpha-adrenoceptor-mediated processes with TPA in the rabbit papillary muscle is in line with the view that the facilitation of phosphoinositide turnover and subsequent activation of protein kinase C may play a certain role in the coupling of alpha-adrenoceptor occupation by agonists to the process leading to the positive inotropic action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169245
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Pharmacological differentiation of synergistic contribution of L-type Ca2+ channels and Na+/H+ exchange to the positive inotropic effect of phenylephrine, endothelin-3 and angiotensin II in rabbit ventricular myocardium (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1996), S. 87-96 
    Details
    ISSN: 1432-1912
    Keywords: Key words L-type Ca2+ channels ; Na+/H+ exchange ; Phenylephrine ; Endothelin-3 ; Angiotensin II ; Isoprenaline ; Positive inotropic effect ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was designed to delineate pharmacologically the role of sarcolemmal L-type Ca2+ channels and Na+/H+ exchange in the positive inotropic effect (PIE) of phenylephrine mediated by alpha-1 adrenoceptors, endothelin (ET) and angiotensin II (Ang II) that stimulate phosphoinositide (PI) hydrolysis in the rabbit ventricular muscle. The PIE of these receptor agonists was compared with the PIE of isoprenaline that accumulates cyclic AMP. For this purpose, we investigated the influence of a Ca2+ antagonist, verapamil, and of an inhibitor of Na+/H+ exchange, 5-(N-ethyl-N-isopropyl) amiloride (EIPA), alone or in combination, on the cumulative concentration-response curve (CRC) for phenylephrine (with 0.3 μM bupranolol), ET-3 and Ang II in isolated right ventricular papillary muscles of the rabbit, which were electrically stimulated at 1 Hz in Krebs-Henseleit solution at 37°C. Verapamil at 0.3 and 1 μM decreased the basal force of contraction to 37.0 ± 4.0% and 13.2 ± 1.1% of the control, respectively, while EIPA even at 10 μM affected the basal force to much less extent and decreased it to 87.0 ± 1.4%. Verapamil (0.3 and 1 μM) and EIPA (1 and 10 μM), when used alone, each significantly attenuated but did not abolish the PIEs induced by phenylephrine, ET-3 and Ang II, while the simultaneous administration of verapamil (1 μM) and EIPA (10 μM) consistently and almost completely inhibited the PIE induced by these receptor agonists. By contrast, the PIE of isoprenaline was retained even in the presence of verapamil and EIPA. These results indicate that both the influx of Ca2+ ions through L-type Ca2+ channels and activation of Na+/H+ exchange contribute synergistically to the PIE that is mediated by alpha-1 adrenergic, ET and Ang II receptor agonists, while these mechanisms are not essential for the beta-adrenoceptor-mediated PIE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004923
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Potent inhibitory action of chlorethylclonidine on the positive inotropic effect and phosphoinositide hydrolysis mediated via myocardial alpha1-adrenoceptors in the rabbit ventricular myocardium (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 669-673 
    Details
    ISSN: 1432-1912
    Keywords: Chlorethylclonidine ; Alpha1-adrenoceptors ; Positive inotropic effect ; [3H]prazosin binding ; Phosphoinositide hydrolysis ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of the alphalb-adrenoceptor-selective antagonist chlorethylclonidine on the alpha1-adrenergic positive inotropic effect and the phosphoinositide hydrolysis induced by phenylephrine was investigated in the rabbit ventricular myocardium. Pretreatment of membrane fractions derived from the rabbit ventricular muscle with 10−5 mol/l chlorethylclonidine decreased the specific binding of [3H]prazosin (at a saturating concentration of 10−9 mol/l) from the control value of 11.27±0.48 to 4.18±1.87 fmol/mg protein. The inhibition by adrenaline of the binding of [3H]prazosin (slope factor and affinity) was not affected by chlorethylclonidine. The positive inotropic effect of phenylephrine (in the presence of 3 × 10−7 mol/l bupranolol) was inhibited by chlorethylclonidine in a concentration-dependent manner (10−7−10−5 mol/l) and abolished by 10−5 mol/l chlorethylclonidine. The concentration of chlorethylclonidine to inhibit the phenylephrine-induced maximum response to 50% was 2.4 × 10−6 mol/l. The accumulation of [3H]inositol monophosphate and [3H]inositol trisphosphate induced by 10−5 mol/l phenylephrine was inhibited by chlorethylclonidine in the same concentration range. These findings indicate that the myocardial alpha1-adrenoceptors mediating a positive inotropic effect in the rabbit ventricular myocardium may belong to the chlorethylclonidine-sensitive alpha1b-subtype, and that the subcellular mechanism of action involve phosphoinositide hydrolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184301
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Pharmacological characteristics of adenosine-induced inhibition of dog ventricular contractility: dependence on the pre-existing level of β-adrenoceptor activation (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 70-78 
    Details
    ISSN: 1432-1912
    Keywords: Adenosine ; Phenylisopropyladenosine ; Negative inotropic effect ; Cyclic AMP ; Ventricular myocardium of the dog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments were carried out to characterize the adenosine-induced negative inotropic effect in relation to the extent of β-adrenoceptor activation in the isolated dog left ventricular myocardium. Adenosine and R-N6-phenylisopropyladenosine inhibited the positive inotropic effect of isoprenaline (10−7 mol/1 and lower) about 20% of its maximal response, which was antagonized by an A1 adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine in a concentration-dependent manner. The negative inotropic effect of adenosine disappeared and that of R-N6-phenylisopro-pyl-adenosine decreased when the isoprenaline concentration was elevated to the level higher than 10−7 mol/1. Adenosine deaminase (1.5 U/ml) that abolished the negative inotropic effect of adenosine enhanced the effect of R-N6-phenylisopropyladenosine, indicating that endogenous adenosine released by high isoprenaline concentration (10−6 mol/1) modulates the interaction. The maximal response to adenosine and R-N6-phenylisopro-pyladenosine determined in the presence of 10−7 mol/1 isoprenaline was 50% of that of carbachol which elicited the maximal inhibition even in the presence of 10−6 mol/1 isoprenaline. The negative inotropic effects of R-N6-phenylisopropyladenosine and carbachol were additive to the maximal response equivalent to that of carbachol. The difference in the efficiency between the adenosine and muscarinic receptor agonists may be partly ascribed to the difference in densities of the respective receptors in the dog ventricular myocardium. The negative inotropic effect of R-N6-phenylisopropyladenosine in the presence of isoprenaline was associated with decrease in cyclic AMP levels elevated previously by isoprenaline. The elevation of cyclic AMP levels caused by isoprenaline (3 × 10−7 mol/1) was abolished by R-N6-phenylisopro-pyladenosine (10−4 mol/1), while the contractile response was reduced only by 30% with R-N6-phenylisopro-pyladenosine. In the absence of β-adrenoceptor stimulation R-N6-phenylisopropyladenosine elicited a negative inotropic effect without changes in cyclic AMP levels, but this effect was less than 10% of the basal force of contraction. It is concluded that in the dog ventricular myocardium adenosine receptors play a role for the inhibitory regulation of contractility, which is influenced markedly by the pre-existing level of β-adrenoceptor activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167384
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Acetylcholine and adenosine activate the G protein-gated muscarinic K+ channel in ferret ventricular myocytes (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 610-617 
    Details
    ISSN: 1432-1912
    Keywords: Ferret ; Ventricular myocytes ; Acetylcholine ; Adenosine ; Muscarinic K+ ; channel ; G protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The properties of the K+ channel activated by acetylcholine (ACh) and adenosine (Ado) were examined in single ferret ventricular myocytes using patch-clamp techniques. In the whole-cell configuration, ACh and Ado induced an inwardly rectifying K+ current and shortened the action potential duration. The effect of ACh was blocked by atropine, while the Ado effect was interrupted by 8-cyclopenty1,1,2-dipropyl xanthine, a specific Ado A1 receptor antagonist. In cell-attached recordings, ACh and Ado added to the pipette solution activated a single population of inwardly rectifying K+ channels, distinct from the i K1 channel. The channel had a slope conductance of ∼ 40 pS in symmetrical 150 mM K+ solutions and a mean open time of 0.8 ms. Excision of the patch into the inside-out patch configuration in guanosine triphosphate (GTP)-free solution abolished the channel activity. The channel was reversibly reactivated by adding GTP to the intracellular side of the patch. GTPγS activated the channel irreversibly. When the inside-out patch was treated with the A protomer of pertussis toxin (PTX), intracellular GTP no longer activated the K+ channel. The results show that ferret ventricular myocytes possess a K+ channel activated by both muscarinic and Ado A1 receptors. Its electrophysiological properties and the gating by a PTX-sensitive G protein in a membrane-delimited fashion are identical with those of the muscarinic K+ channels in nodal and atrial tissues of other species. In conclusion, the G protein-gated muscarinic K+ channel is expressed in ferret ventricular myocardium and may underlie the direct negative inotropism of ACh and Ado in this tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170160
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Relationship between the level of cAMP and the contractile force under stimulation of α- and β-adrenoceptors by phenylephrine in the isolated rabbit papillary muscle (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 109-115 
    Details
    ISSN: 1432-1912
    Keywords: α-Adenoceptors ; β-Adrenoceptors ; Phenylephrine ; cAMP ; Papaverine ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The time course of changes of the level of 3′,5′-cyclic AMP (cAMP) and of the tension developed under stimulation of α- and β-adrenoceptors by phenylephrine was investigated in the isolated rabbit papillary muscle. Furthermore the doseresponse relationships for increases of cAMP and of developed tension elicited by phenylephrine were determined. 1. A submaximally effective concentration of phenylephrine (10−5 M) increased significantly the level of cAMP of the papillary muscle at 15 and 30 s by 45 and 36%, respectively; the level of cAMP returned to the control value at 60 s after the administration. The developed tension increased significantly not before 45 s and reached its maximal level at 180 s. 2. When α-adrenoceptors were blocked by phentolamine (10−6 M), the positive inotropic effect of phenylephrine was decreased significantly but the increase of cAMP induced by phenylephrine was not reduced. In the presence of phentolamine the increase of cAMP induced by phenylephrine lasted longer than in the control experiments. 3. The effects of phenylephrine (10−5 M) both on the level of cAMP and the developed tension mediated via stimulation of β-adrenoceptors in the presence of phentolamine were enhanced by the phosphodiesterase inhibitor papaverine throughout the course of responses. 4. Phenylephrine produced an increase in developed tension as well as in cAMP. The corresponding dose-response curves run parallel to each other but differed by about 1.5 log units whereby the developed tension was evoked by lower concentrations. Phentolamine (10−6 M) shifted the curve for the positive inotropic action by about 1.5 log units but did not affect that for increase in cAMP. Therefore, in the presence of the α-adrenolytic drug phentolamine the difference between both curves became smaller so that both curves were superimposed. Papaverine (10−5 M) shifted the whole curve for cAMP upwards and enhanced the maximal contractile response to phenylephrine mediated by stimulation of β-adrenoceptors. 5. The present results indicate that the positive inotropic action of phenylephrine in lower concentrations (〈10−5 M) induced by stimulation of α-adrenoceptors is independent of the level of cAMP. The positive inotropic action of the higher concentrations of phenylephrine induced via stimulation of β-adrenoceptors was preceded by an accumulation of cAMP; the inhibition of the cAMP phosphodiesterase activity by papaverine enhanced the actions of phenylephrine both on the level of cAMP and on the contractile force.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499441
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Pronounced direct inhibitory action mediated by adenosine A1 receptor and pertussis toxin-sensitive G protein on the ferret ventricular contraction (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 282-289 
    Details
    ISSN: 1432-1912
    Keywords: Adenosine ; Phenylisopropyladenosine ; Adenosine receptors ; Negative inotropic effect ; G proteins ; Ferret ventricular myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An adenosine A1 receptor agonist R-N6-phenylisopropyladenosine (R-PIA) elicited a pronounced negative inotropic effect with the EC50 value of 0.69 μmol/1 in the presence of a β-adrenoceptor blocking agent bupranolol (0.3 μmol/1) in the isolated ferret papillary muscle. The negative inotropic effect of R-PIA was not associated with changes in cyclic AMP level. Adenosine and other A1 receptor agonists also elicited a negative inotropic effect. DPCPX (1,3-dipropyl-8-cyclopentyl xanthine) antagonized the negative inotropic effect of R-PIA in a competitive manner (pA2 value = 8.4). The inhibitory action of R-PIA was markedly attenuated in the ventricular muscle preparation isolated from ferrets pretreated with pertussis toxin that caused ADP-ribosylation of 39 kDa proteins in the membrane fraction. In the membrane fraction derived from the ferret ventricle, [3H]-DPCPX bound to a single binding site in a saturable and reversible manner with high affinity (Kd value = 1.21±0.41 nmol/l; B max = 12.8±3.02 fmol/mg protein; n = 7). The binding characteristics of [3H]-DPCPX in the rat ventricle (Kd value = 1.51 ±0.09 nmol/l; B max = 12.7±1.47 fmol/mg protein; n = 5) were similar to those in the ferret. On the other hand, the content of Go, a major pertussis toxin-sensitive G protein in the ferret heart, was much higher in the ferret than in the rat ventricle. The present results indicate that adenosine receptors may play an important role in the inhibitory regulation of ventricular contractility in the ferret in contrast to other mammalian species. The signal transduction process subsequent to agonist binding to A1 receptors including the pertussis toxin-sensitive G protein and ion channels may be responsible for the unique inhibitory action of adenosine in this species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169157
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Role of alpha1A adrenoceptor subtype in production of the positive inotropic effect mediated via myocardial alpha, adrenoceptors in the rabbit papillary muscle: influence of selective alpha1A subtype antagonists WB 4101 and 5-methylurapidil (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 578-585 
    Details
    ISSN: 1432-1912
    Keywords: WB 4101 ; 5-Methylurapidil ; Alpha1 adrenoceptors ; Positive inotropic effect ; [3H]CGP-12177 ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to elucidate the contribution of alpha1A subtype to the positive inotropic effect mediated by myocardial alpha, adrenoceptors, the influence of the alpha1A selective antagonists WB 4101 and 5-methylurapidil on the alpha,-mediated positive inotropic effect (induced by phenylephrine in the presence of a beta adrenoceptor blocking agent bupranolol) was assessed in the isolated rabbit papillary muscle. WB 4101 (10−9-10−7mol/l) shifted the concentration-response curve of the alpha,-mediated positive inotropic effect to the right in parallel, but the slope of Schild plot did not meet the competitive antagonism: WB 4101 shifted the curve by log one unit at 10−9 mol/1, whereas it did not cause further shift at higher concentrations of 10−8 and 10−7 mol/l. WB 4101 did not affect the beta adrenoceptor-mediated positive inotropic effect. 5-Methylurapidil (10−9 to 10−7 mol/l) shifted the curve of alpha1-mediated positive inotropic effect to the right and downwards in a concentration-dependent manner; the slope of Schild plot calculated at the level of 20% of the maximum response to phenylephrine was close to unity. 5-Methylurapidil at 3 × 10−7 mol/1 abolished the alpha1-mediated positive inotropic effect. In addition, 5-methylurapidil inhibited the beta adrenoceptor-mediated positive inotropic effect in the same concentration range as it antagonized the alpha1-mediated positive inotropic effect, indicating that 5-methylurapidil is not selective for myocardial alpha, adrenoceptors. In the membrane fraction derived from the rabbit ventricular muscle, 5-methylurapidil displaced the specific binding of [3H]CGP-12177 with high affinity, whereas WB 4101 did not affect the [3H]CGP-12177 binding in the concentration range that it antagonized the alpha,-mediated positive inotropic effect. The present results indicate that alpha1A adrenoceptor subtype plays a role in production of the positive inotropic effect mediated by myocardial alpha, adrenoceptors, but the extent is less than that mediated by alpha1B subtype in the rabbit ventricular myocardium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168952
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Stimulation by phenylephrine of adrenergic alpha- and beta-receptors in the isolated perfused rabbit heart (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 282 (1974), S. 307-310 
    Details
    ISSN: 1432-1912
    Keywords: Isolated Perfused Rabbit Heart ; Phenylephrine ; dp/dt max ; Heart Rate ; Adrenolytic Drugs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the isolated perfused rabbit heart the effect of phenylephrine on the left ventricular dp/dt max and on heart rate was investigated. 1. The positive inotropic effect of phenylephrine 3×10−7 to 3×10−6 M was abolished by the α-adrenolytic drug phentolamine (3×10−6 M), whereas the β-adrenolytic drug pindolol (10−8 M) was ineffective. On the other hand, the positive inotropic effect evoked by higher concentrations (10−5 to 10−4 M) of phenylephrine was blocked by pindolol while phentolamine was without any effect. 2. The positive chronotropic effect of phenylephrine was antagonized by pindolol. Phentolamine was ineffective. 3. The results presented here show that the ventricular myocardium of the rabbit contains both β- and α-adrenoceptors responsible for the mediation of the positive inotropic effect of phenylephrine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501238
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Positive inotropic effects of phenylephrine in the isolated rabbit papillary muscle mediated both by α-and β-adrenoceptors (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 284 (1974), S. 133-148 
    Details
    ISSN: 1432-1912
    Keywords: Adrenoceptors ; Phenylephrine ; Phosphodiesterase Inhibitors ; Rabbit Papillary Muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary On the isolated papillary muscle of the rabbit experiments were performed in order to study whether β-and/or α-adrenoceptors mediate the positive inotropic effect of phenylephrine and, for comparison, of other sympathomimetic drugs. 1. The positive inotropic effect of phenylephrine in concentrations of up to 3×10−6M was antagonized by the α-adrenolytic drug phentolamine, while that evoked by higher concentrations was inhibited by the β-adrenolytic drug pindolol. The intrinsic activity of phenylephrine amounted to 0.6 compared with that of isoprenaline. 2. Pretreatment with reserpine altered neither the pD2-value for phenylephrine nor its intrinsic activity. 3. The inhibitors of phosphodiesterase, theophylline (10−4M) and papaverine (10−5M) enhanced the effect of higher concentrations of phenylephrine—mediated mainly by stimulation of β-adrenoceptors, whereas that of lower concentrations—mediated by stimulation of α-adrenoceptors—was not affected. Papaverine strongly increased the intrinsic activity of phenylephrine, which then reached that of isoprenaline. 4. The α-adrenoceptor stimulating drugs, methoxamine, naphazoline and oxymetazoline did not cause positive inotropic effects but, on the contrary, negative ones. The positivei notropic effect of noradrenaline was not changed by phentolamine, whereas that of adrenaline in concentrations of up to 10−5 M was inhibited. 5. From these results it is concluded that in the rabbit papillary muscle not only β- but also α-adrenoceptors are of functional importance for the mediation of the positive inotropic effect of some sympathomimetic drugs. The nature of these α-adrenoceptors is apparently distinct from those of other organs since these receptors were stimulated only by phenylephrine and adrenaline but not by noradrenaline, methoxamine, naphazoline and oxymetazoline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501118
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...