bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endogenous inotropic factor‐induced endothelium‐dependent relaxation of vascular smooth muscle
Authors: Han Chao , Khatter Jagdish C. 
Published: July 2012

Possible contractile or relaxation effects of an endogenous inotropic factor (EIF) isolated and purified from porcine heart left ventricle were examined in rat isolated aortic ring preparations.
EIF induced a dose‐dependent relaxation of the rat isolated aortic ring preparation pre‐contracted with 0.4 μm phenylephrine (PE); 200 μl (in 5 ml bath) of EIF caused relaxation of aortic rings by as much as 67.4±4.5%. In another set of experiments, in the presence of 100 μl EIF, the PE concentration‐response contractile curve shifted to the right, the maximal contractile force was reduced by as much as 32.8% and the EC50 of PE increased from 0.2 to 0.3 μm.
The relaxation effect of EIF was demonstrated to be endothelium‐dependent. Additional experiments demonstrated that EIF‐induced relaxation in an isolated aortic ring could be inhibited by 2 μm NG‐nitro‐L‐arginine methyl ester, a nitric oxide synthase inhibitor, suggesting the involvement of nitric oxide in EIF‐induced relaxation of the muscle.
Atropine (0.2 μm) or indomethacin (10 μm) had no significant effect on EIF‐induced relaxation.
These data suggest that EIF, a novel endogenous inotrope from porcine myocardium, also acts as an endothelium‐dependent vasodilator substance mediating relaxation in the rat isolated aorta mainly by release of nitric oxide. The possibility of EIF acting through muscarinic receptor and the involvement of prostacyclin were excluded.
Comparison of desulfatohirudin (REVASC) and heparin as adjuncts to thrombolytic therapy with reteplase in a canine model of coronary thrombosis
Authors: Martin Ulrich , Dörge Liesel , Fischer Stephan 
Published: July 2012

We compared the direct thrombin inhibitor, desulfatohirudin (REVASC) and the indirect thrombin inhibitor, heparin, as adjuncts to thrombolytic therapy with reteplase in a canine model of coronary artery thrombosis.
Reteplase (BM 06.022) is a recombinant unglycosylated variant of human tissue‐type plasminogen activator. Thrombus formation in anaesthetized open chest dogs was induced by electrical injury. Left circumflex coronary artery blood flow was monitored for 210 min with an electromagnetic flow probe. Twenty eight dogs were randomized to receive i.v. heparin (120 iu kg−1 bolus plus 80 iu kg−1 per h) or i.v. hirudin (2.0 mg kg−1 bolus plus 2.0 mg kg−1 per h) 10 min before thrombolysis preceded by i.v. acetylsalicyclic acid (20 mg kg−1) 5 min prior to anticoagulation. Every dog received an i.v. double bolus injection of 0.14±0.14 u kg−1 (= 0.24±0.24 mg kg−1) reteplase, 30 min apart, 1 h after thrombus formation.
At comparable reperfusion rates (12 out of 12 vs. 15 out of 16 dogs), hirudin enhanced time to reperfusion (14.3±1.4 vs. 23.2±3.4 min; P<0.05) and completely prevented reocclusion after reperfusion in contrast to heparin (0 out of 11 vs. 7 out of 11 dogs; P<0.05). Coronary blood flow quality was improved by hirudin as shown by a higher maximum blood flow after reperfusion (130±14.3 vs. 83±9.3% of baseline; P<0.05), a higher blood flow level at 20, 30, 40, and 50 min after onset of thrombolysis (P<0.05) and a longer cumulative patency time (195±1.7 vs. 166±12 min; P<0.05). Activated partial thromboplastin time and buccal mucosa bleeding time were prolonged (P<0.05) by either anticoagulant, but did not differ significantly between groups.
The direct thrombin inhibitor, desulfatohirudin, enhanced thrombolysis, prevented reocclusion and increased blood flow as compared with the indirect thrombin inhibitor, heparin, when investigated at one dose level each and used in conjunction with reteplase.
Receptors for kinins in the human isolated umbilical vein
Authors: Gobeil F. , Pheng L.H. , Badini I. , Nguyen‐Le X.K. , Pizard A. , Rizzi A. , Blouin D. , Regoli D. 
Published: July 2012

The human umbilical vein has been found to contract in response to bradykinin (BK) and desArg9BK.
The rank order of potency of agonists, in the presence of the B1 receptor antagonist Lys[Leu8]desArg9BK, is as follows: [Hyp3, Tyr(Me)8]BK (pD2 8.88) = [Hyp3]BK (pD2 8.86) = LysBK (pD2 8.81) ≥BK (pD2 8.60) > >[Aib7]BK (pD2 6.38) > >desArg9BK and LysdesArg9BK (inactive).
Hoe 140 (pA2 8.42) inhibits the effects of BK while other B2 receptor peptide antagonists are very weak and WIN 64338 is practically inactive.
Venoconstrictor responses to desArg9BK of fresh tissues increase with time during the in vitro incubation and reach a maximum after 4–6 h. The activity of Hoe 140 (pA2 5.48) is negligible against B1 receptor agonists.
When measured in the presence of the selective B2 receptor antagonist Hoe 140 (400 nM), the order of potency of kinin related peptides on the B1 receptor is Lys[desArg9]BK (pD2 8.60)>desArg9BK (pD2 6.69). BK, LysBK, [Hyp3]BK and other B2 receptor agonists are inactive.
The B1 receptor antagonist, Lys[Leu8]desArg9BK (pA2 7.99), inhibits the response of the human vein to B1 receptor agonists (LysdesArg9BK or desArg9BK), but do not alter the effect of BK.
The results summarized in this paper indicate that the human isolated umbilical vein is a sensitive preparation containing both B1 and B2 receptors. The human B2 receptor shows some similarity with that of the rabbit (at least for agonist potencies) and differs from the B2 receptor of the guinea‐pig. Compared to the rabbit B1 receptor, the human B1 receptor shows low sensitivity to peptides that lack the N‐terminal Lys.
Regional haemodynamic effects of antagonists of angiotensin II, endothelin and adrenoceptors in conscious, vasopressin‐deficient, genetically hypertensive rats
Authors: Gardiner S.M. , March J.E. , Kemp P.A. , Bennett T. 
Published: July 2012

Male, vasopressin‐deficient, normotensive (DI/N) and hypertensive (DI/H) rats were chronically instrumented (all surgery under sodium methohexitone anaesthesia) to allow assessment of resting haemodynamic status and responses to antagonism of AT1‐receptors (Experiment 1), ETA‐ and ETB‐ receptors (Experiment 2) or adrenoceptors (Experiment 3).
Before any treatment, mean arterial blood pressure (MAP) was higher, and hindquarters vascular conductance was consistently lower in all groups of DI/H rats than in DI/N rats.
In Experiment 1, losartan (10 mg kg−1 i.v.), an AT1‐receptor antagonist, was given 5 h after s.c. injection of saline, (DI/N, n = 8; DI/H, n = 8) or hyperoncotic polyethylene glycol, (DI/N, n = 9; DI/H, n = 9) to induce isosmotic hypovolaemia. In the volume‐replete state, losartan caused similar small falls in MAP in the two groups (maximum Δ MAP; DI/N, −9±2; DI/H, −15±5 mmHg), but the mesenteric and hindquarters vasodilatations were greater in DI/N rats. In the volume‐depleted state the effects of losartan were augmented (Δ MAP; DI/N, −32±3; DI/H. −31±3 mmHg), but its vasodilator effects were still greater in DI/N than in DI/H rats.
In Experiment 2, infusion of the ETA‐ETB‐receptor antagonist, SB 209670 (600 μg kg−1 h−1; DI/N, n = 8; DI/H, n = 9), had haemodynamic effects that were not different from those during saline infusion in DI/N (n = 7) and DI/H rats (n = 8).
In Experiment 3, sequential administration of the β2‐adrenoceptor antagonist, ICI 118551 (0.2 mg kg−1 bolus, 0.1 mg kg−1 h−1 infusion), the α2‐adrenoceptor antagonist, idazoxan (0.75 mg kg−1 bolus, 1 mg kg−1 h−1 infusion), and losartan (10 mg kg−1 bolus) had only slight haemodynamic effects in DI/N (n = 8) and DI/H (n = 9) rats. Subsequent administration of the α1‐adrenoceptor antagonist, prazosin (0.5 mg kg−1 bolus, 0.8 mg kg−1 h−1 infusion) caused marked hypotension, although MAP was still higher in DI/H (95±4 mmHg) than in DI/N (75±4 mmHg) rats. However, in this circumstance there were no significant differences between renal, or mesenteric, or hindquarters vascular conductances in the two groups.
The results indicate that the hypertension and hindquarters vasoconstriction in DI/H rats is not dependent on All or endothelin. Moreover, the relative elevation in MAP in DI/H persists in the presence of antagonism of β2, α2‐ and α1‐adrenoceptors, in spite of no significant difference in regional vascular conductances.
The mechanism of relaxation induced by atrial natriuretic peptide in the porcine renal artery
Authors: Seguchi Hiroshi , Nishimura Junji , Toyofuku Kazuki , Kobayashi Sei , Kumazawa Joichi , Kanaide Hideo 
Published: July 2012

The mechanisms underlying the relaxation of the porcine renal artery induced by atrial natriuretic peptide (ANP) were investigated, using front‐surface fluorimetry with fura‐2 and receptor‐coupled permeabilization by α‐toxin.
ANP decreased the cytosolic Ca2+ concentration ([Ca2+]i) and tension during the contraction induced by a high external K+ solution, in a concentration‐dependent manner. This ANP‐induced decrease in [Ca2+]i during the contraction induced by high K+ solution was composed of two phases, an initial rapid phase, followed by a maintenance phase. The initial rapid decrease in [Ca2+]i, but not the maintained decrease in [Ca2+]i, was inhibited when the tissue was treated with thapsigargin, a selective Ca2+ pump inhibitor of the sarcoplasmic reticulum. When the tissues were treated with thapsigargin and external Ca2+ was replaced by Ba2+, which cannot be transported by the Ca2+ pump, ANP did not induce a decrease in [Ba2+]i, even though the elevation of tension induced by Ba2+ was strongly inhibited.
In the absence of extracellular Ca2+, ANP inhibited the release of Ca2+ from the intracellular store induced by noradrenaline (NA).
The [Ca2+]i (abscissa scale)‐tension (ordinate scale) relationship observed during the contraction induced by various concentrations of high external K+ solution was shifted downwards by the addition of 10−8 m ANP, indicating that, at any given [Ca2+]i, the tension generated by high K+ solution was considerably inhibited by the additon of 10‐8 m ANP. The [Ca2+]i‐tension curve of the contraction obtained by the cumulative application of external Ca2+ (0–3.75 mM) during depolarization with 118 mM K+ solution was shifted to the left by 3 × 10−7 m NA. This NA‐induced [Ca2+]i‐tension relationship was shifted to the right by 10−8 m ANP, indicating that the ANP‐induced reduction of Ca2+‐sensitivity operates during the contraction induced by NA.
In α‐toxin‐permeabilized preparations, ANP induced relaxation of tissues precontracted with a mixture of 3 × 10−7 m Ca2+, 10−5 m guanosine 5′‐triphosphate (GTP) and 10−6 m NA. Thus a component of ANP‐induced relaxation took place by way of a reduction in the Ca2+ sensitivity of the myofilaments, independent of changes in [Ca2+]i.
These results indicate that ANP induces relaxation of the porcine renal artery by: (1) reducing [Ca2+]i mainly via the activation of the Ca2+ pumps located on the sarcoplasmic reticulum and sarcolemma, as well as via inhibition of agoinist‐induced release of Ca2+ from the intracellular store; and (2) decreasing the Ca2+‐sensitivity of the contractile elements.
Actions of long chain alcohols on GABAa and glutamate receptors: relation to in vivo effects
Authors: Dildy‐Mayfield J.E. , Mihic S.J. , Liu Y. , Deitrich R.A. , Harris R.A 
Published: July 2012

The effects of n‐alcohols on GABAa and glutamate receptor systems were examined, and in vitro effectiveness was compared with in vivo effects in mice and tadpoles. We expressed GABAa, NMDA, AMPA, or kainate receptors in Xenopus oocytes and examined the actions of n‐alcohols on receptor function using two‐electrode voltage clamp recording.
The function of GABAa receptors composed of α1β1 or α1β1γ21 subunits was potentiated by all of the n‐alcohols studied (butanol‐dodecanol).
In contrast to GABAA receptors, glutamate receptors expressed from mouse cortical mRNA or from cRNAs encoding AMPA (GluR3)‐ or kainate (GluR6)‐selective subunits were much less sensitive to longer chain alcohols. In general, octanol and decanol were either without effect or high concentrations were required to produce inhibition.
In contrast to the lack of behavioural effects by long chain alcohols reported previously, decanol produced loss of righting reflex in short‐ and long‐sleep mice, indicating that the in vivo effects of decanol may be due in part to actions at GABAa receptors. Furthermore, butanol, hexanol, octanol, and decanol produce similar potentiation of GABAa receptor function at concentrations required to cause loss of righting reflex in tadpoles, an in vivo model where alcohol distribution is not a compromising factor.
Thus, the in vivo effects of long chain alcohols are not likely to be due to their actions on NMDA, AMPA, or kainate receptors, but may be due instead to potentiation of GABAA receptor function.
Relaxation of guinea‐pig trachea by sodium nitroprusside: cyclic GMP and nitric oxide not involved
Authors: Sadeghi‐Hashjin Gudarz , Folkerts Gert , Henricks Paul A.J. , van de Loo Peet G.F. , Dik Ilse E.M. , Nijkamp Frans P. 
Published: July 2012

Sodium nitroprusside (SNP) completely relaxed the guinea‐pig isolated, perfused trachea in a concentration‐dependent manner. Although SNP was less potent by about 2 orders of magnitude, its maximal effect was 25% higher compared to isoprenaline.
SNP (3.2 μm) increased cyclic GMP levels by 300% and relaxed guinea‐pig isolated, perfused trachea by 54%. The SNP‐induced relaxations of the preparations were not affected by the guanylate cyclase inhibitor, methylene blue. Moreover, zaprinast, a cyclic GMP‐specific phosphodiesterase inhibitor which was supposed to enhance SNP‐induced relaxations, decreased the maximal relaxation by 22% (P < 0.001).
In contrast, 8Br‐cyclic GMP (10 μm) increased the cyclic GMP levels by 1100% without inducing a marked relaxation.
SNP (10 μm) and S‐nitroso‐N‐acetylpenicillamine (SNAP; a direct donor of nitric oxide; 10 μm), relaxed the tissues by 75% and 25%, respectively, without any nitric oxide (NO) release by SNP (< 1 pmol 100 μl−1), but a substantial NO release by SNAP (560 pmol 100 μl−1).
It is concluded that the SNP‐induced tracheal relaxations are probably not mediated by cyclic GMP and NO.
Drug‐induced in vitro inhibition of neutrophil‐endothelial cell adhesion
Authors: Pellegatta Fabio , Lu Yan , Radaelli Antonella , Zocchi Maria Raffaella , Ferrero Elisabetta , Chierchia Sergio , Gaja Gianfranco , Ferrero Maria Elena 
Published: July 2012

Leukocyte‐endothelial cell interactions play an important role during ischaemia‐reperfusion events. Adhesion molecules are specifically implicated in this interaction process.
Since defibrotide has been shown to be an efficient drug in reducing damage due to ischaemia‐reperfusion in many experimental models, we analysed the effect of defibrotide in vitro on leukocyte adhesion to endothelial cells in basal conditions and after their stimulation.
In basal conditions, defibrotide (1000 μg ml−1) partially inhibited leukocyte adhesion to endothelial cells by 17.3% ± 3.6 (P < 0.05), and after endothelial cell stimulation (TNF‐α, 500 u ml−1) or after leukocyte stimulation (fMLP, 10−7 m), it inhibited leukocyte adhesion by 26.5% ± 3.4 and 32.4% ± 1.8, respectively (P < 0.05).
In adhesion blockage experiments, the use of the monoclonal anntibody anti‐CD31 (5 μg ml−1) did not demonstrate a significant inhibitory effect whereas use of the monoclonal antibody anti‐LFA‐1 (5 μg ml−1) significantly interfered with the effect of defibrotide.
This result was confirmed in NIH/3T3‐ICAM‐1 transfected cells.
We conclude that defibrotide is able to interfere with leukocyte adhesion to endothelial cells mainly in activated conditions and that the ICAM‐1/LFA‐1 adhesion system is involved in the defibrotide mechanism of action.
The mechanism of acidic pH‐induced contraction in aortae from SHR and WKY rats enhanced by increasing blood pressure
Authors: Furukawa Ken‐Ichi , Komaba Junji , Sakai Hiroyuki , Ohizumi Yasushi 
Published: July 2012

Effect of pH on vascular smooth muscle contraction was analyzed by use of biochemical and pharmacological techniques.
In the aorta isolated from spontaneously hypertensive rats (SHR) decreasing extracellular pH (pHo) caused a rapid acidification of intracellular pH accompanied by a pHo‐dependent increase in tension. The contraction of the SHR aorta was remarkable compared with that of the Wistar Kyoto rat (WKY) aorta.
Removal of NH4Cl caused a transient decrease in intracellular pH followed by a marked increase in tension.
Both contraction and intracellular Ca2+ mobilization induced by acidic pHo were markedly inhibited by removal of extracellular Ca2+, verapamil and adenosine, whereas these were not affected by tetrodotoxin or Gd3+, a stretch‐activated cation channel blocker. Furthermore, cromakalim (a K+ channel opener) inhibited acidic pHo‐induced contraction (APIC).
Acidic pHo induced a depolarization of cultured smooth muscle cells from SHR aorta.
Blood pressure elevated with increasing age of WKY and SHR accompanied by an increase in APIC. Feeding WKY with NG‐nitro‐L‐arginine, an inhibitor of nitric oxide synthases caused a marked elevation of their blood pressure followed by an increase in APIC.
These results suggest that APIC is caused by Ca2+ influx mediated through the activation of voltage‐sensitive Ca2+ channels mainly due to acidic pHo‐induced depolarization of the plasma membrane of smooth muscle cells. It is also suggested that APIC is strengthened by the elevation of blood pressure.
Activation of potassium currents by inhibitors of calcium‐activated chloride conductance in rabbit portal vein smooth muscle cells
Authors: Toma C. , Greenwood I.A. , Helliwell R.M. , Large W.A. 
Published: July 2012

The conventional whole‐cell recording technique was used to study the effects of the chloride channel inhibitors ethacrynic acid, anthracene‐9‐carboxylic acid (A‐9‐C) and indanyloxyacetic acid (IAA) on membrane currents in rabbit portal vein smooth muscle cells at a holding potential of 0 mV.
Using a pipette solution that contained 1 × 10−4 m 1, 2‐bis (2‐aminophenoxy)‐ethane‐N,N,N′,N′‐tetraacetic acid (BAPTA) and a normal bathing solution the addition of ethacrynic acid (2 × 10−4 m to 1 × 10−3 m) inhibited spontaneous transient outward currents (STOCs) and evoked a concentration‐dependent current at a holding potential of 0 mV. A similar current was activated by IAA (5 × 10−4 m to 1 × 10−3 m) but not by A‐9‐C (1–5 × 10−3 m) at a holding potential of 0 mV.
The amplitude of the current evoked by ethacrynic acid and IAA was linearly related to potential between −30 and 0 mV and displayed outward rectification at positive potentials. The current induced by A‐9‐C was evident only at potentials positive to +20 mV.
Glibenclamide (1 × 10−5 m) abolished the current evoked by ethacrynic acid and IAA at potentials negative to +10 mV and partially inhibited the current positive to +10 mV. The glibenclamide‐insensitive current at positive potentials was completely inhibited by 1 × 10−3 m TEA. The A‐9‐C‐evoked current was insensitive to glibenclamide and abolished by 1 × 10−3 m TEA.
The glibenclamide‐sensitive current activated by ethacrynic acid was not sustained and declined to control levels in the continued presence of ethacrynic acid. However, the outwardly rectifying current recorded at +50 mV was well maintained over the same period.
Outwardly rectifying currents evoked by ethacrynic acid and A‐9‐C were observed with a pipette solution containing 1 × 10−2 m BAPTA in cells bathed in Ca‐free extracellular solution containing 5 × 10−4 m BAPTA and 1 × 10−5 m cyclopiazonic acid.
It is concluded that all three chloride‐channel blockers activated an outwardly rectifying, TEA‐sensitive current. Moreover, ethacrynic acid and IAA evoked an additional glibenclamide‐sensitive current which was present at all potentials between −30 and +50 mV.
Endothelins‐induce cyclicAMP formation in the guinea‐pig trachea through an ETA receptor‐ and cyclooxygenase‐dependent mechanism
Authors: EL‐Mowafy Abdalla M. , Abou‐Mohamed Gamal A. 
Published: July 2012

The non‐selective endothelin agonist, endothelin‐1 (ET‐1), and the selective ETB receptor agonist, sarafotoxin‐S6c (SRTX‐c), contracted guinea‐pig isolated trachea in a concentration‐dependent manner. The EC50 value for ET‐1 (11 ± 2.1 nM) was significantly higher than that of SRTX‐c (3.2 ± 0.21 nM) and the maximal developed tension due to SRTX‐c was 42.8 ± 2.3% higher than that produced by ET‐1 (P < 0.05).
Pretreatment with the ETA antagonist, BQ‐610, appreciably enhanced the developed tension due to ET‐1 but not SRTX‐c. Likewise, the cyclo‐oxygenase inhibitor, indomethacin, markedly potentiated the contractile responses to ET‐1, but not to SRTX‐c. Combining BQ‐610 with indomethacin was not more effective than either of them in augmenting ET‐1‐evoked tension.
ET‐1 significantly increased cyclic AMP formation in the trachea in concentration‐ and time‐dependent manners. A t1/2 value of 4.3 min, an EC50 value of 20 ± 3 nM and a maximal cyclic AMP increment of 124% above the basal level, were obtained for ET‐1. Similarly but less effectively, ET‐3 (0.1 μm) increased cyclic AMP level (35 ± 3.7% compared to 94 ± 7.8% for the same concentration of ET‐1). By contrast, SRTX‐c did not alter the cyclicAMP level when applied in concentrations up to 1 μm.
Pre‐incubation of the trachea with BQ‐610 (1 μm) or indomethacin (1 μm) prevented cyclicAMP formation by either ET‐1 or ET‐3.
The results of the present study indicate a negative regulatory role mediated by the ETA receptor on the ETB‐triggered mechanical response. This effect is likely to be mediated by activation of adenylate cyclase through a cyclo‐oxygenase‐dependent mechanism.
Evidence for two distinct P2‐purinoceptors subserving contraction of the rat anococcygeus smooth muscle
Authors: Najbar Alicja T. , Li C.G. , Rand Michael J. 
Published: July 2012

The effects of the P2‐purinoceptor agonists, adenosine 5′‐triphosphate (ATP), α, β‐methylene ATP (α, β‐MeATP), β, γ‐methylene ATP (β, γ‐MeATP), L‐β, γ‐methylene ATP (L‐β, γ‐MeATP), adenosine‐5′‐O‐(2‐thiodiphosphate) (ADPβS), and 2‐methylthio ATP (2‐MeSATP) were investigated on the isometric tension of the rat anococcygeus muscle.
Non‐cumulative additions of ATP (100–1500 μm), α, β‐MeATP (1–300 μm), β, γ‐MeATP (10–300 μm), L‐β, γ‐MeATP (3–100 μm) and ADPβS (1–100 μm) produced concentration‐dependent contractions, whereas 2‐MeSATP (1–100 μm) had no effect. The rank order of potency was α, β‐MeATP > L‐β, γ‐MeATP ≥ ADPβS > β, γ‐MeATP > > ATP > 2‐MeSATP.
Contractions to cumulative additions of ATP, α, β‐MeATP, β, γ‐MeATP and L‐β, γ‐MeATP were subject to desensitization whilst those to ADPβS were unaffected.
Contractions to ATP, α, β‐MeATP, β, γ‐MeATP and ADPβS were abolished by the non‐selective P2X/P2Y‐purinoceptor antagonist, suramin (100 μm). In contrast, contractions to ATP, α, β‐MeATP and β, γ‐MeATP were not affected by the non‐selective P1‐purinoceptor antagonist 8‐(p‐sulphophenyl)‐theophylline (8SPT, 30 μm). Blockade of P2X‐purinoceptors with the selective P2X‐purinoceptor antagonist pyridoxal‐phosphate‐6‐azophenyl‐2′, 4′‐disulphonic acid (PPADS, 10 μm) or desensitization with L‐β, γ‐MeATP (10 μm) abolished contractions to α, β‐MeATP, but enhanced those to ADPβS. The P2Y‐purinoceptor antagonist, reactive blue 2 (RB2, 100 μm) enhanced contractions to ATP and α, β‐MeATP but abolished those to ADPβS.
Simultaneous addition of α, β‐MeATP and ADPβS produced an additive contraction.
The findings suggest that in the rat anococcygeus, smooth muscle cells are endowed with two distinct P2‐purinoceptors which subserve contractions: a P2X‐purinoceptor activated by ATP and its analogues, and another type of P2‐purinoceptor activated by ADPβS.