Implementing health promotion activities using community-engaged approaches in Asian American faith-based organizations in New York City and New Jersey.

Faith-based organizations (FBOs) (e.g., churches, mosques, and gurdwaras) can play a vital role in health promotion. The Racial and Ethnic Approaches to Community Health for Asian Americans (REACH FAR) Project is implementing a multi-level and evidence-based health promotion and hypertension (HTN) control program in faith-based organizations serving Asian American (AA) communities (Bangladeshi, Filipino, Korean, Asian Indian) across multiple denominations (Christian, Muslim, and Sikh) in New York/New Jersey (NY/NJ). This paper presents baseline results and describes the cultural adaptation and implementation process of the REACH FAR program across diverse FBOs and religious denominations serving AA subgroups. Working with 12 FBOs, informed by implementation research and guided by a cultural adaptation framework and community-engaged approaches, REACH FAR strategies included (1) implementing healthy food policies for communal meals and (2) delivering a culturally-linguistically adapted HTN management coaching program. Using the Ecological Validity Model (EVM), the program was culturally adapted across congregation and faith settings. Baseline measures include (i) Congregant surveys assessing social norms and diet (n = 946), (ii) HTN participant program surveys (n = 725), (iii) FBO environmental strategy checklists (n = 13), and (iv) community partner in-depth interviews assessing project feasibility (n = 5). We describe the adaptation process and baseline assessments of FBOs. In year 1, we reached 3790 (nutritional strategies) and 725 (HTN program) via AA FBO sites. Most AA FBOs lack nutrition policies and present prime opportunities for evidence-based multi-level interventions. REACH FAR presents a promising health promotion implementation program that may result in significant community reach.

Preliminary results of the luna aneurysm embolization system in a rabbit model: a new intrasaccular aneurysm occlusion device.

BACKGROUND AND PURPOSE: Recent advances in endovascular devices have been aimed at providing high density, mesh-like metallic materials across the aneurysm neck, in place of coil technology. Therefore our aim was to report the in vivo preclinical performance of a self-expanding intrasaccular embolization device. MATERIALS AND METHODS: Elastase-induced aneurysms were created in 12 rabbits. Each aneurysm was embolized with a Luna AES. DSA was performed preimplantation; 5, 10, and 30 minutes postimplantation; and at 1 month in 12 rabbits and at 3 months in 8 rabbits. Early postimplantation intra-aneurysmal flow was graded as unchanged, moderately diminished, or completely absent. One- and 3-month DSAs were graded by using a 3-point scale (complete, near-complete, or incomplete occlusion). Aneurysms were harvested for gross and microscopic histologic evaluation at 1 month (n = 4) and at 3 months (n = 8). Tissues within the aneurysm dome and across the aneurysm neck were assessed by using HE staining. RESULTS: Ten (83%) of 12 aneurysms demonstrated complete cessation of flow within 30 minutes of device implantation. At 1-month follow-up, 10 (83%) of 12 aneurysms were completely occluded. At 3 months, 7 of 8 (88%) aneurysms remained completely occluded. One-month gross examination in 4 rabbits demonstrated that membranous tissue completely covered the device in 3 subjects (75%). Microscopic examination showed that 3 aneurysms had loose connective tissue filling the aneurysm cavity. Three-month gross and microscopic examinations demonstrated membranous tissue completely covering the device, loose connective tissue filling the aneurysm cavity, and neointima formation crossing the aneurysm neck in 8 of 8 (100.0%) subjects. CONCLUSIONS: The Luna AES achieved high rates of complete angiographic occlusion and showed promising histologic findings in the rabbit aneurysm model.

Coil Knotting during Endovascular Coil Embolization for Ruptured MCA Aneurysm. A Case Report.

SUMMARY: Complications during coil embolization of cerebral aneurysms include thromboembolic events, hemorrhagic complications related to procedural aneurysmal rupture and parent vessel perforation, and coil-related complications. The present report describes a rare coil-related complication involving spontaneous coil knotting.

A double catheter technique for elongated middle cerebral artery bifurcation aneurysm. A case report.

SUMMARY: We report a case of an elongated middle cerebral artery bifurcation aneurysm which was managed using an endovascular double catheter technique. After positioning two microcatheters, one at the distal dome and the other at the proximal dome, two coils were subsequently deployed through each microcatheter.We created a proximal supporting coil frame using one microcatheter and preserved the parent artery, and then deposited subsequent packing coils at the distal aneurysm sac region using the other microcatheter. The proximal framing coils did not detach prior to obtaining satisfactory aneurysm packing through the distally positioned microcatheter. This approach allowed for the proximal coil to be withdrawn if there was any evidence of the proximal coil frame changing shape or of parent artery protrusion. This double microcatheter technique provided safe and effective treatment of an elongated middle cerebral artery bifurcation aneurysm.

Receptor signaling mechanisms underlying muscarinic agonist-evoked contraction in guinea-pig ileal longitudinal smooth muscle.

1 In guinea-pig ileal longitudinal muscle, muscarinic partial agonists, 4-(N-[3-chlorophenyl]-carbomoyloxy)-2-butynyl-trimethylammonium (McN-A343) and pilocarpine, each produced parallel increases in tension and cytosolic Ca(2+) concentration ([Ca(2+)]c) with a higher EC(50) than that of the full agonist carbachol. The maximum response of [Ca(2+)]c or tension was not much different among the three agonists. The Ca(2+) channel blocker nicardipine markedly inhibited the effects of all three agonists 2 The contractile response to any agonist was antagonized in a competitive manner by M(2) receptor selective antagonists (N,N'-bis[6-[[(2-methoyphenyl)methyl]amino]hexyl]-1,8-octanediamine tetrahydrochloride and 11-[[2-[(diethlamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H-pyrido[2,3-b][1,4] benzodiazepine-6-one), and the apparent order of M(2) antagonist sensitivity was McN-A343>pilocarpine>carbachol. M(3) receptor selective antagonists, 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide and darifenacin, both severely depressed the maximum response for McN-A343, while darifenacin had a similar action in the case of pilocarpine. Both M(3) antagonists behaved in a competitive manner in the case of the carbachol response. 3 McN-A343 failed to release Ca(2+) from the intracellular stores, and the Ca(2+)-releasing action of pilocarpine was very weak compared with that of carbachol. All three agonists were capable of increasing Ca(2+) sensitivity of the contractile proteins. 4 McN-A343 rarely produced membrane depolarization, but always accelerated electrical spike discharge. Pilocarpine effect was more often accompanied by membrane depolarization, as was usually seen using carbachol. 5 The results suggest that muscarinic agonist-evoked contractions result primarily from the integration of Ca(2+) entry associated with the increased spike discharge and myofilaments Ca(2+) sensitization, and that Ca(2+) store release may contribute to the contraction indirectly via potentiation of the electrical membrane responses. They may also support the idea that an interaction of M(2) and M(3) receptors plays a crucial role in mediating the contraction response.

Mechanisms of NO-resistant relaxation induced by acetylcholine in rabbit renal arteries.

The effects of K+ channel blockers and P2Y receptor agonist/antagonist on the vasorelaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) were investigated in the rabbit renal artery. Acetylcholine (ACh, 1 nM-10 microM) induced endothelium-dependent relaxation of arterial rings precontracted with norepinephrine (NE, 1 microM) in a concentration-dependent manner. NG-nitro-L-arginine (L-NAME. 0.1 mM), an inhibitor of NO synthase, partially inhibited the ACh-induced endothelium-dependent relaxation. The ACh-induced relaxation was only partially inhibited by L-NAME whereas combined addition of L-NAME and 30 mM KCl completely inhibited the relaxation. The ACh-induced relaxation observed in the presence of L-NAME was significantly reduced by a combination of iberiotoxin (0.1 microM) and apamin (1 microM), and almost completely blocked by 4-aminopyridine (5 mM). The ACh-induced relaxation was antagonized by P2Y receptor antagonist, cibacron blue (10 and 100 microM) in a concentration-dependent manner. Furthermore, ADPbetaS, a potent P2Y agonist, induced the endothelium-dependent relaxation, and this relaxation was markedly reduced by either the combination of iberiotoxin and apamin or by cibacron blue alone. In conclusion, ACh may activate the release of ATP from endothelial cells which in turn activates a P2Y receptor on the endothelial cells followed by a release of EDHF, resulting in a vasorelaxation via a mechanism that involves activation of both the voltage-gated K+ channels and the Ca2+-activated K+ channels. EY WORDS: ATP, K+ channel, rabbit renal artery.

Mechanisms of acetylcholine-induced vasorelaxation in high K+-stimulated rabbit renal arteries.

To characterize the mechanisms of acetylcholine (ACh)-induced vasorelaxation in rabbit renal arteries precontracted with high K+ (100 mM), muscle tension and cytosolic free Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded arterial strips. In the artery with endothelium, high K+ increased both [Ca2+]i and muscle tension. Addition of ACh (10 microM) during high-K+ induced contraction significantly relaxed the muscle and induced additional increase in [Ca2+]i. In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM). ACh increased [Ca2+]i without relaxing the muscle. In the artery without endothelium, high K+ increased both [Ca2+]i and muscle tension although ACh was ineffective, suggesting that ACh acts selectively on endothelium to increase [Ca2+]i. 4-DAMP (10 nM) or atropine (0.1 microM) abolished the ACh-induced increase in [Ca2+]i and relaxation. However, pirenzepine (0.1 microM), AF-DX 116 (1 microM) and tropicamide (1 microM) were ineffective. The ACh-induced increase of [Ca2+li and vasorelaxation was significantly reduced by 3 microM gadolinium, 10 microM lanthanum or 10 microM SKF 96365. These results suggest that, in rabbit renal artery, ACh-evoked relaxation of 100 mM K+-induced contractions is mediated by the release of endothelial NO. ACh may stimulates the M3 subtype of muscarinic receptor in the endothelial cells, resulting in the opening of the nonselective cation channels followed by an increase of [Ca2+]i and stimulation of NO synthase.

NO donor sodium nitroprusside inhibits excitation-contraction coupling in guinea pig taenia coli.

In guinea pig taenia coli, the nitric oxide (NO) donor sodium nitroprusside (SNP, 1 microM) reduced the carbachol-stimulated increases in muscle force in parallel with a decrease in intracellular Ca(2+) concentration ([Ca(2+)](i)). A decrease in the myosin light chain phosphorylation was also observed that was closely correlated with the decrease in [Ca(2+)](i). With the patch-clamp technique, 10 microM SNP decreased the peak Ba(2+) current, and this effect was blocked by an inhibitor of soluble guanylate cyclase. Carbachol (10 microM) induced an inward current, and this effect was markedly inhibited by SNP. SNP markedly increased the depolarization-activated outward K(+) currents, and this current was completely blocked by 0.3 micorM iberiotoxin. SNP (1 microM) significantly increased cGMP content without changing cAMP content. Decreased Ca(2+) sensitivity by SNP of contractile elements was not prominent in the permeabilized taenia, which was consistent with the [Ca(2+)](i)-force relationship in the intact tissue. These results suggest that SNP inhibits myosin light chain phosphorylation and smooth muscle contraction stimulated by carbachol, mainly by decreasing [Ca(2+)](i), which resulted from the combination of the inhibition of voltage-dependent Ca(2+) channels, the inhibition of nonselective cation currents, and the activation of Ca(2+)-activated K(+) currents.

The involvement of K+ channels and the possible pathway of EDHF in the rabbit femoral artery.

Experiments were designed to characterize the cellular mechanisms of action of endothelium-derived vasodilator substances in the rabbit femoral artery. Acetylcholine (ACh, 10(-8)-10(-5) M) induced a concentration-dependent relaxation of isolated endothelium-intact arterial rings precontracted with norepinephrine (NE, 10(-6) M). The ACh-induced response was abolished by the removal of endothelium. NG-nitro-L-arginine (L-NAME, 10(-4) M), an inhibitor of NO synthase, partially inhibited ACh-induced endothelium-dependent relaxation, whereas indomethacin (10(-5) M) showed no effect on ACh-induced relaxation. 25 mM KCl partially inhibited ACh-induced relaxation by shifting the concentration-response curve and abolished the response when combined with L-NAME and NE. In the presence of L-NAME, ACh-induced relaxation was unaffected by glibenclamide (10(-5) M) but significantly reduced by apamin (10(-6) M), and almost completely blocked by tetraethylammonium (TEA, 10(-3) M), iberiotoxin (10(-7) M) and 4-aminopyridine (4-AP, 5 x 10(-3) M). The cytochrome P450 inhibitors, 7-ethoxyresorufin (7-ER, 10(-5) M) and miconazole (10(-5) M) also significantly inhibited ACh-induced relaxation. Ouabain (10(-6) M), an inhibitor of Na+, K(+)-ATPase, or K(+)-free solution, also significantly inhibited ACh-induced relaxation. ACh-induced relaxation was not significantly inhibited by 18-alpha-glycyrrhetinic acid (18 alpha-GA, 10(-4) M). These results of this study indicate that ACh-induced endothelium-dependent relaxation of the rabbit femoral artery occurs via a mechanism that involves activation of Na+, K(+)-ATPase and/or activation of both the voltage-gated K+ channel (Kv) and the large-conductance, Ca(2+)-activated K+ channel (BKCa). The results further suggest that EDHF released by ACh may be a cytochrome P450 product.

Position paper of the American Council on Science and Health: lead and human health.

The potential human health risk of lead in the environment remains a topic of current debate and concern. Given sufficient exposure, lead can exert severe and chronic health effects. Today, due to successful efforts to reduce the commercial use of lead and control its release to the environment, lead "poisoning" is uncommon in our society. Blood-lead levels among the U.S. population, including those of children, have decreased dramatically over the past decade and according to current surveillance programs continue to decline. Because lead poisoning among children is no longer as prevalent as it once was, the focus has shifted to the long-term effects lead may exert on the intellectual development of children. Continued toxicological and epidemiological research will expand the understanding of this important facet of the lead issue. Trace levels of lead in consumer products remain a low health risk to humans, despite the fear and uncertainty which often accompany such concerns. Future efforts to reduce lead exposure should be aimed at high-risk groups which include the socioeconomically disadvantaged and certain minority sectors of the population. Through educational programs, improvement in personal hygiene practices, and abatement of lead-containing paint (when warranted), blood lead levels should continue to decline, reducing the health risk to lead in the environment.

Isoproterenol changes the relationship between cytosolic Ca2+ and contraction in guinea pig taenia caecum.

To determine the role of beta-adrenoceptors in the regulation of intestinal smooth muscle, the action of isoproterenol (ISO) on cytoplasmic Ca2+ level ([Ca2+]cyt) and mechanical activity in the isolated guinea pig taenia caecum was examined. Spontaneous changes in [Ca2+]cyt and contraction were inhibited by ISO (0.1-1 microM) without changing resting [Ca2+]cyt. ISO more strongly inhibited the histamine-induced contraction than the high K(+)-induced contraction. ISO inhibited muscle tension more strongly than [Ca2+]cyt stimulated by high K+ and thus shifted the [Ca2+]cyt-tension curve to the lower-right. In the muscle stimulated by histamine, on the other hand, ISO inhibited both [Ca2+]cyt and tension. Salbutamol, a beta 2-selective agonist, showed similar effects as ISO on spontaneous, high K(+)- and histamine-stimulated [Ca2+]cyt and tension. Stimulation of beta-adrenoceptors by ISO increased cyclic AMP content without changing cyclic GMP content. These results suggest that activation of beta 2-adrenoceptors by ISO inhibits the contractions by two mechanisms of action: decrease in Ca2+ sensitivity of contractile elements in the muscle stimulated by K(+)-depolarization and decrease in [Ca2+]cyt in the muscle stimulated by histamine. These effects may be mediated by cyclic AMP.

Membrane potential and current responses to neurotensin in the longitudinal muscle of the rectum of the fowl.

1. The effects of neurotensin (NT) on membrane potential and membrane current of the longitudinal smooth muscle of chicken rectum were investigated by intracellular recording and whole-cell voltage clamp. 2. NT (3 nM-1.2 microM), when applied via the bathing medium, produced a concentration-dependent membrane depolarization with an EC50 of 18 +/- 2 nM (n = 7) which was accompanied by an increase in the membrane conductance. The effect was biphasic: an initial, rapid depolarization reached a peak within 2-3 min and then declined to a lower but still elevated level which was sustained until washout. 3. Excitatory junction potentials (e.j.ps), which were non-adrenergic non-cholinergic (NANC) in nature, were decreased in amplitude and total duration in the presence of NT (0.6 microM). The depression of the e.j.p. was due mainly to the reduction of the membrane resistance. 4. When NT was applied locally by means of pressure ejection from a micropipette containing NT, some cells responded with a membrane depolarization and some failed to respond, whereas e.j.ps could invariably be elicited from all of them. 5. In single muscle cells enzymatically isolated from the muscle and dialyzed under voltage clamp at -50 mV with a CsCl-rich solution, NT (5 or 10 microM) produced an inward current. NT-induced inward currents were obtained with inclusion of 10 mM EGTA in the pipette solution and their reversal potential was around 0 mV. In cells dialyzed under voltage clamp at 0 mV with a KCl-rich solution, NT (5 microM) produced a brief outward current followed by abolition of spontaneous transient outward currents.6. The present results suggest that the membrane depolarization, which may arise from activation of non-selective cation channels, and release of calcium from internal stores produced by neurotensin are responsible for its contractile activity in the longitudinal smooth muscle of chicken rectum. Further, the depolarizing effect may provide support for the involvement of NT in the NANC transmission in this preparation.

Changes in cytosolic CA2+ and contraction induced by various stimulants and relaxants in canine tracheal smooth muscle.

Effects of stimulants and relaxants on the cytosolic Ca2+ level [(Ca2+]cyt) and contraction were examined in isolated canine tracheal smooth muscle. High K+ and carbachol induced a sustained increase in [Ca2+]cyt and muscle tension. Cumulative addition of KCl induced a graded increase in [Ca2+]cyt and muscle tension. Cumulative addition of carbachol induced greater contraction than high K+ at a given [Ca2+]cyt 12-Deoxyphorbol 13-isobutyrate (DPB) (50 nmol/l) induced a small sustained contraction with little effect on [Ca2+]cyt. A higher concentration (1 mumol/l) of DPB induced a larger sustained contraction with a decrease in [Ca2+]cyt. DPB (50 nmol/l) potentiated the KCl-induced contraction without or with only a small additional increase in [Ca2+]cyt. By contrast, 1 mumol/l DPB potentiated the high-K(+)-induced contraction with a decrease in [Ca2+]cyt. Addition of 50 nmol/l or 1 mumol/l DPB in the presence of carbachol inhibited both [Ca2+]cyt and muscle tension. Verapamil, isoprenaline and forskolin did not change or slightly decreased [Ca2+]cyt and muscle tension in resting trachea. Verapamil inhibited the contraction and [Ca2+]cyt stimulated by high K+ and carbachol. Isoprenaline and forskolin inhibited the high-K(+)-induced contraction without changing [Ca2+]cyt, whereas these inhibitors inhibited carbachol-induced contraction with a relatively small decrease in [Ca2+]cyt. These results suggest that (a) sustained contractions induced by high K+ and carbachol are due to the sustained increase in [Ca2+]cyt, (b) carbachol increases the sensitivity of contractile elements to Ca2+, and (c) isoprenaline and forskolin inhibit the contraction by the decrease in [Ca2+]cyt and also by the decrease in the sensitivity of contractile elements to Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of endothelin on the mechanical activity and cytosolic calcium level of various types of smooth muscle.

1. Effects of porcine/human endothelin (endothelin-1), a novel vasoconstrictor peptide, on various smooth muscles were examined. 2. In rat aorta, endothelin (1 pM-30nM) induced contraction in a concentration-dependent manner. Removal of endothelium shifted the concentration-response curve to the left. When added during the sustained contraction induced by 0.1 microM noradrenaline, endothelin (1 nM) induced a relaxation that was inhibited by removing endothelium or by methylene blue. 3. In rat aorta without endothelium, endothelin (1-30 nM) increased cytosolic Ca2+ level [( Ca2+]cyt) followed by contraction. Endothelin induced less contraction than high K+ at a given [Ca2+] cyt when the concentration of endothelin was lower (1-3nm) and/or during the early phase of the contraction (less than 10 min). In contrast, endothelin induced a greater contraction than KCl after prolonged exposure to high concentrations (greater than 10 nM). 4. The increase in [Ca2+]cyt due to endothelin was strongly inhibited by 10 microM verapamil or 0.3 microM nicardipine although muscle contraction was only partially inhibited. 5.In Ca2+ -free solution, endothelin (30 nM) induced a transient increase in [Ca2+] cyt and a slow increase in muscle tension. After a prolonged incubation in Ca2+-free solution, endothelin (30 nM) still induced a slow increase in tension without changing [Ca2+]cyt. This contraction was inhibited by 1 microM sodium nitropusside or 10 microM forskolin. 6. In canine trachea and guinea-pig uterus, endothelin (30 nM) induced sustained contraction with an increase in [Ca2+]cyt. In the absence of external Ca2+, endothelin (30 nM) induced a sustained contraction in canine trachea without changing [Ca2+]cyt. In guinea-pig vas deferens, taenia caeci and ileal longitudinal muscle, endothelin induced small increases in [Ca2+]cyt and tension. 7. In permeabilized smooth muscles, endothelin (30 nM) did not change the muscle tone. 8. These results suggest that endothelin acts on the endothelium and increases the synthesis or release of endothelin-derived relaxing factor (EDRF). These results also suggest that endothelin acts directly on smooth muscle and increases [Ca2+]cyt by releasing Ca2+ from sites and increasing Ca2+ influx through the verapamil- and 1,4-dihydropyridine-sensitive pathway. Endothelin seems to decrease Ca2+ -sensitivity of contractile elements at lower concentrations and/or during the early phase of the contraction, whereas it increases Ca2+ -sensitivity at higher concentrations during the sustained phase of the contraction. Furthermore, endothelin induces a contraction that is not dependent on [Ca2+]cyt.

Possible role of plasma neurotensin in regulating the excitatory neural control of the rectum of the fowl.

Effects of neurotensin (NT) applied via the blood vessel on the responses to stimulation of Remak's nerve (RNS) were investigated in the chicken isolated and perfused rectums. NT (5 ng-2 micrograms/ml) produced a concentration-dependent inhibition of the constituent contraction but not relaxation of the responses to RNS. In addition, high concentrations of NT (over 80 ng/ml) produced a contraction of the rectal muscle. Propranolol, a beta-adrenoceptor blocking agent, and guanethidine, an adrenergic neurone blocking agent, were able to reduce the inhibitory effect of NT on the response to RNS while potentiating the contractile effect of NT on the rectal muscle. NT (0.1 and 1 microgram/ml), like norepinephrine, decreased the flow rate of perfusate from the isolated rectum which was perfused at a constant pressure. Guanethidine enhanced norepinephrine-induced vasoconstriction, and phentolamine, an alpha-adrenoceptor blocking agent, plus propranolol was able to abolish it. Either of these prior applications resulted in a small but significant reduction of NT-induced vasoconstriction. These findings suggest that NT in plasma may function as a circulating hormone to exhibit an inhibitory action on the excitatory neural input to the rectum in the chicken, and that catecholamine release from adrenergic nerve terminals by NT may account for some but not all of the activity.

Effects of prolonged exposure to alpha,beta-methylene ATP on non-adrenergic, non-cholinergic excitatory transmission in the rectum of the chicken.

1. Effects of prolonged exposure to alpha,beta-methylene ATP (alpha,beta-Me ATP) on contractions and excitatory junction potentials (e.j.ps) evoked by non-adrenergic, non-cholinergic (NANC) excitatory nerve stimulation have been investigated in the chicken isolated rectum and longitudinal muscle strip from chicken rectum pretreated with atropine (0.5 microM), methysergide (2 microM) and pyrilamine (3 microM). 2. Alpha,beta-Me ATP (20 nM-4 microM) caused a rapid rise in tension of the longitudinal muscle of the isolated rectum preparation which returned to the baseline levels after a few minutes. The magnitude of the contractile response to NANC nerve stimulation was reduced after exposure to the drug. The inhibitory effect was related to the drug concentration; at 4 microM the nerve-mediated contraction was abolished and frequently converted to a relaxation. 3. Adenosine 5'-triphosphate (ATP, 100 microM), bovine neurotensin (2.5 nM) and K+-rich solutions (30 nM and 60 nM) all produced a transient contraction of the isolated rectum preparation. The exposure to alpha,beta-Me ATP (0.2 and 4 microM) also rendered the preparation less sensitive to these stimulant substances. 4. Alpha,beta-Me ATP (0.2 and 4 microM) caused a membrane depolarization in cells of the longitudinal muscle strip. The depolarization reached a peak within 2-3 min after application and then decayed to a steady level that was still more positive than the baseline level. The electrotonic potentials were reduced in amplitude to 44 +/- 8% (n = 7) of the normal amplitude if measured at the peak depolarization produced with 0.2 microM alpha,beta-Me ATP, and to 62 +/- 10% (n = 7) if measured at the steady-state depolarization. With 4 microM, the corresponding percentages were 33 +/- 7% (n = 8) and 55 +/- 7% (n = 8), indicating a decrease in membrane resistance. 5. The e.j.ps in response to field stimulation of the intramural nerves and Remak's nerve stimulation were decreased in amplitude and duration during exposure to alpha,beta-Me ATP (0.2 and 4 microM). 6. The smooth muscle cells regained normal membrane resistance and sensitivity to ATP on washout of alpha,beta-Me ATP (4 microM) more rapidly than the responses to NANC nerve stimulation. 7. It can be argued from the results that the suppression by alpha,beta-Me ATP of the contraction and e.j.p. evoked by NANC nerve stimulation in the chicken rectum, unlike the mammalian preparation described previously, is due mainly to a change in the electrical properties of the membrane of the smooth muscle cells, rather than being due, or only partly due, to desensitization of the purine receptor.