Sympathetic neuroeffector transmission in the rat anococcygeus muscle

Bramich, Narelle J.; Hirst, G. D. S.

doi:10.1111/j.1469-7793.1999.101aa.x

Cited by 11 publications

(12 citation statements)

References 33 publications

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“…In contrast to the parenchyma, transmural nerve stimulation initiated α‐adrenergic EJPs which are composed of two components in the sac; the initial, rapid component and the second slow component which lasted for over 10 s. Similar sequences of membrane potential change occur following sympathetic nerve stimulation in the rat anococcygeus muscle (Bramich & Hirst, 1999). EJPs often triggered action potentials and caused oscillatory contractions.…”

Section: Discussionmentioning

confidence: 94%

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Hashitani

2000

The Journal of Physiology

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Using intracellular recording techniques, two distinct layers of smooth muscle were identified in the rat penile bulb. The inner muscle layer (parenchyma) exhibited spontaneous action potentials, while the outer sheet (sac) was electrically quiescent. In the parenchyma, transmural stimulation initiated non‐adrenergic, non‐cholinergic (NANC) inhibitory junction potentials (IJPs) which were abolished by Nωnitro‐L‐arginine (LNA) or 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ). The amplitude of IJPs was reduced by ouabain, dinitrophenol or decreasing the extracellular potassium concentration ([K+]o) but not by several K+ channel blockers. The parenchyma also received an excitatory innervation mediated by α‐adrenoceptors which caused a contraction that was not associated with a membrane potential change. In the sac, transmural stimulation initiated two component excitatory junction potentials (EJPs) mediated by α‐adrenoceptors and associated action potentials. The initial component was more dramatically suppressed than the secondary component by caffeine, ryanodine or cyclopiazonic acid (CPA). Lowering of the extracellular chloride concentration ([Cl−]o) selectively inhibited the rapid component of EJPs, while niflumic acid was less potent. These results suggest that IJPs in the parenchyma result from the release of NO which stimulates sodium pump activity following the activation of guanylate cyclase. In the sac, the activation of α‐adrenoceptors initiates EJPs by releasing Ca2+ from intracellular stores which activates Ca2+‐activated channels.

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Section: Discussionmentioning

confidence: 94%

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Hashitani

2000

The Journal of Physiology

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“…The simplest explanation for these observations is that NA increases the sensitivity of contractile proteins to calcium as reported in vascular smooth muscles (Kitazawa et al 1988, 1991). Alternatively, calcium released from intracellular stores has better access to contractile proteins, and thus triggers contraction more readily than calcium which enters via calcium channels as proposed for other smooth muscles (Morgan & Morgan, 1984; Bramich & Hirst, 1999).…”

Section: Discussionmentioning

confidence: 99%

Cellular mechanisms of nitric oxide‐induced relaxation of corporeal smooth muscle in the guinea‐pig

Hashitani

Fukuta

Dickens

et al. 2002

The Journal of Physiology

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The cellular mechanism of nitric oxide (NO)‐induced relaxation in corporeal smooth muscle (CSM) of the guinea‐pig was investigated. Changes in the intracellular concentration of calcium ions ([Ca2+]i), membrane potential and isometric tension were measured. CSM cells exhibited spontaneous depolarizations and transient increases in [Ca2+]i (Ca2+ transients) which were accompanied by contractions. This spontaneous activity was abolished by nifedipine (10 μm). NO released by 3‐morpholino‐sydnonimine (SIN‐1, 10 μm) hyperpolarized the membrane and prevented the generation of spontaneous depolarizations. SIN‐1 also abolished Ca2+ transients and associated contractions. These effects of SIN‐1 were blocked by 1H‐[1,2,4]oxadiazole[4,3‐a]quinoxalin‐1‐one (ODQ, 10 μm), an inhibitor of guanylate cyclase. Noradrenaline (NA, 1 μm) increased [Ca2+]i to levels similar to those produced by high potassium‐containing solution (high K+ solution, [K+]o= 40 mm), however, NA‐induced contractions were three times greater in amplitude than those induced by high K+ solution. In NA precontracted preparations, SIN‐1 inhibited 80 % of the contraction and decreased [Ca2+]i by 20 %. In contrast, nifedipine reduced [Ca2+]i by 80 %, while the level of contraction was decreased by only 20 %. SIN‐1‐induced reduction in [Ca2+]i but not the tension effect, was abolished by pretreatment with cyclopiazonic acid (CPA, 10 μm). In high K+ precontracted preparations, SIN‐1 inhibited 80 % of the contraction and reduced [Ca2+]i by 20 %. Nifedipine, however, largely abolished increases in both [Ca2+]i and tension under these circumstances. These results suggest that decreasing the sensitivity of contractile proteins to Ca2+ is probably the key mechanism of NO‐induced relaxation in CSM of the guinea‐pig.

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“…In some experiments, changes in [Ca 2ϩ ] i were determined as described previously (4). In brief, preparations were loaded with fura PE3 and subsequently illuminated with light of two wavelengths (340 and 380 nm), alternating at a frequency of 12 Hz.…”

Section: Methodsmentioning

confidence: 99%

Vagal inhibition in the antral region of guinea pig stomach

Dickens

Edwards

Hirst

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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The effects of vagal stimulation in the presence of a muscarinic antagonist were examined on three distinct rhythmically active cells located in guinea pig antrum. Vagal stimulation inhibited contractions of the circular muscle layer but did not change their rate of occurrence. With the use of intracellular recording techniques, these stimuli were found to initiate inhibitory junction potentials in the circular layer but produced smaller potential changes in driving and follower cells. Inhibition of the circular muscle layer involved two separate components. The dominant component was independent of changes in membrane potential and was abolished by nitro-L-arginine. After abolishing Ca(2+) entry into smooth muscle cells with a Ca(2+) antagonist, vagal stimulation continued to inhibit the residual contractions associated with each slow wave. When the cyclic changes in intracellular Ca(2+) concentration associated with each slow wave were measured, they were found to be unchanged by vagal stimulation. The observations suggest that vagal inhibition of stomach movements does not alter pacemaker activity in the stomach; rather, it results from a change in the sensitivity of smooth muscle contractile proteins to Ca(2+).

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Sympathetic neuroeffector transmission in the rat anococcygeus muscle

Cited by 11 publications

References 33 publications

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb

Cellular mechanisms of nitric oxide‐induced relaxation of corporeal smooth muscle in the guinea‐pig

Vagal inhibition in the antral region of guinea pig stomach

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