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A Brading

Publications and source records attributed to A Brading.

6 recordsLinked to original sources
PubMed1993

In vitro response of the human anal canal longitudinal muscle layer to cholinergic and adrenergic stimulation: evidence of sphincter specialization.

A study was performed to determine the in vitro response of the longitudinal smooth muscle layer (conjoined longitudinal coat) of the human and canal to cholinergic and adrenergic stimulation, and to compare this with similar features of the internal anal sphincter (IAS) and rectal smooth muscle. Tissue was obtained from abdominoperineal and anterior resection specimens, and strips of muscle mounted for isometric tension recording in superfusion organ baths. Both conjoined longitudinal coat and IAS strips generated and maintained spontaneous myogenic tension (mean(s.e.m.) 0.10(0.01) and 0.48(0.04) g per mg tissue respectively), whereas equivalent rectal smooth muscle did not. Stimulation of muscarinic (cholinergic) receptors caused contraction of strips from the conjoined longitudinal coat and rectal smooth muscle layers in a dose-dependent manner (10(-7)-10(-4) mol/l); however, IAS strips relaxed (10(-6)-10(-4) mol/l). Activation of alpha-adrenergic receptors in conjoined longitudinal coat and IAS strips produced concentration-dependent contraction (10(-7)-10(-4) mol/l). In comparison, rectal smooth muscle relaxed. All muscle layers relaxed in response to beta-adrenoceptor stimulation. These data indicate that in the anal canal both the conjoined longitudinal coat and IAS are specialized sphincteric smooth muscles.

Aged↗
PubMed1993

Nerve mediated relaxation of the human internal anal sphincter: the role of nitric oxide.

The aim of this study was to determine if nitric oxide (NO) is the non-adrenergic, non-cholinergic neurotransmitter, released by enteric inhibitory nerves, which mediates relaxation of the human internal anal sphincter. Isolated muscle strips were mounted for isometric tension recording in superfusion organ baths. Sodium nitroprusside, an exogenous donor of NO, relaxed the strips in a concentration dependent manner. In the presence of atropine and guanethidine, transmural field stimulation produced tetrodotoxin sensitive relaxations, which were inhibited in a dose dependent and enantiomer specific manner by antagonists of NO synthase; completely by L-nitroarginine and partially by L-N-monomethyl arginine. The effect of these antagonists was reversed by L-arginine but not D-arginine. Oxyhaemoglobin, a scavenger of nitric oxide, also abolished the relaxations but methaemoglobin had no such effect. These results strongly suggest that NO is, or is very closely associated with, the non-adrenergic, non-cholinergic neurotransmitter mediating neurogenic relaxation of the human internal anal sphincter.

Aged↗
PubMed1969

The effect of temperature on the membrane conductance of the smooth muscle of the guinea-pig taenia coli.

1. The effect of temperature on the membrane conductance of the smooth muscle of guinea-pig taenia coli was investigated electrophysiologically, using the double sucrose gap method, and by ion-flux determinations.2. In the range between 19 degrees C and 37 degrees C, the membrane conductance increased with rising temperature and decreased with cooling (Mean Q(10) about 2.5).3. When the Cl concentration in the external medium was low (Cl(-) substitution with benzene-sulphonate), the effect of changing the temperature was smaller (Mean Q(10) about 1.5).4. In muscle depolarized by excess K (27 mM) in a solution containing low Cl, cooling repolarized the membrane and markedly increased membrane resistance.5. The slow phases of the (42)K- and (36)Cl-exchange were greatly slowed by cooling which did not change the rate constants of the (24)Na-efflux curve. Thus observations on the rate of exchange of ions agreed with the electrophysiological findings indicating a reduction of K- and Cl-conductance of the cell membrane at low temperature.6. The depolarization produced by lowering the external Ca-concentration was greatest at high temperature (37 degrees C). With cooling the membrane was repolarized and membrane resistance increased.7. The sustained state of depolarization observed when the external Ca was replaced by Ba (2.5 mM) at high temperature (37 degrees C) was terminated by cooling.8. The observations may be interpreted by the hypothesis that Ca, located at two different membrane sites, controls, independently, at the outer layer mainly Na- (and Ba-) permeability and at the inner layer mainly K-permeability, the Ca-binding at these sites being affected by temperature in the opposite direction.

Animals↗
PubMed1969

The effect of sodium and calcium on the action potential of the smooth muscle of the guinea-pig taenia coli.

1. Spontaneous spike activity and action potentials evoked by external field stimulation were recorded, intracellularly and with the double sucrose gap method, from the smooth muscle of guinea-pig taenia coli.2. Replacement of external NaCl with sucrose (leaving 10 mM-Na in the buffer) caused hyperpolarization and stopped spontaneous activity within 10 min. Spikes could, however, be evoked for 2-3 hr. The amplitude, the overshoot and rate of rise of the spike were increased.3. In 10 mM-[Na](o) the intracellular Na concentration was reduced from 35 to 24 mM, shifting the Na-equilibrium potential from +34 to -22 mV.4. Excess Ca (12.5 mM) caused hyperpolarization and increased membrane conductance. The amplitude and the rate of rise of the spike were increased, the threshold was raised and the latency of the spike evoked by threshold stimulation became shorter.5. The effect of reducing the external Ca concentration depended on the Na concentration present, being greater with higher external [Na](o). When the membrane was depolarized and spikes deteriorated in low Ca (0.2-0.5 mM) reduction of Na to 10 mM caused repolarization and recovery of the action potential.6. Mn (0.5-1.0 mM) blocked spontaneous spike discharge after 20 min. Higher concentrations (more than 2.0 mM) were required to block the evoked action potential.7. The results indicate that the smooth muscle spike in taenia is due to Ca-entry and that Na influences spike activity indirectly by competing with Ca in controlling the membrane potential.

Action Potentials↗