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Biomedical subjects

J M Noble

Publications and source records attributed to J M Noble.

24 records · Page 2Linked to original sources
PubMed1992

Atriopeptin: an endogenous corticotropin-release inhibiting hormone.

Activation of the hypothalamic-pituitary-adrenocortical axis is a major component of the body's response to stress. Current theories on the pathophysiology of disorders associated with hyperfunction of the axis, such as depression and Cushing's stress, are based on the concept that anterior pituitary adrenocorticotropin (ACTH) secretion is stimulated by hypothalamic corticotropin-releasing hormones and inhibited by adrenal corticosteroids. Hypothalamic inhibitory control of pituitary ACTH secretion has been also postulated, but has not gained general acceptance because of the lack of definitive evidence for a corticotropin-release inhibiting hormone. It is shown here that in conscious rats stress-induced secretion of ACTH and corticosterone is markedly enhanced by the immunoneutralisation of atriopeptin. Therefore, we propose that atriopeptin is a physiologically relevant corticotropin-release inhibiting hormone.

Adrenal Cortex↗
PubMed1991

Acceptance of quantity recipes with zero added salt by a military population.

The average civilian young man consumes approximately 5.5 g sodium daily in food plus an additional 20% as added salt. The average intake of military personnel may exceed this civilian level. The Surgeons General of the Military Services established 1,700 mg sodium per 1,000 kcal as the goal for sodium content in menus served in military dining facilities. We tested the acceptability of quantity recipes with zero added salt and control recipes with added salt in military dining facilities. Twenty-eight test recipes with zero added salt were prepared and offered on the regular serving line. Military personnel selecting the test items rated them for acceptability on a nine-point hedonic scale. Only 6 of the 28 recipes with zero added salt were rated significantly less acceptable than the control recipes. Chemical analysis of the test recipes showed an 11% to 87% reduction in sodium and a 28% to 80% reduction in chloride. Our results indicate that dietitians and/or foodservice managers can produce quantity food recipes that are reduced in sodium and acceptable to customers.

Chlorides↗
PubMed1985

The secretory action of barium chloride in rat colon.

BaCl2, applied serosally, caused a rise in the p.d. and short-circuit current (s.c.c), and a decrease in tissue resistance in stripped sheets of rat colon. This response was dose dependent. Mucosal application of BaCl2 was without effect. The BaCl2-induced rise in s.c.c. was inhibited by reducing the serosal Na+ concentration to 25 mM. Lowering the mucosal Na+ concentration was without effect. Ouabain (10(-3) M in serosal fluid) and furosemide (10(-3) M in serosal fluid) both reduced the rise in s.c.c. induced by BaCl2. Flux determinations indicated that BaCl2 inhibited Na+ absorption and stimulated Cl- secretion by the colon. In vivo, BaCl2 increased fluid accumulation within the colonic lumen, an effect that was associated with a rise in the transcolonic p.d. Increasing the serosal K+ concentration to 20 mM reduced the responses to BaCl2, acetylcholine and theophylline, and this could not be entirely accounted for by the concomitant reduction in the serosal Na+ concentration. As high serosal K+ did not mimic the secretory response it would appear that BaCl2 does not act by blocking K+ channels. The rise in s.c.c. induced by BaCl2 was not reduced by Ca2+-free conditions, but it was inhibited by 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) and trifluoperazine. BaCl2 did not alter cyclic AMP production by colonic scrapes. It is concluded that BaCl2 induces colonic secretion by the release of intracellular Ca2+, which then combines with calmodulin to activate the secretory process.

Action Potentials↗
PubMed1984

The involvement of calcium in the intestinal response to secretagogues in the rat.

The involvement of Ca2+ in the regulation of intestinal secretion was investigated in stripped sheets of rat mid-intestine. Removal of serosal Ca2+ together with the addition of EGTA at concentrations of 0.5 and 1 mM inhibited the rise in short-circuit current (s.c.c.) induced by both acetylcholine and theophylline, a similar degree of inhibition being observed with both secretagogues. Ca2+-free serosal fluid with 0.5 mM-EGTA added reduced significantly the rises in s.c.c. induced by A23187, acetylcholine, 5-hydroxytryptamine, theophylline, dibutyryl cyclic AMP and prostaglandin E2, but not the increased s.c.c. associated with glucose absorption. The Ca2+ channel blocker verapamil produced similar results. The calmodulin antagonist trifluoperazine inhibited secretagogue action while its sulphoxide derivative was without effect at the same concentration. The intracellular Ca2+ antagonist TMB-8 reduced the increased s.c.c. observed with acetylcholine and dibutyryl cyclic AMP. The net Cl- secretion, but not the decreased mucosal-to-serosal Na+ flux, induced by acetylcholine was abolished in Ca2+-free conditions. There was no consistent effect on the reduction in the residual ion flux caused by acetylcholine. Absence of Ca2+ converted the stimulation of Cl- secretion induced by dibutyryl cyclic AMP observed under control conditions to an enhancement of net Na+ and Cl- absorption. It is concluded that intestinal secretagogues, whether they act through cyclic AMP or not, require both internal and external sources of Ca2+ if they are to produce their full effects. Moreover, it appears that the nature of the response to dibutyryl cyclic AMP depends on the prevailing Ca2+ concentration.

Acetylcholine↗
PubMed1983

The effect of barium chloride on intestinal secretion in the rat.

The addition of BaCl2 to the serosal solution, at concentrations from 0 X 25 mM to 10 mM, caused increases in potential difference, short-circuit current and resistance across stripped sheets of rat mid-intestine, although mucosal application had little effect. The response to BaCl2 was significantly greater than that obtained with the same concentration of CaCl2. An increase in net Cl- secretion entirely accounted for the rise in short-circuit current induced by BaCl2. BaCl2 inhibited net fluid uptake by everted sacs. It also enhanced the accumulation of fluid by intestinal loops in vivo and this was associated with an increased potential difference. The response to BaCl2 in vitro was not reduced in the absence of serosal Ca2+ ions. The effect of BaCl2 was abolished by trifluoperazine and also by TMB-8 (8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride). BaCl2 did not alter cyclic AMP production by isolated enterocytes. It is concluded that BaCl2 induces intestinal secretion by releasing Ca2+ from intracellular stores which then combines with calmodulin to stimulate the secretory process.

Animals↗