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D G Ward

Publications and source records attributed to D G Ward.

40 records · Page 3Linked to original sources
PubMed1976

Role of atrial receptors in the control of ACTH.

Sinusoidal volume changes (+/- 1 ml) were applied at 1 Hz to the right or left atrium of 25 anesthetized cats. Changes in firing rates of single vagal fibers and in plasma ACTH and cortisol were observed in response to start and stop of atrial pulsation. Decreased activity of right atrial and/or septal B-receptors was associated with increased ACTH. Changes in left atrial B-receptor activity were associated with a change in ACTH only if right atrial/septal receptors or baroreceptors also changed their activity in the same direction. The activity of atrial A-receptors did not change in response to atrial pulsation. A quantitative analysis suggested strongly that right atrial and/or septal B-receptors dominate in the response of ACTH to hemodynamic stimuli. Arterial receptors appear less effective, and left atrial B-receptors appear least effective in the hemodynamic control of ACTH.

Adrenocorticotropic Hormone↗
PubMed1976

Inhibitory and facilitatory areas of the dorsal medulla mediating ACTH release in the cat.

To define the role of the dorsal medulla in the control of release of ACTH, the authors stimulated electrically (30 sec, 100 muA, 50 Hz) 50 sites in the vicinity of the solitary nuclei of 11 cats anesthetized with chloralose/urethane. Responses of arterial pressure to electrical stimulation were not correlated significantly with release of ACTH. Indirect effects of changes in arterial pressure could not explain changes in release of ACTH. Concentrations of ACTH were measured by radioimmunoassay. Active areas associated with the solitary nucleus were : 1) lateral inhibitory: ventral and lateral to the solitary tract (mean delta ACTH:-153, -86, -97 pg/ml at 1.5, 3.0 and 6.0 min respectively; P less than 0.01); 2) medial inhibitory: medial dorsal motor nucleus of the vagus and extending to the midline (mean delta ACTH: -81, -107, -67 pg/ml; P less than 0.01); and 3) intermediate facilitatory: lateral nucleus intercalatus and adjacent reticular formation (mean delta ACTH: +105, +158, +4 pg/ml; P less than 0.01). The former two areas contain neurons activated by atrial stretch, and the latter area contains neurons inhibited by atrial stretch. Since changes in ACTH levels are inversely correlated with atrial stretch, the results suggest that the changes in release of ACTH are the result of direct stimulation of neural systems of the solitary nuclei mediating release of ACTH in response to hemodynamic changes.

Adrenocorticotropic Hormone↗
PubMed1976

Inhibitory and facilitatory areas of the rostral pons mediating ACTH release in the cat.

To define the role of the rostral pons in the control of release of ACTH, we stimulated electrically (30 sec, 200 muA, 50 Hz) 128 sites in the dorsal rostral pons of 20 cats anesthetized with chloralose/urethane. Responses of arterial pressure to electrical stimulation were prevented by lesions placed previously in the medulla. Plasma concentrations of ACTH were measured by radioimmunoassay. Active areas consisted of three regions: 1) lateral inhibitory: Locus subcoeruleus and anteroventral locus coeruleus (mean deltaACTH: -189, -164, -145 pg/ml at 1.5,3.0 and 6.0 min respectively, P less than 0.01);2) intermediate facilitatory:principal locus coeruleus and lateral ventral tegmental nucleus (mean deltaACTH: +81, +68, +37 pg/ml; P less than 0.05); and 3) medial inhibitory: dorsal tegmental nucleus, dorsal raphé and medial ventral tegmental nucleus (mean deltaACTH; -211, -212, -115 pg/ml; P less than 0.01). The former two areas received direct projections from medullary neurons activated or inhibited by atrial stretch, and, in turn, give rise to adrenergic and cholinergic projections to the medial hypothalamus. Since the release of ACTH is inversely correlated with right atrial stretch, the results suggest that the lateral inhibitory area and the intermediate facilitatory area are involved in mediation of changes in release of ACTH in response to hemodynamic changes.

Adrenocorticotropic Hormone↗