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Biomedical subjects

G A Hedge

Publications and source records attributed to G A Hedge.

70 records · Page 4Linked to original sources
PubMed1976

Correlation between hypothalamic catecholamine synthesis and ether stress-induced ACTH secretion.

The rates of synthesis of norepinephrine (NE) and dopamine (DA) in several regions of the hypothalamus have been estimated after exposure of rats to stresses that increase ACTH secretion. The rate of 3H-NE and 3H-DA accumulation from 3H-tyrosine in vitro was used as an index of catecholamine synthesis rates. Exposure to ether vapor, 30 min of cold environment, or laparotomy increased ACTH secretion significantly, as indicated by plasma corticosterone levels. However, only the ether stress affected hypothalamic catecholamines; both NE and DA synthesis rates were increased in the arcuate nucleus are (ANA), but not in the median eminence (ME) or the residual hypothalamus (RH). Dexamethasone treatment blocked the stress-induced ACTH secretion, but had no affect on basal or stress-induced rates of amine synthesis. It is concluded that catecholamines in the ANA participate in mediating ether stress-induced ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1976

Suppression of thyrotropic hormone secretion by prostaglandin synthesis inhibitors.

In order to determine whether endogenous prostaglandins (PGs) are involved in the secretion of thyrotropic hormone (TSH), we monitored plasma TSH levels in female rats receiving indomethacin (Ind) or aspirin (Asp) to inhibit PG synthesis. TSH secretion was induced by either exogenous thyrotropin-releasing hormone (TRH) or by throidectomy. On the basis of preliminary experiments, Ind was found to inhibit thyroid secretion directly. Subsequently, thyroidectomized rats receiving thyroxine (T4) replacement (2-4 mug/100 g BW/day) were used to avoid this complicating factor. These replacement regimens were judged to be adequate on the basis of the measurement of plasma triiodothyronine and T4 levels, and the lack of a compensatory rise in plasma TSH levels. Under these conditions, Ind significantly inhibited, but did not abolish, the TSH response to exogenous TRH (250 ng/100 g BW iv). Thyroidectomy-induced TSH secretion was abolished by Ind, and could be reversed upon cessation of Ind treatment. Aspirin was also found to inhibit significantly the compensatory TSH rise following thyroidectomy. These findings suggest that endogenous pituitary PGs mediate the stimulation of TSH secretion by TRH or by reduced feedback of thyroid hormones.

Animals↗
PubMed1968

Corticotropin release: inhibition by intrahypothalamic implantation of atropine.

Anterior hypothalamic implantations of crystalline atropine markedly inhibit the adrenocortical responses evoked by surgical stress, ether anesthesia, or intravenolus injection of arginine vasopressin. Similar implants in nearby regions of the brain or sham implantations in the same region were ineffective. The data suggest that the hypothalamic control of pituitary corticotropin may have a cholinergic component.

Adrenal Glands↗
PubMedDate not supplied

Lack of effect of vasoactive intestinal peptide antagonists on blood flow in the rat thyroid.

We used three putative vasoactive intestinal peptide (VIP) antagonists: 1) [4C1-D-Phe6,Leu17]VIP, 2) [N-Ac-Tyr1,D-Phe2] GRF(1-29)-NH2, and 3) VIP(10-28) to assess the involvement of endogenous VIP in the regulation of thyroid hormone secretion and thyroid blood flow (BF). We measured thyroid BF in ketamine-pentobarbital-anesthetized rats using the microsphere technique. Increases in thyroid BF induced by VIP administration (30 pmol-1.5 nmol/100 g b.wt.) were not affected by any of the three compounds tested at doses 10-100 times higher than that of VIP. These compounds (3-15 nmol/100 g b.wt.) also failed to affect basal thyroid BF or hormone secretion. Increases in pancreatic and salivary gland BFs induced by VIP (30 pmol/100 g b.wt.) were also not affected by [4C1-D-Phe6,Leu17]VIP or [N-Ac-Tyr1,D-Phe2]GRF(1-29)-NH2 (3 nmol/100 g b.wt.). These results indicate that the three compounds tested are not effective inhibitors of VIP receptors in the thyroid vasculature and, therefore, they cannot be used in the investigation of the functional significance of endogenous VIP in the regulation of thyroid BF.

Animals↗
PubMedDate not supplied

Sympathetic thyroidal vasoconstriction is not blocked by a neuropeptide Y antagonist or antiserum.

Sympathetic nerve fibers to thyroid blood vessels contain both norepinephrine (NE) and neuropeptide Y (NPY). To assess the involvement of endogenous NPY in the sympathetic neural control of thyroid blood flow, appropriate doses of a selective NPY antagonist, alpha-trinositol, and an NPY antiserum (NPY-AS) were used during cervical sympathetic trunk stimulation in anesthetized rats. During all experiments, thyroid blood flow was continuously monitored by laser Doppler blood flowmetry. Neither alpha-trinositol nor NPY-AS blocked the thyroidal vasoconstriction evoked by either the first or second stimulation of the cervical sympathetic trunks. Our results suggest that NPY is not involved either directly or indirectly during acute sympathetic vasoconstriction in the rat thyroid gland.

Animals↗