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Biomedical subjects

A V Edwards

Publications and source records attributed to A V Edwards.

At least 55 records · Page 3Linked to original sources
PubMed1991

Muscarinic adrenal responses to acetylcholine in conscious calves.

1. Adrenal responses to intra-aortic infusions of acetylcholine (4.5 nmol min-1 kg-1 for 10 min) have been investigated in hypophysectomized conscious calves given exogenous adrenocorticotrophic hormone (ACTH) (2 ng min-1 kg-1 I.V.) in the presence and absence of hexamethonium. 2. Acetylcholine produced a significant increase in adrenal cortisol output and plasma cortisol concentration. In the absence of nicotinic blockade with hexamethonium this was apparently accounted for by an increase in adrenal ACTH presentation secondary to increased adrenal blood flow. However, administration of hexamethonium revealed a direct steroidogenic action of acetylcholine in the presence of exogenous ACTH. 3. Adrenal medullary responses to acetylcholine, including the release of catecholamines, enkephalins and corticotrophin-releasing factor (CRF), were not significantly reduced by nicotinic blockade. 4. It is concluded that both adrenal medullary and cortical responses to intraaortic infusions of acetylcholine at a low dose are mediated mainly by muscarinic receptors, as it has previously been shown that they are substantially reduced in the presence of atropine.

Acetylcholine↗
PubMed1990

The effect of splanchnic nerve stimulation on the uptake of atrial natriuretic peptide by the adrenal gland in conscious calves.

A technique has been developed with which it has been possible to quantify the output of a wide variety of agonists including catecholamines, glucocorticoids, mineralocorticoids, enkephalins and various peptides, from the adrenal gland in the conscious unrestrained calf; also to investigate responses to electrical stimulation of the peripheral end of the splanchnic nerve below any behavioural threshold. In the present study this methodology has been employed to investigate the extent to which stimulation of the splanchnic sympathetic innervation affects adrenal handling of atrial natriuretic peptide as this peptide has been identified within the adrenal medulla in this species. Stimulation of the splanchnic nerve at frequencies which raised the concentration of atrial natriuretic peptide like-immunoreactivity (ANP) by 25% led to an abrupt increase in the uptake of the peptide by the right adrenal gland by about 250%. During nerve stimulation more than 20% of the ANP that was estimated to be presented to the gland was taken up, by comparison with less than 13% of the amount presented which was taken up before and after stimulation. These results suggest that stimulation of the splanchnic nerve may specifically enhance the uptake of ANP by the adrenal gland and represent the first report of such a mechanism in respect of any biologically active peptide so far as we are aware.

Adrenal Glands↗
PubMed1990

Release of adrenocorticotrophin from the adrenal gland in the conscious calf.

1. The effect of stimulation of the splanchnic nerve on the output of ACTH-related peptides from the adrenal gland has been investigated in conscious, functionally hypophysectomized calves, previously fitted with an 'adrenal clamp'. 2. Stimulation of the splanchnic nerve elicited a small, but statistically significant, increase in the output of ACTH-like immunoreactivity at each frequency tested. This response was frequency-dependent over the range 40-70 Hz when stimulating intermittently for 1 s at 10 s intervals and was potentiated by stimulating intermittently. Thus, the average mean output during stimulation in burst at 70 Hz (25 +/- 5 fmol min-1 kg-1) was significantly higher than the corresponding value during continuous stimulation at 7 Hz (6 +/- 1 fmol min-1 kg-1; P less than 0.01) even though the total number of impulses delivered was identical in each case. 3. There was also a small but significant rise in the output of cortisol from the gland with intermittent stimulation, which was linearly related to the output of ACTH-like immunoreactivity at the lower frequencies (4 and 7 Hz). 4. Separation of the ACTH-related peptides which were extracted from the adrenal effluent plasma of these animals during splanchnic nerve stimulation revealed the existence of two clear forms: ACTH (1-39) accounted for about 60% of total ACTH immunoreactivity and pro-opiomelanocortin (POMC) for about 30%. 5. It is concluded that small amounts of ACTH are released within the adrenal gland during splanchnic nerve stimulation in the functionally hypophysectomized calf and that this may possibly contribute towards the steroidogenic effect of stimulating the splanchnic nerve.

Adrenal Glands↗
PubMed1990

The effect of changes in adrenal blood flow on adrenal cortical responses to adrenocorticotrophin in conscious calves.

1. The effect of varying adrenal blood flow on the rate at which it was estimated that adrenocorticotrophin (ACTH) was presented to the adrenal gland was related to right adrenal cortisol output in conscious calves fitted with 'adrenal clamps'. 2. Intra-aortic infusions of endothelin at either 15.0 or 7.5 pmol min-1 kg-1 produced a substantial fall in right adrenal blood flow which was dose-related over this range. There was an associated fall in right adrenal cortisol output and cortisol output was linearly related to estimated ACTH presentation to the gland over the whole range investigated. The changes in adrenal cortisol output were reflected by changes in the concentration of cortisol in the peripheral plasma, which could be attributed entirely to the fluctuations in adrenal cortisol output. 3. It is concluded that delivery of ACTH to the adrenal gland is flow dependent over the physiological range in these animals and that changes in adrenal cortical blood flow can therefore be expected to result in changes in adrenal output due to variations in the presentation rate of ACTH.

Adrenal Cortex↗
PubMed1990

Adrenal responses to corticotrophin-releasing factor in conscious hypophysectomized calves.

1. Adrenal responses to intra-aortic infusions of pure synthetic ovine corticotrophin-releasing factor (CRF) have been investigated in functionally hypophysectomized calves previously fitted with an adrenal clamp. 2. CRF caused an increase in the output of cortisol from the adrenal gland, which was dose related over the range 4-8 pmol min-1 and maximal at the higher of these doses; this response was observed at a dose below that which produced any change in adrenal vascular resistance. Cortisol output was also found to be related linearly to the rate at which CRF was estimated to be presented to the gland during these infusions. 3. The infusions of CRF also provoked the release of small, but readily detectable, amounts of adrenocorticotrophin-like peptides (ACTH) from the gland. This was mainly in the form of ACTH1-39 with some pro-opiomelanocortin (POMC) also being released. 4. Comparison of the adrenal steroidogenic response to exogenous CRF with that to synthetic ACTH1-24 showed that CRF was the more potent; in each case cortisol output was related linearly to the presentation rate of the peptide. 5. It is concluded that the adrenal cortex in the calf is capable of releasing cortisol in response to exogenous CRF at low concentrations and is even more sensitive to CRF than it is to exogenous ACTH over the dose range that was employed.

Adrenal Cortex↗
PubMed1990

Submandibular responses to stimulation of the parasympathetic innervation in bursts in the anaesthetized ferret.

1. Submandibular salivary and vascular responses to different patterns of stimulation of the parasympathetic innervation have been investigated in anaesthetized ferrets in the presence and absence of atropine. 2. At low stimulus frequencies likely to fall within the physiological range (0.5-2.0 Hz continuously; 5.0-20.0 Hz in 1 s bursts at 10 s intervals) secretion of fluid and protein were both potentiated by the bursting pattern of stimulation and the latency of the secretory response was reduced. Over a somewhat lower range (0.5-1.0 Hz continuously; 5.0-10.0 Hz in bursts) the submandibular vascular response was also significantly potentiated by employing this intermittent pattern of stimulation. Above these frequency ranges no such potentiation occurred. 3. Pre-treatment with atropine (2.0 mg kg-1) blocked the submandibular secretory responses to stimulation of the chorda-lingual nerve at these low frequencies and the residual responses at higher frequencies were not significantly affected by changing the pattern of stimulation. The vascular response was somewhat reduced after atropine but that which persisted was enhanced by stimulating in bursts. 4. It is concluded that the release of some transmitter from postganglionic terminals in the submandibular gland of the ferret must be potentiated by the arrival of action potentials at short intervals and possible mechanisms are considered.

Anesthesia, Intravenous↗
PubMed1989

Adrenal responses to calcitonin gene-related peptide in conscious hypophysectomized calves.

1. Right adrenal and various cardiovascular responses to an intra-aortic infusion of calcitonin gene-related peptide (CGRP; 4 micrograms min-1) have been investigated in the presence and absence of exogenous adrenocorticotrophin ACTH1-24 (2 or 5 ng min-1 kg-1, I.V.). The adrenal clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-7 days previously. 2. At the higher dose (5 ng min-1 kg-1) the I.V. infusion of ACTH raised mean plasma ACTH concentration by about 1000 pg ml-1 and mean right adrenal cortisol output by about 750 ng min-1 kg-1. Under these conditions the intra-aortic infusion of CGRP had no apparent effect on adrenal cortisol output by about 750 ng min-1 kg-1. Under these conditions the intra-aortic infusion of CGRP had no apparent effect on adrenal function, other than to produce moderate adrenal vasodilatation. In contrast, in the absence of exogenous ACTH, the same dose of CGRP produced a substantial rise in cortisol output, which rose steadily to a peak mean value of 409 +/- 31 pg min-1 kg-1 at 10 min. It also significantly inhibited the release of free, but not of total, met5-enkephalin-like immunoreactivity from the gland (P less than 0.001) together with a significantly greater fall in adrenal vascular resistance (P less than 0.001). 3. At the lower dose of ACTH (2 ng min-1 kg-1, I.V.) CGRP raised mean plasma cortisol output from 314 +/- 31 to 486 +/- 44 ng min-1 kg-1 (P less than 0.01) and this effect was not attributable to an increase in the adrenal presentation rate of ACTH. 4. It is concluded that this peptide exerts a steroidogenic action on the adrenal cortex which is manifest in the absence of exogenous ACTH in the functionally hypophysectomized calf.

Adrenal Cortex↗
PubMed1989

Neuroendocrine responses to stimulation of the splanchnic nerves in bursts in conscious, adrenalectomized, weaned lambs.

1. Effects of stimulation of the peripheral ends of the splanchnic nerves below behavioural threshold at either 4 or 7 Hz continuously for 10 min, or at 40 or 70 Hz for 1 s at 10 s intervals for 10 min. have been compared in conscious adrenalectomized lambs. 2. Both patterns of stimulation resulted in an abrupt rise in mean aortic blood pressure of closely similar extent which was associated with reflex bradycardia. 3. At the lower frequencies both patterns of stimulation elicited a closely similar rise in mean plasma glucose, glucagon and pancreatic polypeptide concentration, but the fall in mean plasma insulin concentration was significantly greater during continuous stimulation. 4. Unlike other species in which the release of NPY and bombesin-like immunoreactivity (BLI) is potentiated by intermittent high-frequency stimulation, no significant differences were produced by changing the pattern of stimulation. The release of BLI was found to be frequency related over the ranges tested (4-7 Hz continuously and 40-70 Hz in bursts) whereas the release of NPY was not. 5. Splanchnic nerve stimulation also produced detectable rises in the mean plasma concentrations of noradrenaline and adrenaline. The mean average concentration of noradrenaline during stimulation in bursts was significantly higher than that during continuous stimulation (P less than 0.02). There was also a steady rise in mean plasma 3,4-dihydroxyphenylacetic acid (DOPAC) during stimulation followed by a further rise to significantly higher values (P less than 0.02) following stimulation in bursts at 40 Hz. 6. It is concluded that the pattern of stimulation is a less important determinant of autonomic responses to splanchnic nerve stimulation in sheep than in certain other species.

Adrenalectomy↗
PubMed1989

Adrenal responses to splanchnic nerve stimulation in conscious calves given naloxone.

1. The effects of stimulating the peripheral end of the right splanchnic nerve in the presence of naloxone (2 mg kg-1) have been investigated in conscious 3 to 6-week-old calves. 2. Mean aortic blood pressure rose to significantly higher levels during splanchnic stimulation in bursts at 40 Hz for 1 s at 10 s intervals than it did during stimulation at the corresponding continuous frequency (4 Hz). Furthermore, naloxone significantly reduced the fall in mean vascular resistance in response to both patterns of stimulation. 3. The output of catecholamines from the adrenal gland, together with the proportion of noradrenaline released, was significantly enhanced by stimulating the splanchnic nerves in bursts in animals pre-treated with naloxone and the proportion of noradrenaline released also increased. In both cases the output of adrenaline and noradrenaline was within the same range as that reported previously in normal control animals. 4. Naloxone significantly increased the amounts of enkephalin-like immunoreactivity and corticotrophin-releasing factor (CRF)-like immunoreactivity released from the adrenal gland in response to splanchnic nerve stimulation and raised the proportion of total to free met5-enkephalin that was secreted. 5. Naloxone also inhibited the rise in plasma adrenocorticotrophic hormone (ACTH) concentration during continuous stimulation at 4 Hz, but not during stimulation at 40 Hz in bursts. Under these latter conditions the output of cortisol apparently directly from the adrenal gland was inhibited. The finding that splanchnic nerve stimulation can potentiate the output of cortisol in response to ACTH was confirmed. 6. These results provide evidence that release of enkephalins and of CRF from the adrenal is inhibited by activating opioid receptors within the gland itself.

Adrenal Glands↗
PubMed1988

Submandibular responses to stimulation of the sympathetic innervation following parasympathetic denervation in cats.

1. The effects of continuous stimulation of the ascending cervical sympathetic nerve were compared with those of intermittent stimulation in bursts, so arranged as to deliver the same total number of impulses, in cats under chloralose anaesthesia 3 weeks after excision of the chorda tympani. 2. Parasympathetic denervation of the gland in this way enhanced the vasodilator component of the vascular response during sympathetic stimulation in bursts. During continuous stimulation this was manifested as a reduced rise in submandibular vascular resistance (SVR). It also produced a profound increase in the secretory response to sympathetic stimulation at low intensity (2 Hz continuously). 3. Enhancement of the salivary secretory responses by stimulating intermittently at relatively high frequencies resembled that which developed following parasympathetic denervation in that there was no change in the secretory capacity during maximal or supramaximal stimulation. 4. Pre-treatment with atropine substantially reduced the flow of saliva in response to sympathetic stimulation at low frequencies (2 and 5 Hz continuously) and combined pre-treatment with atropine and propranolol effectively reversed the increase in secretory sensitivity due to parasympathetic denervation indicating that beta-adrenergic and muscarinic responses are involved. Additional pre-treatment with dihydroergotamine effectively abolished the secretory response to sympathetic stimulation. 5. Stimulation in bursts was found to have a significantly greater vasodilator effect than continuous stimulation at the corresponding frequency after parasympathetic denervation. 6. Neither pre-treatment with atropine nor combined pre-treatment with atropine and propranolol had any significant effect on the changes in mean SVR at any frequency tested during or after either pattern of stimulation. Additional pretreatment with dihydroergotamine effectively abolished the vascular responses to sympathetic stimulation both continuous (5 Hz) and in bursts (50 Hz), leaving a small vasoconstrictor response that may be due to release of neuropeptide Y (NPY). 7. These results suggest that cholinergic beta-adrenergic and NPY supersensitivities are not involved in the submandibular vascular changes that result from parasympathetic denervation, but that alpha-mediated secondary vasodilator mechanisms are thereby enhanced.

Animals↗
PubMed1988

The adrenal contribution to the neuroendocrine responses to splanchnic nerve stimulation in conscious calves.

1. The extent to which the adrenal gland contributes to neuroendocrine responses to electrical stimulation of the peripheral end of the splanchnic nerve has been investigated in conscious calves in which the right nerve was stimulated either at 4 Hz continuously for 10 min or at 40 Hz in 1 s bursts at 10 s intervals for the same period. 2. It was confirmed that the release of neuropeptide Y (NPY) and of gastrin-releasing peptide (GRP) is potentiated by stimulation in bursts at a relatively high frequency and shown that the adrenal gland made a negligible contribution to these responses. 3. There was no detectable change in the concentration of vasoactive intestinal peptide (VIP) in the arterial plasma but the existence of a very small but highly significant rise in the output of VIP from the adrenal provided evidence that it was released within the gland in response to splanchnic nerve stimulation. 4. The concentration of calcitonin gene-related peptide (CGRP) in the arterial and adrenal venous effluent plasma was consistently below the level of detection of the assay. 5. Splanchnic nerve stimulation resulted in an abrupt rise in the output of both free and total met5-enkephalin-like immunoreactivity from the adrenal gland which was substantially potentiated by stimulating in bursts. This pattern of stimulation also increased the proportion released in a high-molecular-weight form. 6. Stimulation in bursts significantly enhanced the output of both adrenaline and noradrenaline from the adrenal and resulted in the release of proportionately more noradrenaline. Small amounts of dopamine and DOPAC were also released during splanchnic nerve stimulation and the output of dopamine was significantly increased by stimulating in bursts. 7. Both patterns of stimulation elicited an abrupt rise in mean plasma adrenocorticotrophic hormone (ACTH) concentration, which was associated with an increase in mean adrenal cortisol output and the former effect was significantly enhanced by stimulating in bursts. 8. It is concluded that certain responses to splanchnic nerve stimulation are significantly potentiated by an intermittent high-frequency pattern of stimulation, including all those that are attributable to adrenal medullary activity, whereas others are apparently unaffected by changes in stimulus pattern.

Adrenal Glands↗
PubMed1988

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

1. The output of corticotrophin releasing factor-like immunoreactivity (CRF) from the adrenal gland has been investigated using the 'adrenal clamp' technique in conscious calves. 2. Stimulation of the peripheral end of the splanchnic nerve for 10 min increased the mean output of CRF progressively, so that it had risen by about twentyfold, to a peak incremental value of 24 +/- 4 pmol min-1 kg-1 at 10 min. This response was significantly increased by stimulating in bursts at 40 Hz for 1 s at 10 s intervals, which raised the mean CRF output by 44 +/- 7 pmol min-1 kg-1 at 10 min (P less than 0.05). 3. The mean output of adrenaline and noradrenaline rose more abruptly in response to splanchnic nerve stimulation with peak incremental values realized within 2.5 min. However, the ratios of adrenal CRF to catecholamine output were closely similar during the later stages of stimulation (7.5-10 min). There was a similarly abrupt rise in adrenal cortisol output in response to splanchnic nerve stimulation which was, nevertheless, linearly related to arterial plasma ACTH concentration throughout. 4. In hypophysectomized calves, administration of adrenocorticotrophic hormone (ACTH1-24) at a dose of 5 ng min-1 kg-1 reduced the output of adrenal CRF in response to splanchnic nerve stimulation by about 50% (P less than 0.05). 5. CRF isolated from adrenal venous effluent plasma, collected both at rest and during splanchnic nerve stimulation, was separated by reverse-phase high-pressure liquid chromatography and found to elute in a position identical to that of human 41CRF. This suggests that adrenal CRF is structurally closely similar to its pituitary counterpart.

Adrenal Glands↗
PubMed1987

The effect of splanchnic nerve stimulation on adrenocortical activity in conscious calves.

1. Right adrenal and various cardiovascular responses to stimulation of the peripheral end of the right splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min-1 kg-1). The adrenal-clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-4 days previously. 2. The I.V. infusion of ACTH1-24 increased mean plasma ACTH concentration by about 1200 pg/ml and mean right adrenal cortisol output by about 500 ng min-1 kg-1. Stimulation of the peripheral end of the right splanchnic nerve at 4 Hz for 10 min produced a further rise in cortisol output, amounting to about 400 ng min-1 kg-1 (P less than 0.01). These changes in output were reflected accurately by changes in peripheral plasma cortisol concentration. 3. Closely similar amounts of adrenaline were released in response to splanchnic nerve stimulation in the presence and absence of exogenous ACTH. In the presence of ACTH the average mean output of noradrenaline (58 +/- 2 ng min-1 kg-1) was significantly less than that of adrenaline (102 +/- 4 ng min-1 kg-1; P less than 0.001), whereas the corresponding values were not significantly different in the absence of ACTH. 4. These results also confirm the fact that the fall in adrenal vascular resistance which occurs during splanchnic nerve stimulation is substantially reduced by ACTH, as is the rise in met5-enkephalin output. 5. It is concluded that the splanchnic innervation is capable of enhancing the secretion of adrenal glucocorticoids in response to ACTH under physiological conditions in the conscious calf.

Adrenal Glands↗
PubMed1987

The effect of splanchnic nerve section on the sensitivity of the adrenal cortex to adrenocorticotrophin in the calf.

1. Adrenal cortical responses to adrenocorticotrophin (ACTH) in conscious 2-6-week-old calves, in which both splanchnic nerves had been cut at least 7 days previously, were compared with those of normal calves of the same age in order to discover whether splanchnic nerve section affects the sensitivity of the adrenal cortex to the trophin. 2. In one series of experiments an increase in the release of endogenous ACTH was elicited by an i.v. infusion of noradrenaline (333 ng min-1 kg-1 for 10 min) and in another the concentration of ACTH in the plasma was artificially increased by infusing synthetic ACTH1-24 intravenously at either 5 or 10 ng min-1 kg-1 for 10 min. 3. In all groups mean plasma ACTH was linearly related to mean plasma cortisol and the sensitivity of the adrenal steroidogenic response to ACTH was found to be substantially reduced 7 or more days after section of both splanchnic nerves.

Adrenal Cortex↗
PubMed1987

Adrenal cortical responses to vasoactive intestinal peptide in conscious hypophysectomized calves.

1. Right adrenal and various cardiovascular responses to an intra-aortic infusion of vasoactive intestinal polypeptide (VIP; 4 micrograms min-1 kg-1) have been investigated in the presence and absence of exogenous adrenocorticotrophin, (ACTH1-24; 5 ng min-1 kg-1, i.v.). The adrenal clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-4 days previously. 2. The i.v. infusion of ACTH1-24 increased mean plasma ACTH concentration by between 1000 and 1100 pg ml-1 and mean right cortisol output by about 700 ng min-1 kg-1. Under these conditions the intra-aortic infusion of VIP produced a further rise in mean adrenal cortisol output, together with a consequential rise in mean arterial plasma cortisol concentration, without affecting the concentration of ACTH in the arterial plasma significantly. In the absence of ACTH the same infusion of VIP had no detectable effect on adrenal cortisol output. 3. In each of the above respects this intra-aortic infusion of VIP closely mimicked the effect of stimulation of the peripheral end of the right splanchnic nerve in these animals, as it also did by causing a substantial fall in adrenal vascular resistance in the absence, but not in the presence, of ACTH. 4. It is concluded that release of this peptide from splanchnic nerve terminals in the adrenal gland most probably accounts, at least in part, for the powerful adrenocortical steroidogenic response to splanchnic nerve stimulation, that occurs in the presence of submaximal doses of ACTH.

Adrenal Cortex↗
PubMed1987

Effects of stimulating the sympathetic innervation in bursts on submandibular vascular and secretory function in cats.

1. The effects of continuous stimulation of the peripheral end of the ascending cervical sympathetic nerve were compared with those of intermittent stimulation, so arranged as to deliver the same total number of impulses, in cats under chloralose anaesthesia. 2. Continuous stimulation caused a flow of saliva at 5-10 Hz, but not at 2 Hz. In contrast, the same total number of impulses delivered intermittently in bursts elicited a prompt secretion at a frequency as low as 20 Hz for 1 s at 10 s intervals (corresponding to 2 Hz continuously) and a significantly higher rate of secretion at 50 Hz in bursts than that obtained in response to 5 Hz continuously. 3. Continuous stimulation also caused a rise in submandibular vascular resistance (s.v.r.), which persisted throughout the period of stimulation, and was followed immediately thereafter by an intense but transient fall in s.v.r. During stimulation in 1 s bursts, each burst was followed first by a brief rise in s.v.r. and shortly after by a fall. The balance between these two components varied widely between individual animals but often led to an overall fall in s.v.r. during stimulation i.e. complete reversal of the mean vascular effect. A further fall in s.v.r. was then recorded when the stimulus was discontinued. 4. Propranolol (1.0 mg/kg) reduced but failed to abolish the secretory response. It also altered the balance between the two phases of the vascular response slightly in favour of a rise in s.v.r. during stimulation, without apparently affecting the size of the after-dilatation. 5. Pre-treatment with dihydroergotamine (1.0 mg/kg) invariably blocked secretion and revealed a small vasodilator response during sympathetic stimulation with either pattern of stimulation; it also blocked the after-dilatation. 6. Following combined pre-treatment with propranolol and dihydroergotamine, to produce total adrenergic blockade, there was a small residual vasoconstrictor component which amounted to an increase in mean s.v.r. of about 20% during stimulation at 10 Hz continuously. This may have been due to release of neuropeptide Y (NPY). 7. Small but significantly greater amounts of NPY were released into the effluent blood during stimulation of the ascending cervical sympathetic nerve at 70 Hz in bursts than during continuous stimulation. No significant release of vasoactive intestinal peptide (VIP), somatostatin, bombesin, substance P or calcitonin gene-related peptide (CGRP) was observed during stimulation at any frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Right medullary and various cardiovascular responses to stimulation of the peripheral end of the splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min-1 kg-1). The adrenal-clamp technique was employed in conscious calves, after the pituitary stalk had been cauterized and they had recovered from anaesthesia. The intravenous infusion of ACTH1-24 increased the plasma ACTH concentration by about 1100 pg ml-1 and right adrenal venous output of cortisol by about 400 ng min-1 kg body weight-1. Stimulation of the splanchnic nerve at 4 Hz for 10 min had no effect on either arterial plasma ACTH concentration or the adrenal output of cortisol. Closely similar amounts of both adrenaline and noradrenaline were released in response to nerve stimulation in the presence and absence of exogenous ACTH. In contrast, the fall in adrenal vascular resistance of about 40%, which normally occurred in response to splanchnic nerve stimulation, was completely abolished by ACTH. The adrenal produced relatively large quantities of met-enkephalin-containing peptides. During splanchnic nerve stimulation the output of these increased 2-100-fold, at which time free met5-enkephalin accounted for only 10-20% of total. During ACTH infusion the output of free met5-enkephalin was reduced at rest and during nerve stimulation, but that of total met-enkephalin-containing peptides was unaffected. These results indicate that ACTH or an adrenal steroid may alter the processing of proenkephalin in the adrenal medulla acutely but not total opiate secretion. Alternatively, the presence of ACTH could act by influencing the population of chromaffin cells activated by splanchnic nerve stimulation.

Adrenal Medulla↗