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Biomedical subjects

M L Forsling

Publications and source records attributed to M L Forsling.

At least 91 records · Page 5Linked to original sources
PubMed1992

Aminergic control of vasopressin secretion in the conscious rat.

The influence of aminergic pathways on basal and stimulated vasopressin (AVP) release was studied in conscious rats, the stimulus for hormone release being an intracerebroventricular (ICV) injection of 5 microliters 0.85M sodium chloride. The animals were treated with either phenoxybenzamine, propranolol or haloperidol prior to administration of the central hypertonic stimulus. Phenoxybenzamine elevated basal plasma vasopressin concentrations, while propranolol and haloperidol had no effect. The secretion of AVP in response to the hypertonic stimulus was potentiated by phenoxybenzamine and haloperidol, but the effect of propranolol was equivocal. The antagonists had no effect on basal arterial pressure at the time of hypertonic saline administration or the pressor response to ICV sodium chloride.

Animals↗
PubMed1991

Central and peripheral doses of cholecystokinin that inhibit feeding in pigs also stimulate vasopressin and cortisol release.

The effects on vasopressin and cortisol secretion of centrally and peripherally administered cholecystokinin octapeptide (CCK) were investigated in conscious prepubertal pigs. Injection of 1.3 micrograms CCK into the lateral cerebral ventricle resulted in a sustained increase in plasma vasopressin after a latency of 5 min but no change in cortisol concentrations. Intravenous injection of 0.7 and 1.3 micrograms/kg CCK initiated a rapid surge (within 2 min) in plasma vasopressin and a later increase in cortisol secretion. The time course of the vasopressin response to the central injection of CCK was found to be similar to the period of behavioural inhibition induced when an equivalent dose of the peptide was given by the same route in an earlier feeding experiment. An analogous situation was also observed when CCK was given peripherally and, in this case, the threshold dose at which the behavioural and endocrine responses were induced was found to be the same.

Animals↗
PubMed1991

Hormonal effects of apomorphine and cholecystokinin in pigs: modification of the response to cholecystokinin by a dopamine antagonist (metoclopramide) and a kappa opioid agonist (PD117302).

Three experiments were carried out to investigate some of the mechanisms involved in the endocrine responses of pigs to the emetic agents apomorphine and cholecystokinin. In Experiment 1, plasma levels of vasopressin and cortisol were measured in prepubertal pigs (N = 5) treated with i.v. apomorphine (25 micrograms/kg) or saline vehicle. In Experiment 2, concentrations of vasopressin and cortisol were determined in pigs given iv sulphated cholecystokinin octapeptide (1.3 micrograms/kg), metoclopramide (300 micrograms/kg), metoclopramide + cholecystokinin, and an oral dose of the kappa opioid agonist PD 117302 (20 micrograms) alone, or followed by i.v. cholecystokinin. In Experiment 3, operant feeding behaviour was quantified in pigs (N = 4) given cholecystokinin (1 microgram/kg) or cholecystokinin preceded by oral PD 117302. Following apomorphine injection in Experiment 1, there was a rapid, transient, rise in plasma vasopressin. Cholecystokinin had a similar effect on vasopressin secretion in Experiment 2 and also induced a later rise in plasma cortisol. Pre-treatment with metoclopramide appeared to reduce both of these effects of cholecystokinin, but only the decrease in cortisol was statistically significant. However, oral administration of PD 117302 abolished the effect of cholecystokinin on vasopressin release and reduced the subsequent rise in cortisol. The inhibitory effect of cholecystokinin on feeding was unaltered by PD 117302 treatment in Experiment 3. The results obtained with apomorphine and metoclopramide, together, suggest that the neuroendocrine effects of cholecystokinin in the pig may involve an action on central dopamine receptors while the effects of PD 117302 indicate that kappa opioids may modify the hormonal responses to cholecystokinin by a peripheral action.

Animals↗
PubMed1991

Influence of oxytocin on sodium excretion in the anaesthetized Brattleboro rat.

The contribution of oxytocin to the maintenance of renal Na+ excretion in the Brattleboro rat has been examined in animals infused with hypotonic saline. Brattleboro rats exhibited hypernatraemia and hyperosmolality associated with greatly increased plasma concentrations of oxytocin by comparison with Long-Evans control rats. Neurohypophysectomy to remove the secretion of the remaining posterior pituitary peptide, oxytocin, led to greatly diminished rates of Na+ excretion in the Brattleboro rat. Oxytocin replacement to achieve plasma levels equivalent to those in intact Brattleboro rats produced a substantial and sustained natriuresis in the neurohypophysectomized animal. Oxytocin secretion evoked in response to saline infusion would thus appear to be effective in promoting renal Na+ excretion in the absence of vasopressin in the Brattleboro rat.

Anesthesia, General↗
PubMed1991

Kappa-opioid modulation of vasopressin secretion in conscious rats.

A series of studies has been performed in the conscious rat to investigate the effect of the intracerebroventricular (i.c.v.) administration of the selective kappa-opioid receptor agonist, U50 488H, on arginine vasopressin (AVP) secretion stimulated by i.c.v. administration of hypertonic NaCl. Similarly, the effect of the i.c.v. administration of morphine and the i.v. administration of naloxone on AVP secretion was investigated. The response of AVP to an i.c.v. injection of hypertonic NaCl was potentiated by naloxone at a dose of 0.4 mg/kg, but a higher dose (1.2 mg/kg) was required to increase the basal plasma concentration of AVP. Prior treatment with U50 488H or morphine attenuated the increase in plasma concentrations of AVP stimulated by i.c.v. injection of hypertonic NaCl from 13.92 +/- 4.44 to 1.22 +/- 0.34 and 1.78 +/- 0.74 pmol/l respectively (n = 7; P less than 0.05). Prior administration of U50 488H also attenuated the potentiating effect of naloxone on AVP secretion stimulated by i.c.v. injection of hypertonic NaCl. These results indicate that basal AVP secretion is under tonic inhibitory control by dynorphin, and that mu- and kappa-opioid receptors mediate an inhibitory influence of endogenous opioids on osmoreceptor-mediated AVP secretion.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1991

The influence of reproductive status on vasopressin release in the rat.

It has been shown that surgical ovariectomy of the rat results in a fall in plasma vasopressin concentrations suggesting that ovarian steroids may influence hormone release. To determine whether a similar fall is found on suppression of the oestrous cycle, vasopressin concentrations were monitored after treatment with the antioestrogen preparation tamoxifen or a long-acting analogue of LH-releasing hormone (LHRH) which suppresses ovarian function. Treatment with either agent was found to result in a fall in circulating vasopressin concentrations, with little effect on fluid balance. To determine whether the ovary could influence the vasopressin release in response to known stimuli, hormone concentrations were measured in ovariectomized animals during extracellular fluid hypertonicity produced by an i.p. injection of hypertonic saline and hypovolaemia produced by an i.p. injection of polyethylene glycol. It was found that after ovariectomy or treatment with tamoxifen, the response to hypertonicity was unaffected but that to hypovolaemia was attenuated. Treatment with LHRH affected the response to both hypovolaemia and hypertonicity.

Animals↗
PubMed1991

Vasopressin release in response to hypovolaemia in the conscious rat and the effect of opioid and aminergic receptor antagonists.

Conscious rats were given i. p. polyethylene glycol (PEG) or dextran injections to compare their efficacy in inducing moderate hypovolaemia. Dextran was found unsuitable, producing large variability in the plasma vasopressin (AVP) concentrations. Putative neurotransmitters involved in the AVP response to hypovolaemia and in basal release were examined using opioid, and beta-adrenoceptor and dopamine receptor-blocking agents. A dose of PEG was chosen to produce a decrease in blood volume of approx 14.5% giving plasma AVP concentrations of 19.0 +/- 4.6 pmol/l. Naloxone and phenoxybenzamine failed to influence AVP release under both hypovolaemic and basal conditions. Prazosin also failed to influence the AVP response. In contrast propranolol elevated the plasma AVP concentrations in both conditions. Haloperidol enhanced basal AVP release but did not influence release during hypovolaemia. Guanethidine pretreatment partially blocked the response to hypovolaemia, but did not affect basal plasma AVP. Thus it appears that aminergic pathways have an inhibitory influence on AVP release under hypovolaemic and basal conditions. However, endogenous opioids do not appear to contribute significantly to the hypovolaemic response.

Adrenergic alpha-Antagonists↗
PubMed1991

The renal actions of oxytocin in the conscious rat.

The renal actions of oxytocin were studied in the conscious unrestrained rat infused with 0.077 M saline at a rate of 150 microliters/min. During the control period volume and sodium excretion reached stable equilibria, the rates being equal to those infused. Administration of oxytocin at 200 pmol/min produced plasma oxytocin levels of 26.0 +/- 2.1 pmol/l and caused a significant diuresis and natriuresis. Renal responses could also be seen with a lower dose of 30 pmol/min which produced plasma levels of 5.1 +/- 0.5 pmol/l while a dose of 15 pmol/min which produced no significant increase in the plasma oxytocin had no renal effect. It appears that oxytocin has a natriuretic action in concentrations within the physiological range.

Animals↗
PubMed1990

The vasopressin response to centrally administered hypertonic solutions in the conscious rat.

1. Intracerebroventricular (I.C.V.) injections of isotonic and hypertonic solutions into the dorsal (D3V) and ventral (V3V) third ventricle were employed to examine the release of vasopressin (AVP) and the mean arterial pressure (MAP) response to elevated cerebrospinal fluid (CSF) osmolality in the conscious rat. 2. The D3V injection of hypertonic sodium chloride solution was associated with a concentration-dependent, transient increase in plasma AVP concentration and MAP. 3. The D3V injection of 5 microliters 0.85 M-sodium chloride elicited a 7-fold increase in plasma AVP and oxytocin concentrations, but had no effect on plasma ACTH concentration. The D3V injection of 1.11 M-mannitol in 0.15 M-sodium chloride had no effect on plasma AVP concentration or MAP. However, the D3V injection of 0.746 M-mannitol in 0.4 M-sodium chloride elicited a significant transient increase in plasma AVP, but had no effect on MAP. 4. The V3V injection of 5 microliters 0.85 M-sodium chloride elicited a prolonged increase in plasma AVP concentration and a transient increase in MAP. The V3V injection of 5 microliters 1.11 M-mannitol in 0.15 M-sodium chloride elicited an equal, but transient, increase in plasma AVP concentration, but had no effect on MAP. 5. The pressor effect of a D3V injection of 0.85 M-sodium chloride was unaffected by prior administration of the V1 (pressor) receptor antagonist (beta-mercapto-beta,beta-cyclopentamethylene propionyl1, O-Me-Tyr2, Arg8)-vasopressin. 6. These results indicate that osmotically induced AVP secretion may be mediated by both sodium receptors and osmoreceptors, although expression of the response may depend upon the maintenance of a 'permissive' concentration of sodium in the CSF. 7. It appears also that the pressor effect is not due to increased plasma AVP concentration, but only results from elevation of the CSF sodium concentration.

Animals↗
PubMed1990

Effect of ovariectomy and treatment with ovarian steroids on vasopressin release and fluid balance in the rat.

Plasma vasopressin concentrations have previously been shown to vary during the oestrous cycle of the rat, being highest on the morning of pro-oestrus and lowest on dioestrus day 1. To determine the effect of gonadal steroids on vasopressin secretion and fluid balance, mature rats were ovariectomized and given oestrogen, progesterone or vehicle alone s.c. for periods of up to 16 days. Plasma vasopressin concentrations fell after ovariectomy and this was reflected in an increase in 24-h urine volume. The normal increase in plasma vasopressin concentrations seen over day-light hours was also suppressed. The change in vasopressin concentrations observed on steroid treatment depended upon both the dose and the duration. High doses of oestrogen were associated with a fall in plasma vasopressin, probably as a result of fluid retention. Thus, of an initial group of rats given silicone elastomer implants containing 50, 500 or 1000 micrograms oestradiol in oil, plasma vasopressin concentrations were reduced after 7 days treatment with 1000 micrograms oestradiol implants in association with reduced plasma sodium concentrations. Daily s.c. injections of 100 micrograms oestradiol benzoate/100 g body weight produced an immediate small increase in plasma vasopressin concentrations, but by 14 days the plasma concentrations of 0.7 +/- 0.16 pmol/l (mean +/- S.E.M.) had fallen significantly and were less than those in the vehicle-treated group (1.2 +/- 0.26 pmol/l). However, after treatment for 14 days with implants containing only 50 micrograms oestradiol, plasma vasopressin concentrations were higher compared with the group receiving vehicle alone, despite the fact that the plasma osmolality was lower in the latter group, suggesting a long term resetting of the osmoreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

The influence of central hypersomotic solutions on drinking and vasopressin release following peripheral hyperosmotic NaCl in the minipig.

The drinking and lysine vasopressin (LVP, porcine vasopressin) responses were measured in minipigs given simultaneous intracarotid (i.c.) (1.28 ml/min) and intracerebroventricular (i.c.v.) (50 microliters/min) infusions of solutions of differing osmolality and sodium content. Observations were made during, and for a further 15 min after, the combined infusions which lasted 15 min. Drinking in response to i.c. infusion of 2.0 Osm NaCl started with a latency of 7 min and was unaffected by simultaneous i.c.v. infusion of 0.15 M NaCl, was additive with the drinking produced by i.c.v. 1.4 Osm NaCl, sucrose or mannitol, and inhibited by i.c.v. infusion of 1.4 Osm urea. LVP release following i.c. hyperosmotic NaCl was observed as early as the first blood sample, at 2 min, and was attenuated by i.c.v. hyperosmotic urea and attenuated, then slightly augmented, by i.c.v. infusions of the hyperosmotic non-electrolyte solutions. These results show that drinking following peripheral administration of an osmotic stimulus in the minipig can add to that induced by central infusions of solutions that would have increased the effective osmotic pressure of the cerebrospinal fluid (CSF) but may have increased or decreased CSF sodium concentration. By contrast, the stimulated LVP release was attenuated by solutions that decreased CSF sodium concentration. Thus, in minipigs, separate osmoreceptors appear to mediate osmotically induced drinking and LVP release.

Animals↗
PubMed1989

Plasma arginine vasopressin levels and arterial pressure during open heart surgery.

A study of plasma arginine vasopressin (AVP) levels and their relation to changes in arterial pressure was undertaken in 13 patients undergoing open heart surgery. Seven of the patients received high doses of intravenous morphine (1 or 2 mg/kg) as part of their anaesthetic, whereas the other six did not. Increases in the AVP levels during cardiopulmonary bypass (CPB) were significant in both groups, but were significantly greater in the patients not receiving morphine (median 86.1 fmol/ml) than in those who did (47.5 fmol/ml). In both groups there was a linear correlation between the natural logarithm of the plasma AVP level and the percentage fall in the mean arterial pressure, although the slope of the relationship was significantly less in the group receiving morphine than in the group not receiving morphine. These results indicate that in patients undergoing cardiac surgery the neuroendocrine reflex control of plasma AVP levels in relation to changes in arterial pressure is intact, but that the sensitivity of the reflex (i.e. the increase in plasma AVP level for a given fall in arterial pressure) is reduced by the administration of high doses of intravenous morphine.

Anesthesia, Intravenous↗
PubMed1989

Two regimens of lithium prophylaxis and renal function.

Two regimens of lithium prophylaxis with different pharmacokinetic characteristics were compared under double-blind conditions in 25 bipolar patients in remission already stabilized on lithium, to determine the relative effects of each regimen on renal function. Once-daily lithium carbonate (Priadal), which gives a peak lithium plasma level 2-3 h post-administration with a low level 24 h later, was compared with twice-daily lithium citrate (Litarex), which maintains a steadier 24 h plasma level. Patients were allocated randomly to one of the 2 regimens. They were seen monthly for clinical ratings over the course of 12 months. A comprehensive battery of renal function tests was undertaken at the start of the trial, between 6-9 months after the start and again after 1 year. No significant differences were observed in clinical outcome, side effects or renal function between the 2 regimens.

Acetylglucosaminidase↗
PubMed1989

Drinking and vasopressin release following central injections of angiotensin II in minipigs.

Angiotensin II (AII; 300 ng) injected into the lateral cerebral ventricle produced significant drinking responses and also stimulated release of lysine vasopressin (LVP) in conscious, water replete, unrestrained minipigs. Plasma LVP concentration, measured by a specific radioimmunoassay, was decreased by drinking. At the end of the experiment the level was inversely proportional to the volume of water drunk in response to the AII, and not to changes in plasma osmolality. These findings suggest that AII-stimulated LVP release is influenced by a negative feed-back mechanism, probably involving oropharyngeal receptors.

Angiotensin II↗
PubMed1989

Plasma and urine electrolyte concentrations and vasopressin levels in patients admitted to hospital for falciparum malaria.

Vasopressin levels, together with plasma and urinary electrolytes, were measured in the acute and convalescent stages of 17 patients with malaria and 11 patients with other febrile illnesses. There was a significantly lower serum sodium in the acute stages of both groups (p less than 0.01 and p less than 0.02). There was no significant difference between the malaria and control groups. There were no significant changes in the vasopressin levels, although one patient with malaria showed evidence of inappropriate vasopressin secretion which returned to normal after treatment. This study suggests the mild hyponatraemia sometimes seen in the acute stages of malaria is not related to inappropriate secretion of vasopressin, although this condition may be of importance in more severe cases of hyponatraemia.

Adolescent↗
PubMed1988

Antagonism of V2-receptor effect of antidiuretic hormone by atrial natriuretic peptide in man.

Human alpha-atrial natriuretic peptide (h-alpha ANP) makes the urine of dehydrated volunteers hypotonic to plasma despite high circulating concentrations of antidiuretic hormone. Urinary dilution with h-alpha ANP also occurs in subjects receiving indomethacin. Therefore, h-alpha ANP antagonises effects of antidiuretic hormone on distal tubular V2-receptors in man, probably without involving prostaglandins.

Arginine Vasopressin↗
PubMed1988

Endocrine and renal response to water loading and water restriction in normal man.

1. Nine normal subjects (eight male, one female) on a fixed daily intake of 150 mmol of sodium and 80 mmol of potassium, were randomized to receive either 3 days of 1.0 litre total water intake/24 h (food + fluid) or 4 days of 6.8 litres total water intake/24 h, and were then crossed over after a 3 day control period (2.7 litres water/24 h). 2. During water restriction, urine volume fell from 1.94 litres/24 h to less than 1 litre/24 h by the first day and was 0.77 litre/24 h on the final day. Plasma atrial natriuretic peptide levels were unchanged from baseline despite a large increase in plasma vasopressin and plasma and urine osmolality. Urinary sodium was unaltered throughout, while urinary potassium was increased on the final 2 days of water restriction. 3. During water loading, urine volume increased from 1.85 litres/24 h to 5.44 litres/24 h on the first day and remained at approximately 6 litres/24 h for the final 3 days. Plasma atrial natriuretic peptide showed no change. Plasma vasopressin and plasma and urine osmolality were reduced. Urinary sodium and potassium output were unchanged from baseline. 4. These results suggest that changes in plasma atrial natriuretic peptide are unlikely to be involved in the normal homoeostatic response to changes in water balance in man.

Adolescent↗