Comparative water metabolism of Barrow Island macropodid marsupials: hormonal versus behavioural-dependent mechanisms of body water conservation.

Seasonal variations in rates of water turnover were measured over a 7-year period in four species of macropodid marsupials (Lagorchestes conspicillatus, Bettongia lesueur, Petrogale lateralis and Macropus robustus isabellinus), on Barrow Island off the arid Pilbara coast of Western Australia. These ranged from over 100 mL kg(-0.82) d(-1) in wet seasons to as low as 28.2 mL kg(-0.82) d(-1) in dry seasons in the Spectacled hare wallaby, L. conspicillatus. Plasma osmolality increased significantly in both Barrow Island euros (M. robustus isabellinus) and Spectacled hare wallabies in November 1994, in the driest year yet recorded on the island. In contrast, there was no change in plasma osmolality of the other two species (Black-footed rock wallaby, P. lateralis and Lesueur's burrowing bettong, B. lesueur) that exploit cool and humid thermal refugia such as caves and underground warrens to avoid diurnal temperature extremes. Plasma levels of the marsupial antidiuretic hormone (ADH), lysine vasopressin (LVP), were for the most part below the detectable limit of the assay of 0.41 pg mL(-1) in rock wallabies and bettongs, but reached high levels of 16.7+/-4.6 pg mL(-1) and 20.25+/-5.1 pg mL(-1) in euros and hare wallabies, respectively, in dry seasons. LVP levels were positively correlated with plasma osmolality in both euros and hare wallabies, and negatively correlated with total body water content in euros, supporting its rôle as an antidiuretic hormone in these two species. The study highlights the importance of environmental features, such as caves and underground warrens, which are critical for the long-term survival of endangered species such as the Black-footed rock wallaby and the Lesueur's bettong. These species appear to lack ADH-controlled renal systems for the conservation of body water and are thus dependent on behavioural strategies for the maintenance of fluid homeostasis in arid environments.

Pre-emptive lidocaine inhibits arterial vasoconstriction but not vasopressin release induced by a carbon dioxide pneumoperitoneum in pigs.

BACKGROUND: We assessed the preventive effects of i.v. or i.p. lidocaine administration on increases in vascular resistance produced by carbon dioxide pneumoperitoneum and related this to vasopressin release. METHODS: Carbon dioxide pneumoperitoneum (14 mm Hg intra-abdominal pressure) was performed in 32 anaesthetized young pigs and monitored using a pulmonary artery catheter. Animals received lidocaine 0.5% (0.5 mg kg(-1)) i.v. (n=9) or 2 ml kg(-1) i.p. (n=9) or saline (n=5) 15 min before the pneumoperitoneum and were compared with a control group (n=9). RESULTS: I.V. and i.p. lidocaine inhibited increases in mean systemic vascular resistance induced by the pneumoperitoneum [2109 (SD 935) and 2282 (895), respectively, vs 3013 (1067) dyne s(-1) cm(-5) in the control group]. Cardiac output was increased. Plasma lidocaine concentrations were threefold higher after i.p. administration than after i.v. administration. After pneumoperitoneum insufflation, plasma lysine-vasopressin concentrations increased in all groups (control 74%, saline 65%, i.p. lidocaine 57%, i.v. lidocaine 74%). CONCLUSIONS: I.V. and i.p. lidocaine blunted systemic vascular responses to carbon dioxide pneumoperitoneum in pigs, but without influencing vasopressin release.

Interrelated adrenocortical and neurohypophysial responses associated with fever in endotoxin-treated pigs.

Low intravenous doses of endotoxin [lipopolysaccharide (LPS), 0.7 microgram/kg] induce monophasic fever, increase anterior and posterior pituitary hormone release, and enhance hypothalamic c-Fos expression in pigs, all of which can be prevented by indomethacin (Ind). The present study shows that the synthetic corticosteroid dexamethasone (Dex, 5 mg/kg) has a similar action to Ind and, when given alone, lowers core temperature. In addition, the corticosteroid synthesis inhibitor metyrapone (Met, 3.3 mg/kg, every one-half hour) reduces LPS fever and amplifies the effect of LPS on vasopressin, but not on oxytocin, release. The similar actions of Dex and Ind suggest that phospholipase A2 pathways controlling prostaglandin synthesis mediate the responses of prepubertal pigs to immunological challenge with LPS. The increased vasopressin release induced when animals receiving Met are also given LPS supports findings in other nonrodent species indicating an inverse relationship between cortisol and vasopressin. The attenuation of LPS fever by Met is suggestive of an endogenous antipyretic mechanism associated with enhanced neurohypophysial vasopressin secretion.

Effects of SR 49059, an orally active V1a vasopressin receptor antagonist, on vasopressin-induced uterine contractions.

OBJECTIVE: To test the effect of SR 49059, an orally active, nonpeptide, selective and specific antagonist of the vasopressin V1a receptors in humans. DESIGN: A placebo-controlled, double-blind, cross-over trial. SETTING: The Department of Obstetrics and Gynaecology, Lund University Hospital, Sweden. PARTICIPANTS: Twelve healthy women, who had previously been sterilised by tubal ligation. INTERVENTIONS: The women participated on days 1, 2 or 3 of two menstrual cycles, with intrauterine pressure recordings and intravenous bolus injections of 10 pmol/kg body weight of lysine vasopressin given 1 h before and at 1, 2 and 3 h after oral administration of 300 mg of the study drug or of placebo. MAIN OUTCOME MEASURE: The area between the recording curve and zero level of pressure. Vital signs, safety parameters and drug plasma concentrations were also measured. RESULTS: The spontaneous uterine activity as well as the response to lysine vasopressin injections before administration of the test drugs were almost identical at the two experiments. Following intake of SR 49059 the area under the recording curve (0-10 min) after the second, third, and fourth injection of lysine vasopressin were reduced by 57, 42, and 66%, respectively, compared with placebo. Trough plasma concentrations of lysine vasopressin were markedly higher and systolic blood pressure slightly lower after antagonist administration than after placebo, whereas no significant difference between treatments was observed in diastolic pressure, heart rate or plasma osmolality. CONCLUSIONS: This study demonstrates for the first time a biological effect of an orally active vasopressin V1a antagonist in humans in vivo and the results support the importance of vasopressin in uterine activation. The differences between study drug and placebo treatments in lysine vasopressin levels and systolic blood pressure, but lack of difference in osmolality indicate that SR 49059 antagonises the effect of lysine vasopressin on the vasopressin V1a receptor, but not that on the vasopressin V2 one. It is suggested that SR 49059 be explored therapeutically in dysmenorrhoea.

Restricting maternal space during parturition in the pig. Effects on oxytocin, vasopressin and cortisol secretion following vagino-cervical stimulation and administration of naloxone.

This experiment studied the effects on endocrine and birth parameters of parturient pigs produced by restricting maternal freedom of movement without otherwise altering environment. Six primiparous pigs (gilts) were each given a jugular catheter under anaesthesia 7 days before parturition and commenced birth in a strawed pen, 2.0 m x 1.5 m in size. Continuous automated blood sampling (3 ml min-1) from unrestrained gilts began following the birth of the first piglet (stage 1) and continued for 2 h. After at least 30 min of blood collection, maternal space was reduced to 2.0 m x 0.55 m by placing rails across the pen (stage 2). The scope for movement in stage 2 was similar to that offered by a farrowing crate. After at least 25 min each gilt was given the opioid antagonist naloxone (1 mg kg-1 i.v.: stage 3). At each stage, vagino-cervical stimulation (VCS) was applied to mimic foetal ejection. Non-cervically stimulated oxytocin (OT) secretion between stages 1 and 2 was unchanged (P > 0.05) but increased significantly relative to both stages 1 and 2 following naloxone treatment for 15-20 min (P < 0.05, paired t-tests on log10 data). Following VCS in all stages plasma OT rose (P < 0.05) for 1-2 min in a similar way to that seen previously following foetal ejection, the increases being proportionally similar irrespective of stage or baseline secretion. Cortisol secretion did not increase as a consequence of space restriction (mean +/- SEM concentrations were 28.6 +/- 8.51 pmol l-1 and 32.3 +/- 11.8 pmol l-1 in stages 1 and 2, respectively). In addition, VCS did not significantly affect cortisol output. Lysine vasopressin concentrations were not affected as a consequence of either stage or VCS. Parturition was not interrupted following space restriction of gilts. These data suggest that reducing maternal space allowance during parturition is not stressful when the process does not involve the movement of animals to novel surroundings.

Hyperthermic and endocrine effects of intravenous prostaglandin administration in the pig.

Experimentally induced fever is accompanied by a variety of hormonal changes, and there is evidence to suggest that some of these responses may be mediated by prostaglandins. However, little is known about the endocrine effects of peripherally administered prostaglandins, especially in domesticated species. In this study, the effects of intravenous prostaglandin E2 (PGE2; 20 micrograms/kg) on deep body temperature and plasma concentrations of cortisol, lysine vasopressin (LVP), and growth hormone were investigated in prepubertal pigs (n = 6) prepared with venous catheters and sampled at 10-min intervals for 3 hr. PGE2-induced hyperthermia, which lasted for the duration of the study, was accompanied by a 70-min increase in cortisol and LVP concentrations. Moreover, this hyperthermic response was checked when LVP levels were high. These results indicate that a fever-inducing intravenous injection of PGE2 produced a marked anterior and posterior pituitary hormone response in growing pigs. Also, the transient increase in LVP may be correlated with a central action of the hormone, limiting the extent of the fever. In addition, because the majority of the animals exhibited mild hyperthermia (0.5 degrees C) under control conditions, the results suggest that, in a given population of pigs, there may be some animals that exhibit stress-induced hyperthermia.

The CCKA receptor antagonist devazepide inhibits the effect of apomorphine on vasopressin release in pigs.

1. A transient increase in plasma vasopressin concentrations represents a physiological correlate of nausea in animals that vomit. 2. The CCKA receptor antagonist devazepide has previously been shown to inhibit vasopressin release induced in pigs by intravenous (i.v.) CCK. 3. This study investigated whether devazepide (70 micrograms/kg i.v.) would affect vasopressin secretion induced in pigs (n = 6) by the emetic drug apomorphine (25 micrograms/kg i.v.). 4. Apomorphine stimulated vasopressin release in the 30 min period following injection; this effect was prevented by prior administration of devazepide. 5. The results suggest that CCKA receptor antagonists may have the ability to prevent nausea and/or emesis.

Reliability of hormonal levels for assessing the hypothalamic-pituitary-adrenocortical system in clinical pharmacology.

Few data are available on the reliability of measurements of adrenocortical and corticotroph hormones for use in clinical pharmacology. Two placebo controlled cross-over trials in 20 normal healthy male subjects offered the opportunity to perform three repeat samplings of adrenocortical and corticotroph hormones at 1 to 5 week intervals during the placebo periods. Measurements of baseline levels of plasma, salivary and urinary cortisol, plasma adrenocorticotroph hormone (ACTH), lipotrophic hormone (LPH), beta-endorphin, post tetracosactrin levels of plasma and salivary cortisol, post corticotrophin releasing hormone (CRH)-lysine vasopressine (LVP) levels of plasma cortisol, ACTH and LPH; and post metyrapone levels of plasma cortisol and 11-deoxycortisol (compound S), ACTH, LPH, beta-endorphin were performed in the same laboratory. The reliability of the measurements was estimated by computing the intraclass correlation coefficient (R) and by using Altman-Bland graphical method. The Rs of baseline parameters varied from 0.18 (for 08.00 h salivary cortisol) to 0.55 (for 08.00 h plasma cortisol and nocturnal urinary cortisol). In contrast, parameters obtained after direct stimulation or inhibition of the producing targets were much more reliable: Rs were above 0.80 for post tetracosactrin levels of plasma and salivary cortisol, post CRH-LVP levels of plasma ACTH and LPH. The Rs were below 0.50 for post metyrapone levels of plasma 11-deoxycortisol, ACTH, LPH and beta-endorphin. The interval between sampling did not affect R estimates. These data show that peak levels of plasma cortisol and ACTH after direct stimulation are highly reliable whereas baseline and main post-metyrapone levels are not.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors associated with vasopressin release in exercising swine.

This study examined the effect of dynamic exercise on vasopressin release in the miniswine and factors that may elicit this response (n = 15). Thus lysine vasopressin (LVP), the catecholamines epinephrine and norepinephrine (EPI and NE), plasma renin activity (PRA), and plasma volume, Na+, and osmolality were measured before and during treadmill running at work intensities of 60, 80, and 100% of each swine's maximal heart rate reserve (HRR). LVP increased in a progressive manner similar to that of humans, ranging from 5.9 +/- 0.4 pg/ml before exercise to 30.1 +/- 4.5 pg/ml during maximal exercise. EPI, NE, and PRA [an index of angiotensin II (ANG II) activity] demonstrated a pattern of response comparable to LVP. Although these hormones can influence the release of LVP, only PRA displayed a strong correlation with LVP (r = 0.84). When ANG II synthesis was blocked (captopril, 1-3 mg/kg, intra-atrial injection) during exercise (80% HRR), plasma LVP was reduced from 9.9 +/- 0.6 to 7.5 +/- 0.6 pg/ml (P < 0.05). In addition, moderate-to-strong correlations were found between plasma concentrations of LVP and plasma osmolality (r = 0.79) and body temperature (r = 0.78). Plasma LVP also correlated with decreases in plasma volume (r = 0.84). These data suggest that the miniswine model is a good one for studying vasopressin effects during exercise and that ANG II appears to be a particularly strong stimulus for the release of this hormone.

CCK-A receptors mediate the effect of cholecystokinin on vasopressin but not on cortisol in pigs.

Bolus intravenous injections of cholecystokinin (CCK) octapeptide induce a rapid rise in plasma vasopressin and a later increase in cortisol in the prepubertal pig. To determine whether these endocrine responses involve CCK-A or CCK-B receptors, this experiment investigated the effect of CCK (1 microgram/kg) in pigs (n = 7) pretreated with the CCK-A antagonist L 364718 (70 microgram/kg) or the CCK-B antagonist L 365260 (10 ng/kg and 10 micrograms/kg). The animals were prepared with jugular vein catheters and given the antagonist vehicle, L 364718, or L 365260 10 min before administration of CCK or saline. Analysis of hormone concentrations in blood samples taken 2, 5, 10, and 20 min after the second injection indicated that an abrupt rise in vasopressin, detectable within 2 min of CCK administration, occurred after vehicle or L 365260 pretreatment but not when CCK was preceded by L 364718. In contrast, the rise in plasma cortisol that was observed approximately 15 min after CCK injection was not prevented by either antagonist. Thus peripherally administered CCK induces vasopressin release by CCK-A receptor activation, in agreement with its inhibitory effect on food intake in this species. However, the effect of CCK on cortisol secretion does not appear to involve either CCK-A or CCK-B receptors.

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.

Neuroendocrine responses to hypertonic saline/dextran resuscitation following hemorrhage.

The neuroendocrine responses to resuscitation with 7.5% hypertonic saline/6% Dextran-70 (HSD) following hemorrhagic hypotension were evaluated in conscious swine. Following hemorrhage (37.5 ml/kg/60 min) animals received 4 ml/kg of HSD (n = 6) or 0.9% saline (n = 8). Administration of normal saline did not alter cardiovascular function nor attenuate an increase in hormones. HSD rapidly improved cardiovascular function and acutely decreased ACTH, plasma renin activity (PRA), cortisol, norepinephrine (NE), epinephrine (E), aldosterone, and lysine vasopressin levels (LVP). The initial decreased in ACTH, cortisol, and aldosterone levels was due primarily to hemodilution associated with the expansion of plasma volume. The reductions in NE, E, LVP, and PRA were greater than those attributed to hemodilution alone. Values for LVP, NE, and E remained at values below those at the end of hemorrhage, but greater than basal levels, while PRA returned to values similar to these at the end of hemorrhage. The decrease in LVP, NE, and E following HSD resuscitation for the treatment of hemorrhagic hypotension may result from and contribute to the rectification of cardiovascular and metabolic function.

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.

Isocratic high-performance liquid chromatography-photodiode-array detection method for determination of lysine- and arginine-vasopressins and oxytocin in biological samples.

A simple, isocratic, sensitive (1 ng), and specific high-performance liquid chromatographic (HPLC) method based on photodiode-array detection (PAD) is described for simultaneous quantitation of the bioactive peptides, lysine vasopressin (LVP), arginine vasopressin (AVP) and oxytocin (OXY). Acidified pig plasma and left ventricular (LV) tissue samples were first extracted with Sep-Pak C18 columns, and the bioactive peptides were eluted with methanol, then dried at 37 degrees C and reconstituted with HPLC mobile phase. The bioactive peptides were separated by HPLC on a Dynamax 3009-A C8 column with a mobile phase of 0.1% trichloroacetic acid-50 mM heptanesulfonic acid-30mM triethylamine-20% acetonitrile in water, pH 2.5 and identified with a Waters 990-PAD system (spectrum index plots in the range 200-400 nm). Standards of LVP, AVP and OXY and their mixtures showed a linear increase in the range 5 to 100 ng and were eluted at 6.1, 6.9 and 4.6 min, respectively. Spectrum analysis showed a distinct absorption peak at 280 nm, corresponding to peptide bonds. The reproducibility of the method coefficient of variation for standards is 6.9, 5.8 and 4.7% for LVP, AVP and OXY, respectively. In plasma and tissue it is much higher: 12.9% (LV tissue) and 18.6% (plasma) for LVP. Pig plasma contains negligible amounts of AVP and OXY; LVP is much higher (0.28 +/- 0.19 ng/ml). In pig tissue, LVP predominates (6.95 ng/g wet weight) compared to AVP (1.45) and OXY (1.50). Spectral analysis is necessary to identify the bioactive peptide peaks among interfering substances and to increase the sensitivity four-fold. The method described here is useful for the simultaneous determination of LVP, AVP and OXY in the nanogram range and can be extended to picogram levels by employing PAD spectral analysis techniques.

Response of prolactin to hemorrhage is similar to that of adrenocorticotropin in swine.

Prolactin (PRL) responds to several stimuli that elicit release of adrenocorticotropin (ACTH), but does not increase in response to hemorrhage in fetal animals. To determine whether PRL increases after hemorrhage in older animals, 11 immature female swine were prepared chronically under halothane and conditioned behaviorally to lie in a sling. They were bled 14 ml/kg over 5 min. PRL, ACTH, cortisol (F), lysine vasopressin (LVP), and pressure renin activity (PRA) were measured by radioimmunoassay. Epinephrine (EPI) and norepinephrine (NE) were separated by high-performance liquid chromatography. Arterial PRL increased at 0.75 and 1 h (P less than 0.01) and paralleled ACTH and F that peaked at 0.75 h (P less than 0.05 and P less than 0.01, respectively). All three hormones recovered significantly by 4 h. In contrast, PRA and LVP peaked transiently at 0.25 h after hemorrhage and recovered by 1.5 h (P less than 0.05, in each case). EPI and NE did not change significantly. In individual pigs, ACTH and F each showed correlations (Spearman) with PRL that were positive in 10 pigs and significant in six and five pigs, respectively. The pig with the smallest ACTH change (8.4 pg/ml peak) showed no increase in PRL. Peaks in PRL were simultaneous with (five pigs) or delayed by 15 min (four pigs) or 30 min (one pig) from peaks in ACTH. Significant correlations of PRL with PRA and with LVP occurred in only two pigs and in one pig, respectively. A common pathway may contribute to other independent mechanisms controlling the release of ACTH and PRL after hemorrhage.

Effect of available surface water on levels of antidiuretic hormone (lysine vasopressin) and water and electrolyte metabolism of the Rottnest Island quokka (Setonix brachyurus).

A sensitive radioimmunoassay was developed to measure circulating levels of the neurohypophysial peptide lysine vasopressin (LVP) in the marsupial quokka (Setonix brachyurus), which is abundant on Rottnest Island off the coast of Western Australia. Animals from locations on the island where free water is completely absent were compared in midsummer with animals from sites where brackish water is available and utilized by the quokkas. In the animals from West End, where free water is absent, circulating levels of LVP averaged 89.2 +/- 19.6 pg/ml, which was significantly higher than the mean level of 35.6 +/- 15.8 pg/ml measured in individuals collected from the Lakes site with access to brackish drinking water. Rates of water and sodium turnover, measured with isotopes, were significantly greater in Lakes than West End animals, as were renal clearances of sodium, chloride, urea, and total osmolytes. Despite an obvious osmotic diuresis resulting from the ingestion of salty water, the Lakes animals were in better physical condition at the end of summer than the West End animals which lack free water, and these latter individuals showed signs of slight dehydration with elevated plasma and urinary electrolyte concentrations and osmolalities.

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.

Endobronchial versus intravenous application of the vasopressin derivative glypressin during diagnostic bronchoscopy.

Glypressin is a vasopressin derivative which is used in the present study to stop pulmonary bleeding. The effects of endobronchially versus intravenously applied glypressin were examined during diagnostic fibreoptic bronchoscopy in 27 patients. Transcutaneously measured blood gases and haemodynamics were analysed after 1 mg glypressin was given. The glypressin plasma level was 251 fold higher after the intravenous than after the endobronchial administration. After endobronchial application no significant changes were observed for blood pressure, heart rate or blood gases. Following the intravenous glypressin application there was a significant increase in diastolic blood pressure. The bronchial mucosa pallor appeared earlier after topical than after systemic glypressin application. The haemostyptic effect was similar for both routes of application.

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.

Osmoregulation of vasopressin secretion and thirst during the estrous cycle of pigs.

The influence of the reproductive cycle on ingestive behaviors, osmotically induced fluid intake, and peripheral blood levels of several hormones involved in fluid electrolyte balance was investigated in young adult female pigs. Food, water, and salt intakes and plasma aldosterone levels were significantly lower during estrus compared with the luteal and follicular phases, whereas plasma sodium (PNa) was higher. Plasma renin activity and lysine vasopressin (LVP) levels did not vary with the cycle. Regression analyses of the relationship between plasma LVP and PNa in unanesthetized, unstressed animals infused for 2 h with intravenous 5% NaCl revealed no significant differences in terms of the osmotic threshold and sensitivity of LVP release at different stages of the reproductive cycle. In contrast, when osmotic loading was carried out with continuous access to water, the osmotic threshold for drinking was found to be significantly higher and the rate of drinking lower during estrus. The results indicate that in the adult female pig the stage of the reproductive cycle has an influence on ingestive behaviors and the osmoregulation of thirst. Osmoregulation of vasopressin secretion, on the other hand, appears to be independent of the estrous cycle in this species.