Effects of morphine and naloxone on the release of oxytocin and on milk ejection in dairy cows

2000 ◽  
Vol 67 (1) ◽  
pp. 13-20 ◽  
Author(s):  
VLADIMIR TANČIN ◽  
WOLF-DIETER KRAETZL ◽  
DIETER SCHAMS
Keyword(s):  
Dairy Cows ◽  
Receptor Agonist ◽  
Opioid System ◽  
Dependent Manner ◽  
Milk Ejection ◽  
Milk Flow ◽  
Oxytocin Release ◽  
Dose Dependent ◽  
Μ Receptor ◽  
Stimulation Of

The aim of this study was to investigate the action of opioids (the μ receptor agonist morphine) and the antagonist naloxone on inhibition of oxytocin release and milk let-down in response to milking in dairy cows. In the first experiment, cows were injected with 0, 21, 70 and 210 mg morphine 10 min before milking on four successive days. Plasma oxytocin levels after 1 min manual stimulation of the udder were reduced by 70 and 210 mg morphine, and milk let-down was inhibited at the latter dose. In the second experiment, cows were injected after a control milking with 210 mg morphine (or 350 mg at 10 min before milking the following day if not effective) to inhibit milk flow. On the following day the inhibiting dose of morphine was given with 210 mg naloxone. Naloxone injection given before morphine had no effect on plasma oxytocin concentrations, but abolished the inhibition of oxytocin release by morphine and potentiated oxytocin release in response to milking. Naloxone alone injected the day after control milking increased oxytocin levels during milking, suggesting involvement of the opioid system in milking. A model has been developed for the control of opioid effects during milking. Morphine suppressed oxytocin release during milking in a dose-dependent manner and the effect was reversible by naloxone.

Effect of stimulation intensity on oxytocin release before, during and after machine milking

2003 ◽  
Vol 70 (3) ◽  
pp. 349-354 ◽  
Author(s):  
Daniel Weiss ◽  
Alen Dzidic ◽  
Rupert M Bruckmaier
Keyword(s):  
Dairy Cows ◽  
Milk Production ◽  
Threshold Level ◽  
Flow Profile ◽  
Milk Ejection ◽  
Machine Milking ◽  
Milk Flow ◽  
Oxytocin Release ◽  
Stimulation Period ◽  
Stimulation Of

Release of oxytocin (OT) is essential for milk ejection in dairy cows (Lefcourt & Akers, 1983; Bruckmaier & Blum, 1998). During milk ejection, alveolar milk is shifted into the cistern, which causes an increase of intracisternal pressure (Bruckmaier et al. 1994). To initiate maximum milk ejection at the start of milking, increasing OT concentration beyond a threshold level is sufficient (Schams et al. 1983). Increasing OT concentration beyond this threshold has no additional effect on intracisternal pressure, i.e., milk ejection (Bruckmaier et al. 1994). Stimulatory effects of milking by hand or by machine or by suckling are well documented (Gorewit et al. 1992; Bar-Peled et al. 1995; Tancin et al. 1995; Bruckmaier & Blum, 1996). At the start of milking, stimulatory effects of machine milking without pre-stimulation or with a manual pre-stimulation and subsequent machine milking cause the release of comparable amounts of OT (Gorewit & Gassman, 1985; Mayer et al. 1985; Bruckmaier & Blum, 1996), whereas the timing of the applied pre-stimulation is important for the shape of the milk flow curve. Should the pre-stimulation period be too short, or absent altogether, the start of the main milk flow is delayed resulting in a bimodal milk flow profile (Bruckmaier & Blum, 1996). Furthermore, the stimulation of only one teat causes an OT release similar to that caused by stimulation of all four teats (Bruckmaier et al. 2001). However, milk production is greater for hand milking or suckling than for machine milking, possibly owing to higher OT concentrations (Gorewit et al. 1992; Bar-Peled et al. 1995).

Lactational changes in oxytocin release, intramammary pressure and milking characteristics in dairy cows

1991 ◽  
Vol 58 (2) ◽  
pp. 159-169 ◽  
Author(s):  
Harald Mayer ◽  
Rupert Bruckmaier ◽  
Dieter Schams
Keyword(s):  
Dairy Cows ◽  
Milk Yield ◽  
Maximum Flow ◽  
Pressure Increase ◽  
Maximum Pressure ◽  
Early Lactation ◽  
Milk Ejection ◽  
Milk Flow ◽  
Oxytocin Release ◽  
Almost All

SummaryTwo experiments were conducted to investigate possible changes of milking-related oxytocin release (Expt 1) and of intramammary pressure and milking characteristics (Expt 2) throughout entire lactations in German Braunvieh dairy cows. Mean oxytocin concentrations after stimulation at onset of milking increased from 18·3 ± 15·9 to 30·7 ± 24·1 pg/ml in Expt 1 and decreased from 23·9 ± 17·6 to 15·4 ± 9·1 pg/ml in Expt 2, respectively, but remained above the level necessary to elicit complete milk ejection in both trials. Premilking baseline intramammary pressure had its maximum in early lactation until about month 4 and then decreased to ∼50% of its initial level. Ejection pressure followed a similar pattern, but dropped only to ∼75% of its maximum. This was due to the constant elevation of pressure increase, reaching its highest level in late lactation. Time from commencement of stimulation until maximum pressure exceeded 1 min in almost all instances even in early lactation and increased throughout lactation. Despite the normal decrease of milk yield average milk flow fell only slightly while maximum flow rate remained almost constant. Pressure increase, milk yield and milk flow were not different after 1 min and after extended stimulation. Thus there were no indications of a decreasing sensitivity of the milk ejection reflex during lactation, and milking characteristics were positively affected by intense teat stimulation. Suggestions for practical dairying are made.

scholarly journals Best combination of pre-stimulation and latency period duration before cluster attachment for efficient oxytocin release and milk ejection in cows with low to high udder-filling levels

2010 ◽  
Vol 78 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Shehadeh Kaskous ◽  
Rupert M Bruckmaier
Keyword(s):  
Storage Capacity ◽  
Latency Period ◽  
Milk Ejection ◽  
Suitable Alternative ◽  
Milk Flow ◽  
Total Milk ◽  
Oxytocin Release ◽  
Actual Degree ◽  
Period Duration ◽  
Stimulation Of

Experiments were designed to investigate the suitability of a combination of a short manual teat stimulation with a short latency period before teat cup attachment to induce and maintain oxytocin release and milk ejection without interruption. In Experiment 1, seven dairy cows in mid lactation were manually pre-stimulated for 15, 30 or 45 s, followed by either 30 s or 45 s of latency period. It was shown that all treatments induced a similar release of oxytocin without interruption until the end of milking. In particular, the latency period of up to 45 s did not cause a transient decrease of oxytocin concentration. In Experiment 2, milking characteristics were recorded in seven cows each in early, mid, and late lactation, respectively. Because the course of milk ejection depends mainly on the degree of udder filling, individual milkings were classified based on the actual degree of udder filling which differs between lactational stages but also between morning and evening milkings. All animals underwent twelve different udder preparation treatments, i.e. 15, 30, or 45 s of pre-stimulation followed by latency periods of 0, 30, 45, or 60 s. Milking characteristics were recorded. Total milk yield, main milking time and average milk flow rate did not differ between treatments if the degree of udder filling at the start of milking was >40% of the maximum storage capacity. However, if the udder filling was <40%, main milking time was decreased with the duration of a latency period up to 45 s, independent of duration of pre-stimulation. Average milk flow at an udder filling of <40% was highest after a pre-stimulation of 45 s followed by a latency period of another 45 s. In contrast, average milk flow reached its lowest values at a pre-stimulation of 15 s without additional latency period. However, average milk flow after a 15-s pre-stimulation increased with increasing latency period. In conclusion, a very short pre-stimulation when followed by a latency period up to 45 s before teat cup attachment remains a suitable alternative for continuous stimulation to induce milk ejection.

scholarly journals Milk yield, oxytocin and β-endorphin gradually normalize during repeated milking in unfamiliar surroundings

1996 ◽  
Vol 63 (2) ◽  
pp. 191-200 ◽  
Author(s):  
Rupert M. Bruckmaier ◽  
Hans-Ulrich Pfeilsticker ◽  
Jürg W. Blum
Keyword(s):  
Dairy Cows ◽  
Milk Yield ◽  
Control Level ◽  
Operating Theatre ◽  
Milk Ejection ◽  
Asymptotic Approach ◽  
Blood Samples ◽  
Milk Flow ◽  
Total Milk ◽  
Oxytocin Release

SummaryFor six successive milkings, six dairy cows were relocated immediately before milking to an unfamiliar operating theatre, a procedure previously shown to inhibit oxytocin release and milk ejection. Two control milkings were performed in familiar surroundings. After milk flow had ceased, two i.v. injections of 1 i.u. oxytocin were given to remove the remaining milk. Milk flow was recorded continuously and blood samples were taken every minute during milking and 10 min after milking. During the first milking in unfamiliar surroundings, no oxytocin was released. Thereby, only 13% of the total milk yield, the cisternal milk, was available and the alveolar milk fraction could only be removed after injection of oxytocin. During subsequent relocations oxytocin release steadily increased toward the control level, although the timing of oxytocin release remained delayed as compared with controls. However, the milk fraction available before oxytocin injection increased with increasing number of removals, following an asymptotic approach to control levels. The concentrations of β-endorphin, cortisol (and perhaps also of prolactin) gradually declined with the number of times the animal was moved to unfamiliar surroundings, i.e. hormone concentrations gradually adjusted to control level. During milking, concentrations of prolactin and cortisol increased, while β-endorphin concentrations decreased (except for the first relocation). We conclude that milking-related oxytocin release and therefore milk ejection adapted gradually to repeated relocations to unfamiliar surroundings. This adaptation was inversely related to β-endorphin concentrations, so it is possible that oxytocin release was suppressed by high circulating β-endorphin concentrations.

α1c- and β2-adrenergic receptor mRNA distribution in the bovine mammary gland detected by competitive RT-PCR

2001 ◽  
Vol 68 (4) ◽  
pp. 699-703 ◽  
Author(s):  
OLGA WELLNITZ ◽  
ANDREAS ZURBRIGGEN ◽  
ROBERT R. FRIIS ◽  
JÜRG W. BLUM ◽  
RUPERT M. BRUCKMAIER
Keyword(s):  
Mammary Gland ◽  
Dairy Cows ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Molecular Techniques ◽  
Milk Ejection ◽  
Milk Flow ◽  
Β Adrenergic Receptors ◽  
Stimulation Of ◽  
Receptor Distribution

Milk ejection and milk removal is considerably influenced by the sympathetic nervous system. Stimulation of α-adrenergic receptors by administration of α-adrenergic agonists inhibits alveolar milk ejection and milk removal in dairy cows due to smooth muscle contraction (Blum et al. 1989; Bruckmaier et al. 1991). However, contraction of the teat in response to α-adrenergic receptor stimulation has no influence on milk flow as long as milk is available in the cistern (Bruckmaier et al. 1997). Therefore, α-adrenergic stimulation causes inhibition of transport of alveolar milk into the cistern. On the contrary, the stimulation of β-adrenergic receptors facilitates milk ejection and milk removal in dairy cows (Bernabé & Peeters, 1980; Bruckmaier et al. 1991) because of muscle relaxation. Therefore, the distribution of α- and β-adrenergic receptors plays an important role in the milkability of dairy cows. However, from these in vivo studies it is not possible to distinguish between the different α1- and α2- and β2-receptor subtypes owing to the non-specific nature of the pharmacological agents used.To date, the precise tissue distribution of these different subtypes, in bovine mammary tissue, is unknown. Using molecular techniques, we were interested in the expression of genes that encode α1c and β2 as a preliminary study towards the understanding of noradrenergic receptor-gene expression and regulation in this important system.In addition, α1c- and β2-adrenergic receptors were determined in front and rear quarters of the mammary gland to investigate differences in receptor distribution within the udder and possible relations between adrenergic receptor distribution and the higher milk flow rates in rear than in front quarters (Rothenanger et al. 1995).

Modulation of Ca2+ transients in neonatal and adult rat cardiomyocytes by angiotensin II and endothelin-1

1996 ◽  
Vol 270 (3) ◽  
pp. H857-H868 ◽  
Author(s):  
R. M. Touyz ◽  
J. Fareh ◽  
G. Thibault ◽  
B. Tolloczko ◽  
R. Lariviere ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Agonist ◽  
Dependent Manner ◽  
Induced Responses ◽  
Ang Ii ◽  
Binding Studies ◽  
Vasoactive Peptides ◽  
Adult Cardiomyocytes ◽  
Etb Receptor ◽  
Dose Dependent

Vasoactive peptides may exert inotropic and chronotropic effects in cardiac muscle by modulating intracellular calcium. This study assesses effects of angiotensin II (ANG II) and endothelin-1 (ET-1) on intracellular free calcium concentration ([Ca2+]i) in cultured cardiomyocytes from neonatal and adult rats. [Ca2+]i was measured microphotometrically and by digital imaging using fura 2 methodology. Receptor subtypes through which these agonists induce responses were determined pharmacologically and by radioligand binding studies. ANG II and ET-1 increased neonatal atrial and ventricular cell [Ca2+]i transients in a dose-dependent manner. ANG II (10(-11) to 10(-7) M) failed to elicit [Ca2+]i responses in adult cardiomyocytes, whereas ET-1 increased [Ca2+]i in a dose-dependent manner. The ETA receptor antagonist BQ-123 significantly reduced (P 7< 0.05) ET-1 induced responses, and the ETB receptor agonist IRL-1620 (10(-7) to 10(-5) M) significantly increased (P < 0.05) [Ca2+]i in neonatal and adult cardiomyocytes. ET-1 binding studies demonstrated 85% displacement by BQ-123 and approximately 15% by the ETB receptor agonist sarafotoxin S6c, suggesting a predominance of ETA receptors. Competition binding studies for ANG II failed to demonstrate significant binding on adult ventricular myocytes, indicating the absence or presence of very few ANG II receptors. These data demonstrate that ANG II and ET-1 have stimulatory [Ca2+]i effects on neonatal cardiomyocytes, whereas in adult cardiomyocytes, ANG II-induced effects are insignificant, and only ET-1-induced responses, which are mediated predominantly via ETA receptors, are preserved. Cardiomyocyte responses to vasoactive peptides may thus vary with cardiac development.

scholarly journals Adrenaline Stimulation of Phospholipid Metabolism in Adipocyte Ghosts

1987 ◽  
Vol 40 (4) ◽  
pp. 405
Author(s):  
David Mann ◽  
Audrey M Bersten
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Adenylate Cyclase ◽  
Phospholipid Metabolism ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Membrane Phospholipids ◽  
Dose Dependent ◽  
Stimulation Of

The incorporation of long-chain fatty acids into phospholipids has been detected in adipocyte ghosts that were incubated with [1_14 C] stearic, [1_14 C] linoleic or [l_14C] arachidonic acid. Adrenaline and adenosine activated this incorporation within 15 s of exposure of the ghosts to the hormones and the response was dose dependent. Maximum incorporation of labelled linoleic acid occurred at 10-5 M adrenaline and 10-7 M adenosine. The a-agonist phenylephrine and the ~-agonist isoproterenol were also shown to stimulate the incorporation of fatty acid in a dose dependent manner. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol were each labelled preferentially with linoleic or arachidonic acid. p-Bromophenacylbromide, quinacrine and centrophenoxine inhibited the adrenaline-stimulated incorporation of fatty acids into ghost membrane phospholipids, and p-bromophenacylbromide also reduced the activation of adenylate cyclase by adrenaline. NaF, an activator of adenylate cyclase, like adrenaline, stimulated the incorporation of linoleic acid into ghost membrane phospholipids.

Interaction of adenosine with vasopressin in the inner medullary collecting duct

1990 ◽  
Vol 259 (4) ◽  
pp. F679-F687 ◽  
Author(s):  
Y. Yagil
Keyword(s):  
Pertussis Toxin ◽  
Receptor Agonist ◽  
Collecting Duct ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effects ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Camp Levels ◽  
Dose Dependent ◽  
Stimulation Of

Administration of adenosine (Ado) into rat renal artery induces dose-dependent diuresis that is independent of changes in glomerular filtration rate or renal blood flow, suggesting a direct effect on tubule H2O reabsorption. To test the hypothesis that Ado modulates cellular action of arginine vasopressin (AVP) as a tubular mechanism for the diuretic effect of Ado, interaction of Ado with AVP was studied in primary cell culture of rat inner medullary collecting duct (IMCD) epithelium. Stimulation of cells with 10(-6) M AVP in presence of 0.1 mM Ro 20-1724, a nonmethylxanthine phosphodiesterase inhibitor that has no effect on Ado receptors, increased adenosine 3',5'-cyclic monophosphate (cAMP) levels twofold or more above baseline. Stimulation of cells with the A1 Ado-receptor agonist N6-cyclohexyladenosine (CHA), the A2-receptor agonist 5'-(N-ethylcarboxamido)-adenosine (NECA), or with the P-site agonist 2',5'-dideoxyadenosine (DDA) significantly inhibited the AVP-stimulated cAMP response. Preincubation with pertussis toxin abolished the inhibitory effects of CHA and NECA, but not of DDA. The data suggest that, in the rat IMCD, Ado modulates AVP action by interfering with its ability to stimulate formation of its second messenger, cAMP. This effect is mediated by the extracellular Ado receptors A1 and A2 and by the intracellular P-site. It occurs by at least two pathways, one sensitive and the other insensitive to pertussis toxin.

Effect of galanin on glucose-, arginine-, or potassium-stimulated insulin release

1989 ◽  
Vol 256 (5) ◽  
pp. E619-E623
Author(s):  
T. Yoshimura ◽  
J. Ishizuka ◽  
G. H. Greeley ◽  
J. C. Thompson
Keyword(s):  
Insulin Release ◽  
High Glucose ◽  
Second Phase ◽  
Dependent Manner ◽  
Perfused Pancreas ◽  
Isolated Perfused Pancreas ◽  
Second Phases ◽  
High Concentrations ◽  
Dose Dependent ◽  
Stimulation Of

We have examined the effect of galanin infusion on glucose-stimulated release of insulin from the isolated perfused pancreas of the rat to better characterize the effect of galanin on the first and second phases of insulin release. The effects of galanin on insulin release stimulated by L-arginine or high concentrations of potassium were also examined. When perfusion of galanin was started 4 min before the start of perfusion of high glucose (16.7 mM), galanin (10(-8)-10(-11) M) inhibited both the first and second phases of insulin release in a dose-dependent manner. When perfusion of galanin (10(-8) or 10(-9) M) was started simultaneously with high glucose (16.7 mM), only the second phase of insulin release was suppressed (P less than 0.05). Galanin (10(-9) M) failed to inhibit insulin release stimulated by L-arginine (10 and 5 mM) or potassium (25 and 20 mM). These findings suggest that the inhibitory action of galanin on glucose-stimulated insulin release is exerted on early intracellular events that occur during the stimulation of insulin release and that are common to both phases. Because galanin does not inhibit insulin release stimulated by L-arginine or potassium, galanin may inhibit glucose-stimulated closure of potassium channels.

Physiological concentrations of insulin and T3 stimulate 3T3-L1 adipocyte acyl-CoA synthetase gene transcription

1996 ◽  
Vol 270 (5) ◽  
pp. E873-E881 ◽  
Author(s):  
M. S. Kansara ◽  
A. K. Mehra ◽  
J. Von Hagen ◽  
E. Kabotyansky ◽  
P. J. Smith
Keyword(s):  
Gene Transcription ◽  
Fold Increase ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Reciprocal Regulation ◽  
Stearoyl Coa Desaturase ◽  
Dose Dependent ◽  
Long Chain ◽  
Stimulation Of

Acyl-CoAsynthetase (ACS) is a key gene for cellular utilization of long-chain fatty acids. We characterized its regulation by physiological concentrations of insulin that acutely regulate metabolism. Our results demonstrate that subnanomolar insulin rapidly and maximally stimulates ACS gene transcription in the absence of protein synthesis; 0.5 nM insulin produced a 2.3 +/- 0.1-fold increase in ACS mRNA levels and induced ACS gene transcription 2.4 +/- 0.3-fold. The insulin sensitivity of ACS was compared with lipoprotein lipase (LPL) and stearoyl-CoA desaturase-1 (SCD-1), which were both less sensitive to insulin. Physiological triiodothyronine (10 nm) also induced ACS mRNA 2.4 +/- 0.1-fold and gene transcription 2.8 +/- 0.3-fold and coordinately induced LPL and SCD-1 mRNA and gene transcription. Because insulin and adenosine 3',5'-cyclic monophosphate often regulate genes involved in lipid and carbohydrate metabolism in a reciprocal manner, we evaluated effects of 1-methyl-3-isobutylxanthine (MIX).ACS mRNA levels were strongly downregulated by MIX in a dose-dependent manner, and ACS gene transcription inhibited in a coordinate manner with LPL and SCD-1. These data demonstrate a uniquely sensitive pattern of stimulation of ACS gene transcription by insulin with reciprocal regulation by MIX, and they suggest a significant role for ACS as a tightly regulated “gatekeeper” gene participating in the control of adipocyte metabolism.

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