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Biomedical subjects

U Knigge

Publications and source records attributed to U Knigge.

At least 91 records · Page 5Linked to original sources
PubMed1988

Noradrenaline as a possible mediator in the renal response to vascular expansion with blood in the cat.

In chloralose anaesthetized cats with renal arterial pressure kept constant at 100 mmHg, vascular expansion with precirculated blood, 20 ml kg b.w.-1, caused significant increments in arterial inflow rates of blood to the deep (ARBFD) and superficial (ARBFS) renal venous drainage area of 35 +/- (SE)10 and 19 +/- 6%, respectively, and in the excretion rates of water and sodium of 73 +/- 24 and 75 +/- 28%, respectively, while GFR remained essentially unchanged. In acutely denervated kidneys the responses to expansion were not significantly different from those of innervated kidneys, which indicated largely humoral mediation. Arterial plasma concentrations of noradrenaline, adrenalin, and vasopressin fell significantly to values of a half to one-third of pre-expansion values, while plasma dopamine was not significantly changed by expansion. The response to expansion could be (1) reversed by a 'substituting' intraaortic infusion of noradrenaline, and (2) imitated, without volume expansion, by an infusion of an alpha-adrenergic blocking agent (phentolamine). It is concluded that the renal response (excretory and vascular) to volume expansion with blood is largely humorally mediated and that circulating noradrenaline may play a causal role in the response.

Adrenergic alpha-Antagonists↗
PubMed1988

Release of NPY in pig pancreas: dual parasympathetic and sympathetic regulation.

Several lines of evidence have connected neuropeptide Y (NPY), a 36-residue polypeptide, to the sympathetic division of the autonomic nervous system. We studied the localization, the molecular characteristics, and the release of NPY and norepinephrine (NE) in the porcine pancreas. Immunohistochemical investigations revealed that NPY nerves around blood vessels were likely to be of adrenergic nature, whereas NPY-immunoreactive fibers close to exocrine and endocrine cells may originate from local ganglia also containing VIP (vasoactive intestinal peptide) and PHI (peptide histidine isoleucine). Electrical stimulation of the splanchnic nerve supply to the isolated perfused pig pancreas resulted in a corelease of NPY and NE into the venous effluent. Stimulation of the vagal nerves caused a sevenfold larger release of NPY without affecting the NE secretion. Characterization of the NPY immunoreactivity in the pancreatic tissue and in the venous effluent by gel filtration, high-performance liquid chromatography, and isoelectric focusing showed that the immunoreactive NPY was indistinguishable from synthetic porcine NPY. It is concluded that, although NPY is associated with sympathetic perivascular neurons, the majority of the pancreatic NPY-containing nerve fibers are likely to belong to the parasympathetic division of the autonomic nervous system.

Animals↗
PubMed1988

Histaminergic mediation of the stress-induced release of prolactin in male rats.

Histamine (HA) is likely to participate in the neuroendocrine regulation of prolactin (PRL) secretion. We, therefore, studied the possible involvement of HA in the stress-induced release of PRL in conscious male rats. HA (30 micrograms) infused intracerebroventricularly 15 min before decapitation elevated PRL plasma levels from 5 +/- 1 to 54 +/- 6 ng/ml (p less than 0.01). Intracerebroventricular infusion of the H2 receptor antagonists cimetidine (CIM: 100 micrograms) or ranitidine (RAN: 125 micrograms) abolished the PRL response to HA (p less than 0.01), while intracerebroventricular infusion of the H1 receptor antagonist mepyramine (MEP; 100 micrograms) inhibited the response only 40% (p less than 0.05). Intra-arterial infusion of CIM (2,000 micrograms) or RAN (2,500 micrograms) inhibited the HA-stimulated PRL secretion 52% (p less than 0.01) or 63% (p less than 0.01), respectively. The H1 receptor antagonists MEP (1,000 micrograms) and SKF-93944 (1,500 micrograms) had no effect following intra-arterial administration. Restraint stress increased the PRL level to 84 +/- 6 ng/ml (p less than 0.01 vs. control). This effect was prevented by intracerebroventricular infusion of CIM or RAN (p less than 0.01) and inhibited 75% by MEP (p less than 0.01). Intra-arterial infusion of CIM, MEP, and SKF-93944 inhibited the stress response about 50% (p less than 0.01), while RAN decreased the response only 25% (p less than 0.05). Ether stress elevated the plasma PRL concentration to 46 +/- 5 ng/ml (p less than 0.01 vs. control). When infused intracerebroventricularly CIM or RAN prevented the response (p less than 0.01), while MEP had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Histaminergic regulation of prolactin secretion: involvement of tuberoinfundibular dopaminergic neurons.

It has been shown that histamine (HA) stimulates prolactin (PRL) secretion via H2 receptors following intra-cerebroventricular infusion and via H1 receptors following systemic (intra-arterial) infusion. Since the effect of HA appears to be exerted at a suprapituitary level, we investigated the involvement of the tuberoinfundibular dopaminergic (TIDA) system in HA-induced PRL secretion in urethane-anesthetized male rats. HA infused intracerebroventricularly (30 micrograms) or intra-arterially (420 micrograms) decreased the dopamine (DA) concentration in pituitary portal blood by 30 and 23%, respectively. Blockade of DA receptors by pimozide did not prevent the stimulation of PRL secretion induced by intracerebroventricular infusion of HA or the H2 receptor agonist dimaprit. Furthermore, during DA receptor blockade intracerebroventricular infusion of the H1 receptor agonist 2-thiazolylethylamine inhibited PRL secretion. In contrast, pimozide prevented the stimulation of PRL secretion induced by intra-arterial infusion of HA and the H1 receptor agonist 2-thiazolylethylamine. In fact, under these conditions intra-arterial infusion of HA or the H2-receptor agonist dimaprit inhibited PRL secretion. During treatment with alpha-methyl-p-tyrosine, which reduced the hypothalamic DA content by 50%, HA infused intracerebroventricularly stimulated PRL secretion, while HA infused intra-arterially inhibited the secretion, which is in accordance with the results obtained during pimozide treatment. Cholinergic blockade by atropine did not prevent the HA-induced PRL release, excluding the possibility that the observed effect of pimozide is due to its anticholinergic property. We suggest that intracerebroventricular infusion of HA by activation of H2 receptors may stimulate PRL secretion partly via inhibition of the TIDA system and partly via other mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Histaminergic regulation of prolactin secretion: involvement of serotoninergic neurons.

The possible involvement of the serotoninergic system in histamine-induced PRL secretion was studied in urethane anesthetized male rats. Intracerebroventricular infusion of histamine (30 micrograms) stimulated PRL secretion 10-fold. This effect was mimicked by the H2-receptor agonist dimaprit (300 micrograms), while the H1-receptor agonist 2-thiazolylethylamine (140 micrograms) had no effect. Pretreatment with the serotonin receptor blockers methysergide (2.5 mg/kg i.p.) or ketanserin (2.5 or 10.0 mg/kg i.p.) reduced the PRL peak response to histamine 75, 54, or 58%, respectively. During serotonin receptor blockade, dimaprit had a stimulatory effect similar to that of histamine, while 2-thiazolylethylamine had no effect. Intraarterial infusion of histamine (420 micrograms) stimulated PRL secretion 6-fold. This effect was mimicked by the H1-receptor agonist 2-thiazolylethylamine (1,900 micrograms), while the H2-receptor agonist dimaprit (3,000 micrograms) had no effect. Pretreatment with methysergide (2.5 mg/kg i.p.) or ketanserin (2.5 or 10.0 mg/kg i.p.) reduced the peak response to histamine 54, 54, or 51% respectively. The effect of histamine was mimicked by 2-thiazolylethylamine, while dimaprit slightly inhibited the PRL secretion. The antiserotoninergic activity of methysergide and ketanserin was demonstrated by their ability to prevent the PRL-releasing effect to serotonin. The effects of methysergide and ketanserin were not due to dopamine-like activity, since none of the drugs affected basal PRL secretion and since the dopamine receptor antagonist pimozide did not prevent the inhibitory effect of methysergide on the histamine-induced PRL release. The findings indicate that histamine-stimulated PRL secretion is mediated in part by serotoninergic neurons.

Dimaprit↗
PubMed1988

Effect of histamine on the secretion of pro-opiomelanocortin derived peptides in rats.

In conscious male rats intracerebroventricular infusion of histamine increased the plasma concentrations of ACTH and beta-endorphin immunoreactivity 2.5-fold (P less than 0.01). Gel filtration of plasma revealed two peaks of beta-endorphin immunoreactivity corresponding to beta-endorphin and beta-lipotropin. The two fractions increased almost equally in histamine-stimulated animals, whereas most of the circulating beta-endorphin immunoreactivity in control animals corresponded to beta-endorphin. Central infusion of the H1-receptor agonist 2-thiazolylethylamine and of the H2-receptor agonists dimaprit or 4-methylhistamine increased the plasma ACTH and beta-endorphin immunoreactivity concentrations 2- and 3-fold, respectively (P less than 0.01). Infused intracerebroventricularly, the H2-receptor antagonists cimetidine or ranitidine prevented the histamine-induced increase in plasma ACTH and beta-endorphin immunoreactivity (P less than 0.01), whereas the H1-receptor antagonist mepyramine inhibited the peptide responses by 70% (P less than 0.01). Infused intra-arterially cimetidine or ranitidine inhibited the histamine-induced increase in plasma ACTH by 80% (P less than 0.01) and plasma beta-endorphin immunoreactivity by 45% (P less than 0.05), whereas mepyramine or the other H1-receptor antagonist SKF-93944 inhibited the ACTH response by 50% (P less than 0.05), but had no effect on the beta-endorphin immunoreactivity. The results indicate that histamine increases the release of the pro-opiomelanocortin derived peptides ACTH, beta-lipotropin and beta-endorphin from the anterior pituitary lobe, whereas an effect of histamine on the release of beta-endorphin from the neurointermediate lobe is possible. The effect of histamine seems primarily mediated by H2-receptors, whereas H1-receptors appear to play a minor role.

Adrenocorticotropic Hormone↗
PubMed1987

Corticotropin-releasing activity of gastrin-releasing peptide in normal men.

Gastrin-releasing peptide (GRP; mammalian bombesin) exerts several functions within the hypothalamus and is a putative regulator of pituitary hormone secretion. We investigated the effect of GRP on the secretion of pituitary hormones and cortisol in normal men. GRP was infused iv as primed infusions of 0.12 pmol/kg BW. min for 30 min (GRP I) and 1.50 pmol/kg. min for an additional 30 min (GRP II). GRP dose-dependently stimulated ACTH secretion compared with the effect of saline [net change in ACTH (delta ACTH) before and after treatment: GRP I, 3 +/- 1 (+/- SEM) vs. 0 +/- 1 pmol/L (P less than 0.05); GRP II, 5 +/- 1 vs. -3 +/- 1 pmol/L; P less than 0.01)]. A further increase in plasma ACTH concentration occurred after cessation of GRP infusion (7 +/- 2 vs. 0 +/- 1 pmol/L; P less than 0.025). GRP caused a similar dose-dependent stimulation of cortisol secretion compared with the effect of saline [delta cortisol before and after treatment: GRP I, -19 +/- 21 vs. -68 +/- 14 nmol/L (P less than 0.05); GRP II, 38 +/- 33 vs. -86 +/- 15 nmol/L (P less than 0.005)]. The serum cortisol concentration increased further after cessation of the GRP infusion (72 +/- 31 vs. -124 +/- 33 nmol/L; P less than 0.0025). GRP dose-dependently stimulated beta-endorphin immunoreactivity compared with the effect of saline [delta beta-endorphin immunoreactivity before and after treatment: GRP I, 6 +/- 1 vs. -3 +/- 1 pmol/L (P less than 0.01); GRP II, 11 +/- 4 vs. -6 +/- 2 pg/mL (P less than 0.025)]. GRP had no effect on PRL or GH secretion. We suggest that GRP participates in the neuroendocrine regulation of the secretion of proopiomelanocortin-derived peptides.

Adrenocorticotropic Hormone↗
PubMed1987

Effects of H2-receptor antagonists on prolactin secretion: specificity and mediation of the response.

The effects on prolactin secretion of histamine H2-receptor antagonists infused intracerebroventricularly were studied in urethane anaesthetized male rats. A dose of 1.6 mumol cimetidine stimulated basal prolactin secretion and did not affect the histamine-induced release, whereas 0.4 mumol cimetidine inhibited basal and histamine-stimulated prolactin secretion. 0.1 mumol cimetidine had no effect. The more potent H2-receptor antagonist ranitidine at doses of 0.1, 0.4, 1.6 mumol had no effect on basal prolactin secretion, whereas 0.4 and 1.6 mumol inhibited the histamine-stimulated secretion completely. SKF-92408, a compound resembling cimetidine in chemical structure but devoid of H2-receptor antagonist activity, stimulated basal prolactin secretion at a dose of 1.6 mumol, but had no effect on the histamine-induced release or at a dose of 0.4 mumol. The H2-receptor antagonists metiamide and oxmetidine (1.6 mumol) stimulated basal prolactin secretion and did not prevent the response to histamine. A dose of 0.4 or 1.6 mumol imidazole (the ring structure contained in cimetidine, SKF-92408, metiamide, and oxmetidine) had no effect on basal or histamine-stimulated prolactin secretion. The findings indicate that cimetidine stimulates prolactin secretion by a non-specific action when infused centrally at high doses. In contrast, when infused at lower doses cimetidine inhibits the basal and histamine-stimulated secretion by blockade of H2-receptors. The prolactin-stimulatory action of cimetidine was not due to an H2-agonist effect, since ranitidine did not prevent the response. Cimetidine did not stimulate prolactin secretion via an effect on the dopaminergic system, since the drug had no effect on the dopamine concentration in hypophysial portal blood or in hypothalamic tissue and since inhibition of the dopamine synthesis by alpha-methyl-p-tyrosine did not prevent the cimetidine-induced prolactin release.

Animals↗
PubMed1987

Effect of anaesthetics on PRL and LH secretion in rats. Importance of pre-anaesthetic adaptation and involvement of monoaminergic neurons.

General anaesthesia has been reported to interact with neuroendocrine functions leading to large variations in basal and stimulated plasma levels of several hormones, but the findings are often contradictory. In the present investigation we have attempted to clarify the importance of the experimental procedure when evaluating the influence of anaesthetics on the secretion of PRL and LH in male rats. One group of rats (non-adapted) were anaesthetized (ip) with pentobarbital (P), urethane (U), ketamine (A), or althesin (A) without being accustomed to the laboratory environment prior to anaesthesia. Another group of rats (adapted) were kept for 90 min in their individual cages before induction of anaesthesia with P or U. In non-adapted rats the plasma concentration of PRL declined rapidly during the first 30 min following administration of all anaesthetics or saline (controls) and attained a steady level after 60 min. Except for a brief rise following U injection, the LH concentration was not affected by anaesthesia in the non-adapted rats. In adapted rats, the concentration of both PRL and LH declined markedly during the pre-anaesthetic adaptation period and had stabilized at the end of that period. Following administration of U, P or saline, no further changes in the hormone concentrations were observed. Injection of the dopamine receptor antagonist pimozide prevented the decrease in plasma PRL during the adaptation period, but had no effect on LH secretion. In pimozide-treated rats, U caused a 5-fold increase in the PRL concentration. This effect of U was inhibited by the serotonin receptor antagonist methysergide. The PRL response to 30 micrograms of histamine was similar in conscious and U-anaesthetized rats, whereas P anaesthesia caused a reduction in the response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1986

Sympathoadrenal and parasympathetic responses to exercise.

Exhaustive exercise is associated with a persistent sensation of weakness and sometimes nausea suggesting abdominal vagal activity. We measured plasma indices of sympathoadrenal (adrenaline, noradrenaline, dopamine) and vagal (pancreatic polypeptide) activity before, during and after submaximal and maximal exercise in healthy young subjects. Plasma adrenaline, noradrenaline and dopamine increased to 8.5 (range 7.4-40.5), 48.0 (32.3-100.5) and 1.8 (1.2-6.6) nmol 1-1 respectively (n = 5), during maximal exercise and decreased towards control values within 15 min of rest. Pancreatic polypeptide (n = 10) increased only during maximal exercise and reached its highest value, 48 (21-145) pmol 1-1, after exertion. The results conform to an increase in sympathetic activity during exercise and a persistent vagal activity after intense exercise which could contribute to the sensation of weakness.

Adult↗
PubMed1986

Histaminergic stimulation of prolactin secretion mediated via H1- or H2-receptors: dependence on routes of administration.

Controversy exists regarding the involvement of H1- or H2-receptors in the PRL-releasing activity of histamine (HA). This could be due to differences in the route of administration of HA and histaminergic compounds. Therefore, we studied the effect on PRL secretion of HA and HA-agonists infused intracerebroventricularly (ICV) or systemically (IA) either alone or in combination with HA-antagonists in male rats. HA administered ICV as well as IA stimulated PRL secretion dose dependently. The stimulatory effect of ICV-infused HA was blocked by the H2-receptor antagonist cimetidine (CIM) and mimicked by the H2-receptor agonists 4-methylhistamine (4-MeHA) and dimaprit (DIM). In contrast, the H1-receptor antagonist mepyramine (MEP) enhanced the PRL-releasing effect of HA while the H1-receptor agonist 2-thiazolylethylamine (2-TEA) had no significant effect. The stimulatory effect of IA-infused HA was blocked by the H1-receptor antagonist MEP and mimicked by the H1-receptor agonist 2-TEA, whereas the H2-receptor antagonist CIM enhanced the PRL-stimulatory effect of HA and the H2-receptor agonist DIM was without effect. 4-MeHA stimulated PRL secretion, but this effect was unrelated to stimulation of H2-receptors. The effect of ICV administered HA was unaffected by IA infused antagonists and the effect of IA administered HA was not altered by ICV infused antagonists. HA had no effect on the PRL release from isolated adenohypophyses, and HA did not stimulate PRL secretion in pituitary stalk-sectioned rats following IA infusion. The findings indicate that HA administered ICV exerts its PRL releasing activity via H2-receptors while HA administered IA stimulates PRL secretion via H1-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Histaminergic regulation of prolactin secretion: dose-response relationship and possible involvement of the dopaminergic system.

Histamine (HA) may participate in the neuroendocrine regulation of pituitary hormone secretion. HA diphosphate infused iv for 120 min in a dose of 9, 18, 30, or 50 micrograms/kg BW.h to six normal men stimulated PRL secretion in a dose-dependent manner [absolute change in PRL (delta PRL) area = 52 X (HA dose) - 618; r = 0.9926; P less than 0.001]. The stimulatory effect of HA was modest and occurred during the second hour of infusion. This increase might be due to the opposing effects of HA on PRL secretion, specifically stimulation via H1 receptors and inhibition via H2 receptors. The PRL-releasing effect of 11 micrograms HA dihydrochloride was not significantly different from that of an equimolar dose of HA diphosphate (18 micrograms). Selective activation of H2 receptors by combined infusion of HA and the H1 receptor antagonist mepyramine inhibited PRL secretion compared to the effect of NaCl [delta PRL, -55 +/- 23 (+/- SEM) vs. -20 +/- 17 microIU/ml; P less than 0.01; n = 6). Mepyramine infused alone had no effect (delta PRL, -43 +/- 22 vs. -33 +/- 30 microIU/ml; n = 6). Selective activation of H1 receptors by combined infusion of HA and the H2 receptor antagonist cimetidine stimulated PRL secretion (delta PRL, 193 +/- 40 vs. -20 +/- 17 microIU/ml; P less than 0.0005; n = 6). When infused alone, cimetidine had only a modest and late stimulatory effect (delta PRL, 35 +/- 22 vs. -27 +/- 15; P less than 0.025; n = 6). Dopamine receptor blockade with metoclopramide (MET; 10 mg, three times daily, orally) did not prevent the PRL-inhibiting action of H2 receptor activation (delta PRL, -374 +/- 70 vs. -184 +/- 107 microIU/ml; P less than 0.01; n = 6), whereas the PRL-stimulating effect of H1 receptor activation was abolished by the drug (delta PRL, -249 +/- 64 vs. -174 +/- 54 microIU/ml; n = 6). The latter effect of MET was not due to exhaustion of the lactotrophs, since 200 micrograms TRH stimulated PRL secretion during MET treatment. These findings suggest that the H1 receptor-mediated PRL-stimulating effect of HA occurs through an inhibition of the dopaminergic system, whereas the H2 receptor-mediated PRL-inhibiting effect of HA does not involve dopaminergic neurons.

Adult↗
PubMed1985

Gastrin-releasing peptide: effect on exocrine secretion and release from isolated perfused porcine pancreas.

The effect of gastrin-releasing peptide (GRP) on pancreatic exocrine secretion was studied by infusing it at four dose levels (0.01, 0.1, 1.0, and 10 nmol/l) into the arterial line of the isolated perfused porcine pancreas. At 1.0 nmol/l GRP stimulated protein (37-fold), fluid (13-fold), and bicarbonate secretion (12-fold). Atropine at 1 mumol/l diminished the protein secretion in response to infusion of GRP at a dose of 1 nmol/l to 45% of control. Fluid and bicarbonate responses were not affected by atropine treatment. Electrical stimulation of the vagus nerves resulted in an increase in pancreatic output of GRP and a concomitant stimulation of exocrine secretion. Infusions of acetylcholine, carbachol, pilocarpine, or dimethylphenylpiperazinium had no effect on the output of GRP, although hexamethonium abolished the response to vagal stimulation. It is concluded that GRP in conjunction with acetylcholine is likely to play a prominent part in parasympathetic regulation of pancreatic exocrine secretion.

Animals↗
PubMed1985

Effect of histamine on basal and TRH/LH-RH-stimulated PRL and LH secretion during different phases of the menstrual cycle in normal women.

The neurotransmitter histamine (HA) may participate in the regulation of some pituitary hormones. We, therefore, investigated the effect of HA (50 micrograms/kg body weight/h, infusion 0-240 min) on basal and thyrotropin-releasing hormone (TRH) and luteinizing hormone releasing hormone (LH-RH) stimulated prolactin (PRL) and LH secretion in 5 normal women during the early follicular and the luteal phases of the same menstrual cycle. HA had no effect on the basal secretion of the two hormones. However, the PRL response to 200 micrograms TRH during the HA infusion was significantly increased compared to the response to a saline control infusion during the early follicular phase (peak responses were 1,902 +/- 398 vs. 1,228 +/- 230 microIU/ml, p less than 0.025) and during the luteal phase (peak responses were 2,261 +/- 335 vs. 1,647 +/- 245 microIU/ml, p less than 0.05). HA potentiated the LH response to 100 micrograms LH-RH during the early follicular phase (peak responses were 37.1 +/- 4.9 vs. 26.9 +/- 4.5 mIU/ml, p less than 0.05) and during the luteal phase (peak responses were 79.3 +/- 22.5 vs. 50.7 +/- 11.4 mIU/ml, p less than 0.025). We, therefore, found HA to have a potentiating effect on TRH/LH-RH-stimulated PRL and LH secretion in women. The results are similar to our previous findings in men, although the potentiating effects of HA were higher in women.

Adult↗