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1. |
PROCEEDINGS OF THE AUSTRALASIAN SOCIETY OF CLINICAL sAND EXPERIMENTAL PHARMACOLOGISTS |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 1-90
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ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb03011.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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2. |
ANTICONVULSANT ACTIVITY OF DI‐N‐PROPYLACETATE AND BRAIN MONOAMINE METABOLISM IN THE RAT |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 11-16
Wadie T. Abed,
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摘要:
SUMMARY1. Sodium di‐n‐propylacetate (DPA) treatment induced significant increases in brain contents of gamma‐aminobutyric acid (GABA), 5‐hydroxyindoleacetic acid (5‐HIAA) and homovanillic acid (HVA). Furthermore, the threshold for pentylenetetrazol (PTZ) clonic convulsions was also increased in response to DPA administration.2. Pretreatment with inhibitors of monoamine synthesis α‐methyl‐p‐tyrosine (AMPT) andp‐chlorophenylalanine (PCPA) did not alter the anticonvulsant activity of DPA, but when given alone, both AMPT and PCPA caused significant decreases in brain monoamine contents and PTZ threshold seizures.3. Experiments using probenecid suggest that the increases in 5‐HIAA and HVA seen after DPA treatment could have resulted from inhibition of their active transport out of the brain. These data indicate that the anticonvulsant action of DPA is not dependent on changes in monoamine met
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01259.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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3. |
EFFECTS OF LOW DOSE INFUSION OF ATRIAL NATRIURETIC FACTOR ON ACUTE INHIBITION OF ANGIOTENSIN CONVERTING ENZYME IN NORMAL MAN |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 17-22
Motoyuki Nakamura,
Naoshi Arakawa,
Yukio Kawata,
Masataka Kato,
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摘要:
SUMMARY1. We have studied the effects of low dose infusions of atrial natriuretic factor (human ANF (99–126), 1.95 pmol/min per kg) on angiotensin converting enzyme (ACE) inhibitor‐induced haemodynamic and hormonal changes in healthy subjects.2. ACE inhibitor (captopril 25 mg, administered orally) was given against a background infusion of physiological saline (placebo day) or ANF (experimental day).3. Compared with the placebo observations, ANF enhanced the fall in plasma aldosterone concentrations induced by captopril (P<0.05).4. The rise of plasma renin activity following administration of ACE inhibitor which was observed during placebo infusion was abolished by ANF (P<0.05).5. The responses of systemic blood pressure and heart rate to the converting enzyme inhibition were not affected by the infusion of ANF.6. These results suggest that variations in endogenous circulating ANF may influence, in part, the response of these hormonal levels during ACE inhibit
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01260.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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4. |
STIMULATION OF β1‐ADRENOCEPTORS ENHANCES ELECTRICALLY EVOKED [3H]‐ACETYLCHOLINE RELEASE FROM RAT PHRENIC NERVE |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 23-32
I. Wessler,
G. Holzer,
A. Künster,
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摘要:
SUMMARY1. The effects of isoprenaline, noradrenaline and fenoterol on the electrically evoked release of [3H]‐acetylcholine from the rat phrenic nerve were investigated.2. Isoprenaline (0.1 μmol/L) and noradrenaline (1 μmol/L) enhanced evoked [3H]‐acetylcholine release by about 90%, an effect which was abolished by CGP 20712A (0.1 μmol/L), a specific antagonist at β1‐adrenoceptors. Noradrenaline still enhanced [3H]‐acetylcholine release in the presence of phentolamine (1 μmol/L).3. The enhancing effect of both isoprenaline and noradrenaline decreased at prolonged exposure times (24–32 min). A pre‐exposure of the tissue to a low concentration (0.01 μmol/L) of isoprenaline prevented the enhancing effect of 0.1 μmol/L isoprenaline.4. Fenoterol, a specific agonist at β2‐adrenoceptors, did not modify evoked [3H]‐acetylcholine release.5. The present results indicate the existence of facilitatory β1‐adrenoceptors on the motor nerve. These receptors appear to be desensitized either by a high concentration of, or by a long exposure to, agonists. Under the present conditions noradrenaline enhances the release of newly synthesized transmitter mainly by stim
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01261.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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5. |
PRELIMINARY STUDY ON THE ANTINOCICEPTIVE EFFECT OF ELEPHANT β‐ENDORPHIN |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 33-37
Chak‐Lam Wong,
Man‐Keung Wai,
Heung‐Chin Cheng,
David Chung,
Donald Yamashiro,
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摘要:
SUMMARY1. Intraventricular administration of human β‐endorphin and elephant β‐endorphin significantly prolonged the tail flick response tested 30 min later. However, elephant β‐endorphin was about 7–8 times more potent than human β‐endorphin in the tail flick test.2. β‐Endorphin1‐27antagonized the antinociceptive effect of both human β‐endorphin and elephant β‐endorphin by the same extent. Naloxone also antagonized the antinociceptive effects of the β‐endorphins but it was less effective than β‐endorphin1‐27.3. Human β‐endorphin and elephant β‐endorphin were of equal potency in inhibiting the abdominal constriction response induced by intraperitoneal (i.p.) acetic acid. Both β‐endorphin1‐27and naloxone antagonized these effects of the β‐endorphins with naloxone being more effective.4. The present study showed that different opioid receptor subtypes may be involved in the tail flick test and the abdominal constriction test. Furthermore, elephant β‐endorphin was a better antinociceptive ag
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01262.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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6. |
EFFECTS OF NEUROPEPTIDE Y ON BAROREFLEX CONTROL OF HEART RATE AND MYOCARDIAL CONTRACTILITY IN CONSCIOUS RABBITS |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 39-49
R. B. Minson,
R. J. McRitchie,
J. P. Chalmers,
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摘要:
SUMMARY1. The effects of intravenous (i.v.) neuropeptide Y (NPY, 10 μg/kg bolus) on the stimulus‐response curves relating changes in heart period (HP) and in peak left ventricular (LV) dP/dt to acute changes in mean arterial pressure (MAP) were determined in conscious, normotensive rabbits.2. The relationship between increases and decreases in MAP and the subsequent changes in HP were represented by a sigmoid‐shaped curve described by a logistic function. Following NPY administration there was a baroreflex‐dependent increase in the maximum slope (sensitivity) at the midpoint of this MAP‐HP curve from 7.0 ± 0.5 to 10.6 ± 1.3 ms/mmHg (P<0.05). NPY caused an upward shift in the whole curve which reflected the NPY‐induced bradycardia and was independent of baroreflexes.3. The relationship between increases in MAP and decreases in peak LV dP/dt was determined during fixed‐rate atrial pacing to prevent the effects of the accompanying bradycardia. Increases in MAP and the corresponding reductions in peak LV dP/dt were represented by an exponential function.The slope of the curve, measured at its origin 5–15 min after NPY administration, was reduced from −0.9 ± 0.2 to −0.4 ± 0.1 units (P<0.05).4. The effects of NPY are consistent with an action on efferent connections of the arterial baroreceptor reflex, mediated through a reduction in cardiac β‐adrenergic tone. They would also be explained through actions on the afferent or central neural conn
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01263.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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7. |
ACUTE MANNITOL AND SALINE VOLUME EXPANSION IN THE RAT: EFFECT ON TRANSEPITHELIAL POTENTIAL DIFFERENCE IN PROXIMAL TUBULES |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 51-59
E. Sugo,
Á. Z. Györy,
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摘要:
SUMMARY1. Transepithelial potential difference (PDte) of proximal tubules was measured in rats under control conditions (C), and mannitol‐saline and saline extracellular fluid volume expansion (MVE, SVE, respectively) under conditions of normal net lumen to basal sodium transport.2. PDtewas measured in kidneys bathed with Hartmann's solution or covered with mineral oil under both volume‐expanded conditions together with their controls.3. PDtewas significantly lower in kidneys bathed with Hartmann's solution than in those covered with oil.4. In MVE rats, with mineral oil covering the kidneys, PDte(expressed as mean and s.e.m.) was for the control 2.20 ± 0.05 (n= 45) mV and MVE 1.97 ± 0.04 (n= 36) mV, lumen positive, a significant reduction of 10% (P<0.001). In SVE rats, with mineral oil covering the kidneys, PDtewas for C = 2.42 ± 0.05 (n= 74) mV and SVE = 1.93 ± 0.03 (n= 67) mV, a significant reduction (P<0.001) of 20%.5. According to thermodynamic considerations, neither of these changes is sufficient to explain the 50% inhibition of Na transport measured previously during MVE and SVE with autologous tubular fluid. The present results offer further evidence supporting the idea that the inhibition of Na transport during MVE and SVE is largely due to inhibition of the active Na transporti
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01264.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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8. |
VASOACTIVE INTESTINAL POLYPEPTIDE AND HUMAN VAGINAL BLOOD FLOW: COMPARISON BETWEEN TRANSVAGINAL AND INTRAVENOUS ADMINISTRATION |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 61-68
Connie Palle,
Helle E. Bredkjaer,
Bent Ottesen,
Jan Fahrenkrug,
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摘要:
SUMMARY1. The present study was performed to examine and compare the effect of increasing doses of vasoactive intestinal polypeptide (VIP) on vaginal blood flow following vaginal subepithelial and intravenous injection in normal women.2. Local vaginal blood flow was measured by a heated oxygen electrode.3. Peripheral blood samples were collected throughout the experiments for VIP analysis by radioimmunoassay.4. Both subepithelial and intravenous injections induced a significant and dosedependent increase in vaginal blood flow (P<0.05), displaying the same efficacy, potency and sensitivity.5. The vaginal flow values correlated with the corresponding plasma VIP concentrations after both routes of administration.6. The systemic vascular side effects; that is, flushing, hypotension and tachycardia, were observed following both subepithelial and intravenous injection.7. The findings indicate that the effect of VIP on vaginal blood flow irrespective of route of administration is part of a systemic vasodilatory effect rather than a local response.
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01265.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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9. |
CONTRACTILE RESPONSES TO α1‐ADRENOCEPTOR STIMULATION DURING MATURATION IN THE AORTA OF THE NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RAT: RELATION TO STRUCTURE |
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Clinical and Experimental Pharmacology and Physiology,
Volume 17,
Issue 1,
1990,
Page 69-82
Krishnankutty Sudhir,
James A. Angus,
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摘要:
SUMMARY1. The significantly greater rise in blood pressure during the first 20 weeks of life in spontaneously hypertensive rats (SHR) when compared with normotensive Wistar‐Kyoto rats (WKY) may be related to increased vasoconstrictor responses caused by enhanced transmitter release or post‐junctional receptor changes.2. The reactivity of rat isolated aorta to post‐junctional α1‐adrenoceptor stimulation by methoxamine and to transmural sympathetic nerve stimulation was studied in ring segments suspended at equivalent transmural pressures in organ baths.3. Wall stress in the SHR aorta was significantly higher at 4 weeks, but lower at 9 and 20 weeks when compared with the WKY aorta, a possible adaptation to the higher pressures seen in the SHR at the latter ages.4. The sensitivity (location of EC50) to methoxamine was similar at all ages in both strains, but the SHR aortae at 9 and 20 weeks generated higher maximal contractile force to this agent compared with the WKY aorta.5. The increase in force to methoxamine parallelled the medial hypertrophy of the SHR aorta, determined from computerized morphometric analysis.6. There was an enhanced response to transmural field stimulation in the SHR aortae at 9 weeks, that was not accounted for by medial hypertrophy or altered neuronal uptake of noradrenaline.7. These studies suggest that enhanced maximal contractile force in the SHR aorta to α1‐adrenoceptor stimulation is accounted for by medial hypertrophy. However, there is an additional enhanced reactivity at 9 weeks in response to nerve stimulation in the SHR aorta that may be related to increased innervat
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1990.tb01266.x
出版商:Blackwell Publishing Ltd
年代:1990
数据来源: WILEY
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