bluuebunny/crossref_metadata_2025_split huggingface dataset:
MATING SYSTEM AND SEXCUL DIMORPHISM IN LARGE TERRESTRIAL, MAMMALIAN HERBIVORES
Authors: JARMAN PETER 
Published: January 2008

SummarySexual dimorphism in mammals is not entirely satisfactorily explained by the models that are advanced to account for it among birds. This may be because species‐specific styles of being dimorphic, and of attaining mature dimorphic state, are not clearly recognized. Mature dimorphism is a syndrome involving body size, appearance and weaponry; each facet and the whole syndrome may have functions in both fighting and signalling. The mature dimorphic stage has to be reached by growth and change from juvenile and sub‐adult states.The occurrence of the separate facets of the dimorphic syndrome are reviewed in species of Bovidae, Cervidae and Macropodidae, large, diverse families of eutherian (the first two) and metatherian mammals, which have broadly similar ecological adaptations. In each family the smallest species tend to be homomorphic, with small, inconspicuous weapons. Greatest dimorphism in size is found in medium‐sized bovids and cervids, and the larger macropodids (in which no species exceeds 100 kg male weight); the range of species showing greatest dimorphism in size also shows the most exaggerated weapons. Mature dimorphism is reached by different patterns of growth, which may be determinate and similar in the sexes (leading to homomorphism), determinate but differing between the sexes, or indeterminate and differing, both of which lead to heteromorphism.The syndromes of dimorphism and patterns of growth are associated and a classification of styles of dimorphism is presented. The adaptiveness of the styles is suggested in terms of what is known of the socio‐ecology, in particular the male reproductive strategies, of the species. The various styles of heteromorphy appear to be associated with males' way of achieving polygyny: such as by non‐resource‐based territoriality, by dominance‐determined access to oestrous females, or by wandering and formation of a consortship with pro‐oestrous females. The relevance of the species' ecology of use of resources to these styles of dimorphism and mate‐acquisition is briefly discussed.
THE EVIDENCE OF REPRODUCTIVE MECHANISMS IN FOSSIL DASYCLADS (ALGAE: CHLOROPHYTA)
Authors: ELLIOTT GRAHAM F. 
Published: January 2008

SummaryDasyclads (members of Order Dasycladales: Algae, Chlorophyta) are reviewed for evidence of reproductive structures in the fossil state, and then compared with what is known of the reproductive processes in living examples. The effects of poor preservation in most of the fossils are shown to result in many uncertainties, and the resulting degree of interpretation required is emphasized. Selected genera of fossil dasyclads considered relevant to this problem are briefly analysed and discussed: Archaeobatophora (Ordovician), Kulikia (Carboniferous), Imperiella (Permian), Stichoporella (Jurassic) and Cympolia (Cretaceous to Recent). The pioneer views of J. Pia on dasyclad reproduction through geological time are seen to need much modification in the light of later work. The fundamental dasyclad nucleus‐fragmentation‐reproduction mechanism is believed to have operated within the great morphological variety of known dasyclads, giving rise to modification in genera where basic evolution was structural. In this way the variety of dasyclads can be seen to be the result of varied morphological evolution, often modified by the consistently simple basic reproductive mechanism.
CAPTOPRIL AND BARORECEPTOR REFLEX RESPONSES TO PRESSOR AND DEPRESSOR STIMULI IN THE RABBIT
Authors: PETTY MARGARET A. , REID J. L. 
Published: January 2008

The reflex effects of intravenous phenylephrine, sodium nitroprusside or acute haemorrhage in rabbits were examined as indices of baroreceptor reflex function.
The slope of the linear regression of heart period: mean arterial pressure relationship was significantly greater (P<0.01) when buffering the pressor stimulus than either depressor stress.
Captopril (1 mg/kg i.v.) had no effect on the slope of the relationship to either pressor or depressor stimuli.
The clinical and experimental observation of hypotension without bradycardia after captopril could not be confirmed in the present study to be a result of changes in baroreflex sensitivity.
PHARMACOLOGICAL APPROACHES TO THE CHARACTERIZATION OF β‐ADRENORECEPTOR POPULATIONS IN TISSUES
Authors: O'DONNELL STELLA R. , WANSTALL JANET C. 
Published: January 2008

The locations of the Schild plots for a selective β‐adrenoreceptor antagonist using different agonists have been used as a means of determining whether the β‐adrenoreceptor population of a tissue is heterogeneous (β1 plus β2) or homogeneous (β1 or β2).
On guinea‐pig trachea, Schild plots for ICI 118,551 (β2‐selective adrenoreceptor antagonist), obtained using fenoterol (β2‐selective) or noradrenaline (β1‐selective) as agonist, were separated, indicating a heterogeneous β‐adrenoreceptor population. In contrast, Schild plots for a non‐selective antagonist, pindolol, using the same two agonists, were superimposed.
On guinea‐pig trachea, the Schild plot for ICI 118,551 with salbutamol (β2‐selective agonist) was superimposed on that with fenoterol (slopes of both plots were close to unity). The Schild plots for ICI 118,551 with adrenaline or rimiterol (β2‐selective agonists) gave pA2 values similar to those obtained with fenoterol or salbutamol as agonist, although the slopes of these plots were less than unity. The Schild plot obtained using any of these β2‐selective agonists was clearly separated from that using noradrenaline. This was in contrast to guinea‐pig atria where Schild plots were superimposed whatever the β‐adrenoreceptor agonist used.
These data confirmed that, in a tissue with a heterogeneous β‐adrenoreceptor population, separated Schild plots for an antagonist are obtained only if the antagonist is selective and if agonists of differing selectivity are used. This is the theoretically predictable result.
Data were also obtained (for the positive chronotropic response of guinea‐pig, rat and cat atria and for the relaxation response of guinea‐pig trachea) using another method for determining whether or not the β‐adrenoreceptor population of a tissue is homogeneous. This method did not require the use of selective agonists.
The concentration ratios obtained for the antagonism of isoprenaline by atenolol (β1‐selective) and ICI 118,551 alone and then in combination, indicated the involvement of a single β‐adrenoreceptor population in responses of guinea‐pig and rat atria but not of cat atria and guinea‐pig trachea. These results were consistent with conclusions from Schild plot experiments that positive chronotropic responses in rat and guinea‐pig atria involve only β1‐adrenoreceptors whereas chronotropic responses in cat atria and relaxation of guinea‐pig trachea involve both β1 and β2‐adrenoreceptors.
THE EFFECTS OF COCAINE AND LIGNOCAINE ON THE RAT RIGHT VENTRICLE IN VITRO
Authors: DOGGRELL SHEILA A. , VINCENT LYNN 
Published: January 2008

The effects of cocaine and lignocaine on the contractile responses to field stimulation and to exogenously applied agents, in the absence of other stimuli, have been investigated in the rat right ventricle using methods we have recently described (Doggrell & Vincent, 1981a). In addition the effects of 3H accumulation from (−)‐[3H]‐noradrenaline and on the spontaneous and field stimulation‐induced overflow of 3H, following preloading of the tissue with (−)‐[3H]‐noradrenaline, are reported.
Cocaine, but not lignocaine, inhibited the accumulation of 3H from (−)‐[3H]‐noradrenaline. The spontaneous overflow of 3H, following preloading of the tissue with (−)‐[3H]‐noradrenaline was not altered by cocaine, 10μ, or lignocaine, 100μM. 10μM Lignocaine had no effect on the overflow of 3H evoked by field stimulation at 5Hz. Lignocaine, 100μM, increased and cocaine, 1 and 10μM, reduced the decline in evoked release of 3H. This effect of lignocaine probably represents a decrease in nerve excitability and that of cocaine inhibition of neuronal uptake of noradrenaline.
Cocaine, μM, reduced the rate of beat response to tyramine, 1μM, alone, probably by inhibiting the neuronal uptake process.
Cocaine, 1 and 10μM, had no effect on the contractile responses to field stimulation (at 2 and/or 5Hz). The rate of beat to (−)‐noradrenaline or (−)‐isoprenaline, 1μM, alone was decreased by cocaine, 10μM. Lignocaine, 10μM, reduced the force of contractions to field stimulation at 5 Hz and the responses to (−)‐noradrenaline or (−)‐isoprenaline alone. It is suggested that the inhibitory effects of cocaine and lignocaine on responses to (−)‐isoprenaline in the rat right ventricle are due to a decreased postjunctional membrane excitability. The inability of 10μM cocaine to potentiate contractile responses to endogenous or exogenous (−)‐noradrenaline as a consequence of the inhibition of neuronal uptake is also probably due in part to decreased post‐junctional excitability of the right ventricle.
IMPAIRMENT BY NIFEDIPINE OF VASOPRESSOR RESPONSES TO STIMULATION OF POSTSYNAPTIC α2‐ADRENORECEPTORS IN GANGLION‐BLOCKED RABBITS. FURTHER EVIDENCE FOR THE SELECTIVE INHIBITION OF POSTSYNAPTIC α2‐ADRENORECEPTOR‐INDUCED PRESSOR RESPONSES BY CALCIUM ANTAGONISTS
Authors: VAN MEEL J. C. A. , ZOETEN K. DE , TIMMERMANS P. B. M. W. M. , VAN ZWIETEN P. A. 
Published: January 2008

After ganglionic blockade and bilateral vagotomy, vasopressor responses induced by activation of postsynaptic α1‐ and α2‐adrenoreceptors were elicited in the intact circulatory system of rabbits.
The hypertensive effects of the selective stimulating agents methoxamine (α1‐agonist) and B‐HT 920 (α2‐agonist) were effectively antagonized by the adrenoreceptor antagonists prazosin and yohimbine, respectively. These findings confirm the existence of two types of postsynaptic α‐adrenoreceptors (α1‐and α2‐type) in vascular smooth muscle of rabbits.
The calcium antagonistic drug nifedipine did not affect the maximal increase in diastolic pressure brought about by methoxamine, whereas it strongly inhibited the hypertensive effects of B‐HT 920.
It is concluded that this confirmation of the selective inhibition of postjunctional α2‐adrenoreceptor‐mediated vasopressor responses by a calcium antagonistic drug, such as nifedipine, indicates that this activity constitutes a general phenomenon. This finding supports the hypothesis that an influx of extracellular calcium is necessary for the vasoconstriction mediated by postsynaptic α2‐adrenoreceptors.
EFFECTS OF CATECHOLAMINES ON PREGNANT RAT UTERUS
Authors: BOYLE FRANCES C. , DIGGES K. G. 
Published: January 2008

The effects of noradrenaline (NA), adrenaline (Adr) and isoprenaline (Iso) have been studied on pregnant rat uterus, at various stages of gestation ‐ on the 10th and 20th days of pregnancy and on the first day post‐partum.
The three catecholamines were inhibitory in all stages of gestation, with the same order of potency as observed in non‐pregnant uteri (ie Iso > Adr > NA). However, mean pD2 values for the catecholamines tended to decrease as gestation progressed.
In 20 day pregnant and 1 day post‐partum uteri, in the presence of propranolol, NA and Adr produced consistent α‐adrenoreceptor mediated motor responses.
It is concluded that in the rat uterus, a form of pregnancy reversal occurs, in that there is a decrease in β‐adrenoreceptor responsiveness, and an increase in α‐adrenoreceptor responsiveness towards the end of gestation, and immediately post‐partum.
THE REGROWTH OF RIGHT ATRIAL NORADRENERGIC NERVES AFTER 6‐HYDROXYDOPAMINE IN GENETICALLY DIABETIC MICE: EFFECTS OF INSULIN TREATMENT
Authors: MAYER J. HEIDI , CLARKE SHARON A. , WILSON HILARY F. , TOMLINSON D. R. 
Published: January 2008

1 This study examined the rate of repletion of right atrial noradrenaline levels after a single dose (100 mg/kg i.p.) of 6‐hydroxydopamine (6‐OH Da) in diabetic and non‐diabetic mice of the C57 BL/KS db/db strain.2 In mice which received no 6‐OH Da there was no significant difference, in endogenous noradrenaline levels, between diabetic and non‐diabetic animals. The depletion of noradrenaline 24 h after 6‐OHDa was slightly more profound in the diabetic mice than in non‐diabetic controls. Thereafter the rate of repletion of noradrenaline was more rapid in the diabetic group.3 The normal noradrenaline content was reinstated in diabetic mice between 7 and 10 days after 6‐OHDa. In the non‐diabetic group levels similar to those found in untreated mice were not reinstated until 14 days after 6‐OHDa.4 Ten days after 6‐OHDa right atria from diabetic mice were markedly more responsive to stimulation of the intramural noradrenergic nerves than were preparations from non‐diabetic mice.5 A group of diabetic mice was treated with insulin (10 m Units/g daily) for 6 weeks. The right atria from these animals, examined 10 days after 6‐OHDa, were similar in their responses to noradrenergic nerve stimulation to the preparations from the non‐diabetic mice.6 All these groups of atria gave similar responses to exogenous noradrenaline. These findings indicate that regrowth of noradrenergic terminals after 6‐OHDa was more rapid in diabetic mice than in either insulin‐treated diabetic mice or non‐diabetic mice.
ARYLAZIDO AMINOPROPIONYL ATP (ANAPP3) ANTAGONISM OF CAT URINARY BLADDER CONTRACTIONS
Authors: THEOBALD R. J. 
Published: January 2008

1 ANAPP3 produces a transient contraction of the urinary bladder of the cat similar to that produced by ATP and hypogastric nerve stimulation.2 ANAPP3 partially antagonizes the inhibition of pelvic nerve‐evoked bladder contractions induced by adenosine, possibly by blocking P1 receptors.3 ANAPP3 antagonizes contractions of the cat urinary bladder induced by ATP, β, γ‐methylene ATP, pelvic nerve stimulation and hypogastric nerve stimulation.4 ANAPP3 produces no antagonism of either noradrenaline‐induced inhibition of pelvic nerve‐evoked bladder contractions or acetylcholine‐induced bladder contractions, thereby substantiating the specificity of the effect of ANAPP3 against purines.
CHOLINERGIC INFLUENCES ON THE SPINAL CARDIOVASCULAR NEURONES
Authors: BHARGAVA K. P. , PANT K. K. , TANGRI K. K. 
Published: January 2008

In bilaterally vagotomized and spinal cord (C1) transected dogs, intrathecal (i.t.) injection of pilocarpine decreased while DMPP increased the blood pressure. These responses were antagonized by i.t. pretreatment with ethylbenztropine and chlorisondamine respectively.
No change in the resting heart rate occurred after intrathecal injection of cholinergic drugs in these animals.
The post‐coronary artery ligation cardiac arrhythmia, in bilaterally vagotomized and spinal (C1) transected dogs, was inhibited by i.t. pilocarpine and chlorisondamine and facilitated by ethylbenztropine and DMPP.
The effects of muscarinic and nicotinic receptor agonists on the arrhythmia were blocked by their respective blockers.
It appears that the muscarinic receptors are inhibitory while nicotinic receptors are facilitatory for spinal control of vasomotor tone and the post‐coronary artery ligation cardiac arrhythmia. However, the spinal muscarinic and nicotinic receptors do not appear to have a significant role in the regulation of normal heart rate.
THE CHRONIC EFFECTS OF β‐ADRENORECEPTOR BLOCKING AGENTS ON TRANSMITTER OVERFLOW IN THE ANOCOCCYGEUS MUSCLE OF THE RAT
Authors: CARR SUSAN S. , DRAPER A. J. , LAMAA MICHEL , REDFERN P. H. 
Published: January 2008

1 The effect of chronic administration of three β‐adrenoreceptor blocking agents, propranolol, timolol and atenolol on transmitter release from sympathetic nerves has been investigated in the isolated anococcygeus muscle of the rat.2 Oral treatment for 11 weeks with either propranolol (12 mg/kg/day), or timolol (1.2 mg/kg/day) but not atenolol (12 mg/kg/day) significantly increased the stimulation‐induced overflow of radioactivity following preincubation of the tissue with 3H‐NA.3 No increase in end‐organ sensitivity, as measured in terms of responsiveness to exogenous acetylcholine, tyramine or NA, was observed.4 The ineffectiveness of atenolol compared to the other β‐adrenoreceptor blocking drugs may be related to the finding that, in acute experiments, atenolol inhibited tissue uptake of 3H‐NA.5 It is postulated that increased release of transmitter may be related to prolonged blockade of presynaptic β‐receptors and a resultant increase in presynaptic receptor sensitivity.
DIFFERENCES BETWEEN RECEPTORS FOR 5‐HYDROXYTRYPTAMINE ON AUTONOMIC NEURONES REVEALED BY NOR‐(–)‐COCAINE
Authors: FOZARD J. R. 
Published: January 2008

1 The interaction between nor‐(–)‐cocaine and 5‐hydroxytryptamine (5‐HT) at autonomic neuronal 5‐hydroxytryptamine (5‐HT) receptors has been investigated on the rabbit heart and guinea‐pig ileum.2 The chronotropic response to 5‐HT mediated through activation of receptors on the terminal sympathetic fibres of the rabbit heart was antagonized selectively and surmountably by nor‐(–)‐cocaine. Schild analysis yielded a pA2 value for the interaction of 7.79 ± 0.11, n = 13.3 On the guinea‐pig ileum induced to contract by activation of 5‐HT receptors on the intramural cholinergic nerves, nor‐(–)‐cocaine was also a selective and surmountable antagonist of 5‐HT, although the concentrations needed were higher than those shown to be effective on the heart. The pA2 value for the interaction was 6.49 ± 0.07, n = 16.4 The differential blocking effect of nor‐(–)‐cocaine in the two tissues suggests that the receptors for 5‐HT on the cholinergic nerves of the ileum and the sympathetic fibres of the heart are different. The data thus lend support to the earlier similar conclusion based on the observation that 5‐methoxytryptamine is a potent agonist on the ileum yet inactive on the heart.
EFFECTS OF PRAZOSIN, PHENTOLAMINE AND YOHIMBINE ON NORADRENERGIC TRANSMISSION IN THE RAT RIGHT VENTRICLE IN VITRO
Authors: BRADLEY LYNN , DOGGRELL SHEILA A. 
Published: January 2008

1 The effects of prazosin, phentolamine and yohimbine on the accumulation of radioactivity from [3H]‐noradrenaline, and on the subsequent spontaneous and field stimulation‐evoked outflow of radioactivity have been investigated in the rat right ventricle in vitro. In addition the effects of these agents on contractions produced by exogenous amines or by field stimulation are reported.2 Prazosin, phentolamine and yohimbine had no effect on the accumulation of radioactivity from [3H]‐noradrenaline.3 The decline in the spontaneous outflow of radioactivity, following loading of the tissue with [3H]‐noradrenaline, was reduced by prazosin (1 times 10‐8 or 1 times 10‐7M) and 1 times 10‐6M yohimbine. Phentolamine and 1 times 10‐7M yohimbine had no effect on the spontaneous outflow of radioactivity.4 Prazosin, phentolamine and yohimbine (all at 1 times 10‐7M) reduced the decline in outflow of radioactivity evoked by field stimulation at 5Hz. In the presence of yohimbine, prazosin or phentolamine had no effect on the evoked outflow. The effect of prazosin, phentolamine and yohimbine alone probably represents antagonism at prejunctional α‐adrenoreceptors.5 The rate of beating and force of contractions evoked by 1 times 10‐6M isoprenaline were not altered by prazosin, phentolamine or 1 times 10‐7M yohimbine. The rate of beating evoked by noradrenaline (1 times 10‐6M) was reduced by prazosin and phentolamine. Yohimbine (1 times 10‐6M) reduced the rate of beating to isoprenaline and to noradrenaline. These effects of prazosin and phentolamine probably represent antagonism at postjunctional α1‐adrenoreceptors and that of yohimbine a decrease in the excitability of the postjunctional membrane.6 In the control tissues the force of contractions evoked by field stimulation at 5Hz declined slowly with successive stimulations at 30 min intervals. In the presence of prazosin (1 times 10‐8 and 1 times 10‐7M), phentolamine (1 times 10‐7 and 1 times 10‐6M) and 1 times 10‐7M yohimbine the responses did not decline with successive stimulations. Yohimbine (1 times 10‐6M) had no effect on the stimulation‐evoked responses.7 Phentolamine or yohimbine (both at 1 times 10‐7M) had no additional effect on the stimulation‐evoked responses in the presence of prazosin (1 times 10‐7M). Prazosin (1 times 10‐8M) and yohimbine (1 times 10‐7M) had no further effect in the presence of phentolamine (1 times 10‐6M). Prazosin or phentolamine (both at 1 times 10‐7M) had no effect on stimulation‐evoked responses in the presence of yohimbine (1 times 10‐7M).8 In the rat right ventricle, the ability of phentolamine and yohimbine to prevent the decline in the stimulation‐evoked responses with successive stimulations is probably due to antagonism at prejunctional α‐adrenoreceptors. However it is suggested that the ability of prazosin to prevent the decline in response is due to a release of endogenous noradrenaline and to antagonism at prejunctional α‐adrenoreceptors.
INTERACTION OF CLONIDINE, ITS METHYLENE‐BRIDGED ANALOG, St 1913, AND THE BENZYLIC HYDROXYL‐SUBSTITUTED DERIVATIVE, St 1965, WITH α1‐ AND α2‐ADRENORECEPTORS
Authors: RUFFOLO R. R. , TIMMERMANS P. B. M. W. M. , VAN ZWIETEN P. A. 
Published: January 2008

The effects of benzylic hydroxyl substitution on the activity of a close structural analog of clonidine was assessed at α1‐ and α2‐adrenoreceptors both in vitro and in vivo in order to uncover possible differences that this substitution may have on the effects of imidazolines and phenethylamines at adrenoreceptors.
In all test systems, the presence of the benzylic hydroxyl group was associated with a consistent and marked decrease in activity. These findings are in agreement with our previous studies with imidazolines having different pharmacological profiles and different physicochemical properties than the clonidine derivatives reported herein.
We conclude, therefore, that the deleterious effects of the benzylic hydroxyl group is ubiquitous among imidazolines and, more importantly, is in marked contrast to the 100–1000 fold enhancement in activity that the benzylic hydroxyl substituent (i.e. β‐hydroxyl group) produces for the phenethylamines.
The results support the concept that imidazolines and phenethylamines may interact differently with α‐adrenoreceptors.
CALCIUM‐DEPENDENCY OF THE PRESSOR RESPONSES TO SELECTIVE 5‐HYDROXYTRYPTAMINE RECEPTOR AGONISTS IN PITHED RATS
Authors: KALKMAN H. O. , BODDEKE H. W. G. M. , TIMMERMANS P. B. M. W. M. , VAN ZWIETEN P. A. 
Published: January 2008

The pressor responses to six selective 5‐HT receptor agonists, quipazine, TMFPP, Org 10155, Ru 24969, 5‐methoxytryptamine and 5‐methoxy‐N,N‐dimethyltryptamine, were quantified and tested for calcium dependency following i.v. administration to pithed normotensive rats.
The pressor responses induced by 5‐methoxytryptamine and 5‐methoxy‐N,N‐dimethyltryptamine were not influenced by calcium entry blockade by means of nifedipine.
The piperazine derivatives quipazine, TMFPP and Org 10155 were full agonists, but the pressor responses to these agonists were sensitive to calcium entry blockade.
5‐Methoxy‐N,N‐dimethyltryptamine and Ru 24969 were found to be partial agonists.
It is submitted as a hypothesis that within the present series of 5‐HT receptor agonists, a restricted side chain flexibility will enhance the dependency of their pressor responses to extracellular calcium.