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Biomedical subjects

A Hilditch

Publications and source records attributed to A Hilditch.

At least 19 recordsLinked to original sources
PubMed1999

Immunisation initiatives in general practice. Important lessons from division projects.

AIM: To examine immunisation projects undertaken by divisions of general practice through the Divisions and Project Grants Program in the period from 1993 to mid 1997. METHOD: A simple descriptive frequency analysis was conducted of information from the National Information Service Divisions Project database and evaluation reports of the project characteristics and methodology such as: year commenced; duration; location; funding; target groups; intervention; needs assessment; aim(s); study design; measurement (assessment) and outcome(s). RESULTS: Forty-four funded immunisation projects were identified and of these, 12 projects with completed evaluation reports were analysed. Most projects were of 12-14 months duration, and were funded for a mean of $56,349 and median of $46,348 for the 44 funded projects and a mean $44,348 and median $40,318 for the 12 with evaluation reports. Most projects included a needs assessment. The main target groups were general practitioners, the general community, and children. Of the wide spectrum of interventions used, education and/or promotion and register and/or reminder systems were the most common. Study designs, the quality of measurement and outcomes were variable. CONCLUSION: In the future with the move to outcome based block funding, it will be important for projects to adopt broader target groups, refine and develop interventions and develop greater sustainability through responding to local needs, improving design and evaluation and ongoing funding.

Australia↗
PubMed1997

Effects of the angiotensin AT1 receptor antagonist GRI38950 on haemodynamic function in dogs.

1. The antagonist activity of the angiotensin AT1 receptor antagonist, GR138950, and its haemodynamic effects have been investigated in beagle dogs. 2. In four anaesthetized dogs, GR138950 (0.1, 1 and 10 mg kg-1 i.v.), displaced dose-response curves to angiotensin II (AngII) rightwards, in a parallel manner; GR138950, at 1 mg kg-1 i.v., produced a 15-fold displacement of the AngII dose-response curve. In four conscious dogs, GR138950 (1 mg kg-1 i.v. or p.o.) antagonized AngII, and produced rightward and parallel displacements of the AngII dose-pressor response curves. Maximum displacements of approximately 33- and 16-fold occurred at 1 h after intravenous and 5 h after oral administration, respectively. The inhibitory effect of GR138950 was long lasting; AngII dose-pressor response curves were still displaced by 10-fold from control values, 24 h after intravenous or oral administration of GR138950. 3. In comparison with its vehicle, GR138950 (0.1-10 mg kg-1) caused a significant decrease in resting blood pressure as a consequence of a significant decrease in total peripheral resistance in anaesthetized dogs. Effects on cardiac output, stroke volume and heart rate were not significantly different between GR138950- or vehicle-treated dogs. 4. Compared with vehicle, GR138950 administration did not significantly affect blood flow to the mesenteric and femoral vascular beds but did significantly increase blood flow to the renal vascular bed. Vascular resistance of the femoral bed was unaffected but that of the mesenteric and renal vascular beds was significantly reduced by GR138950, compared with the changes produced by vehicle treatment. 5. Compared with vehicle, left ventricular end diastolic pressure was significantly reduced by GR138950, but GR138950 had no significant effect on indices of cardiac contractility (+dP/dtmax and +dP/dt@40) or cardiac relaxation during early diastole (-dP/dt). 6. In conclusion, GR138950 acts as a competitive, surmountable antagonist at vascular angiotensin II receptors in beagle dogs. GR138950 reduced arterial blood pressure by reducing total peripheral resistance, attributable partly to reduction in resistance in the mesenteric and renal vascular beds. GR138950 reduced left ventricular end diastolic pressure whilst having no direct effect on cardiac contractility or relaxation.

Administration, Oral↗
PubMed1996

Further investigations into the mechanism of the antihypertensive activity of the angiotensin AT1 receptor antagonist, GR138950.

1. The angiotensin AT1 receptor antagonist, GR138950, produces a long-lasting antihypertensive effect in conscious renal artery ligated hypertensive (RALH) rats but this effect does not correlate temporally with its antagonist profile against angiotensin II (AII). In the present experiments we have compared the inhibitory profiles of GR138950 and enalapril, against angiotensin I (AI), with their respective antihypertensive activities. 2. GR138950 (1 mg kg-1, i.a.) and enalapril (3 mg kg-1, i.a.) reduced blood pressure in RALH rats to a similar degree. Maximum reductions in blood pressure occurred approximately 5-24 h and 3-5 h after administration, respectively. The antihypertensive effect of GR138950 lasted for 24-48 h. However, the effect of enalapril lasted for only 5-24 h. 3. In conscious normotensive rats, inhibition of AI-induced pressor responses was maximal 1 h after systemic administration of GR138950 and enalapril. Dose-response curves to AI were displaced to the right, in a parallel manner, 1406 and 102 fold by GR138950 (1 mg kg-1, i.a.) and enalapril (3 mg kg-1 i.a.), respectively. The inhibitory effect of enalapril lasted for < 24 h whereas that of GR138950 lasted for up to 48 h. 4. Contractile responses to AI were extensively inhibited in aortae removed from either RALH rats or normotensive rats, 1 and 5 h after administration of GR138950 (1 mg kg-1, i.a.). Responses were still significantly reduced 24 h after administration but had returned to control levels after 48 h. Enalapril pretreatment (3 mg kg-1, i.a.) did not inhibit contractile responses to AI in aortae isolated from normotensive rats at any time point. 5. These experiments confirm that GR138950 is an effective and long-lasting antihypertensive agent. GR138950 was a more potent and longer lasting antagonist against AI than has previously been found against AII, and the duration of its antihypertensive activity coincides better with its blockade of responses to AI. Blockade of the effects of AII generated locally within the vascular wall might play an important role in the antihypertensive profile of GR138950.

Angiotensin Receptor Antagonists↗
PubMed1995

Pharmacological effects of GR138950, a novel angiotensin AT1 receptor antagonist.

The antagonist activity of GR138950 (1-[[3-bromo-2-[2-[[(trifluoromethyl)sulphonyl]amino]phenyl]-5- benzofuranyl]methyl]-4-cyclopropyl-2-ethyl-1H-imidazole-5-carboxamide) was investigated at angiotensin AT1 receptors and AT2 receptors in vitro and on blood pressure in conscious rats. GR138950 suppressed and displaced angiotensin II (AII) concentration-effect curves in the rabbit isolated aorta (pKb approximately 9.0-9.7) but had no effect against phenylephrine or serotonin induced-contractions. GR138950 competed with [3H]-AII for angiotensin AT1 receptors in rat liver membranes (pKi = 9.09). GR138950 had no apparent affinity for angiotensin AT2 receptors (bovine cerebellum; pKi < 6.0). GR138950 (1 mg/kg i.a. and p.o.) inhibited pressor responses to AII, but not phenylephrine, in conscious normotensive rats. Parallel displacements in AII dose-response curves occurred without any reduction in the maximum response to AII. The antagonist activity of GR138950 lasted for up to 24 h. GR138950 (> 0.03 mg/kg i.a., > 0.3 mg/kg p.o.) significantly reduced diastolic blood pressure (DBP) in renal artery ligated hypertensive rats. DBP was reduced maximally, 5 to 7 h after administration and the antihypertensive effect of GR138950 lasted for up to 48 h. Daily administration (5 days) of GR138950 to renal artery ligated hypertensive rats produced a sustained reduction in DBP. Acute administration of GR138950 (1 mg/kg i.a.) also significantly reduced DBP in spontaneously hypertensive rats but not in normotensive rats. Heart rate was little changed in renal artery ligated hypertensive rats, normotensive rats and spontaneously hypertensive rats. These experiments demonstrate that GR138950 is a potent, selective and specific angiotensin AT1 receptor antagonist that is orally active and reduces DBP in conscious hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1994

Cardiovascular effects of GR117289, a novel angiotensin AT1 receptor antagonist.

1. The effect of GR117289, an angiotensin AT1 receptor antagonist, on diastolic blood pressure (DBP) was determined in angiotensin-dependent and angiotensin-independent models of hypertension in rats. In addition, the antagonist profile of GR117289 at angiotensin AT1 receptors was determined in conscious renal hypertensive rats and conscious normotensive rats, dogs and marmosets. 2. Intra-arterial and oral administration of GR117289 (0.3-3 mg kg-1, i.a.; 1-10 mg kg-1, p.o.) to 6-day left renal artery ligated hypertensive (RALH) rats (DBP > 140 mmHg) produced significant, dose-related reductions in DBP with little apparent effect on heart rate (< 15%). The antihypertensive effect of GR117289 developed progressively over several hours and with some doses persisted for 24-48 h after administration. 3. Administration of GR117289 (1 mg kg-1, i.a.) on 5 consecutive days to RALH rats reduced DBP on each day. The antihypertensive effect of GR117289 was not cumulative as DBP had almost returned to base-line values, 24 h after administration of each dose. 4. A dose of GR117289 (3 mg kg-1, i.a.), which produced a substantial reduction in DBP (about 70 mmHg) in RALH rats, was administered to rats in which blood pressure was elevated either by unilateral renal artery clipping, sustained infusion of angiotensin II (AII), DOCA-salt administration or genetic inbreeding. GR117289 reduced DBP in rats in which the renin-angiotensin system was activated by renal artery clipping or AII infusion but had little effect in normotensive rats, DOCA-salt rats and SHR. 5. Systemic administration of All to RALH rats and to normotensive rats, dogs and marmosets elicited reproducible pressor responses in all species. Systemic or oral administration of GR1 17289 (3 mg kg-1)inhibited the pressor responses produced by All, resulting in parallel, rightward displacements of All dose-response curves.6. Maximal displacements of All dose-response curves occurred 1 h and 1-7 h after systemic and oral administration, respectively. GR1 17289 produced a 32-246 fold displacement after systemic administration and a 4-12 fold displacement after oral administration. The effect in dogs was short lasting after systemic administration but the effect of GRI17289 lasted for up to 24 h in rats and marmosets and for up to 24 h after oral administration in all species. The antagonist activity appeared specific for angiotensin receptors as GRi17289 did not inhibit pressor responses to phenylephrine or vasopressin.7. These experiments demonstrate that GRI 17289 reduces blood pressure in conscious hypertensive rats after both systemic and oral administration, and is an effective antagonist at angiotensin AT1 receptors in conscious rats, dogs and marmosets.

Administration, Oral↗
PubMed1991

Effects of dopamine DA1-receptor blockade and angiotensin converting enzyme inhibition on the renal actions of fenoldopam in the anaesthetized dog.

Experiments were performed in anaesthetized dogs to characterize the renal effects of the selective dopamine DA1-receptor agonist, fenoldopam. Intrarenal artery infusion of fenoldopam (0.01-10 micrograms/kg per min) caused dose-related renal vasodilation. At low doses (0.01-0.3 micrograms/kg per min), renal vasodilation occurred without concomitant falls in blood pressure but was accompanied by increased urine output. This diuresis was most probably a result of reduced tubular reabsorption since glomerular filtration rate was not increased. Both fenoldopam-induced renal vasodilation and diuresis were blocked to a similar extent by the selective dopamine DA1-receptor antagonist, SCH 23390 (30 micrograms/kg, intravenously), suggesting that both effects were mediated by dopamine DA1-receptors. In the presence of the angiotensin converting enzyme inhibitor, captopril (1 mg/kg, intravenously, + 20 micrograms/kg per min, intrarenal artery), fenoldopam (0.01-0.3 micrograms/kg per min) significantly increased fractional excretion of sodium, despite reducing blood pressure; neither of these effects were observed in captopril-free dogs. These observations support the view that the inhibitory effect of fenoldopam on tubular function, and its vasodepressor activity, may be opposed by angiotensin II resulting from fenoldopam-induced renin release.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Potentiation of the effects of dopamine in the rabbit isolated splenic artery by 3-isobutyl-1-methylxanthine or forskolin.

Dopamine relaxes precontracted rabbit isolated splenic arteries via stimulation of dopamine DA1 receptors on the smooth muscle. However, in many preparations, the effect of dopamine is small. In an attempt to increase the effectiveness of dopamine and thus increase the proportion of usable preparations, we have examined the effects, on the sensitivity of dopamine, of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) and the adenylate cyclase stimulant forskolin. In tissues pretreated with phenoxybenzamine, and in the presence of propranolol, IBMX (1 mumol/l) or forskolin (0.01 mumol/l) produced a small increase in the sensitivity to dopamine in otherwise insensitive preparations. The maximum relaxation of U-46619-induced tone produced by dopamine was increased to around 50%. However, after treatment with higher concentrations of IBMX (10 mumol/l) or forskolin (0.1 mumol/l), previously insensitive preparations relaxed readily to dopamine with EC50 values in the range 1-3 mumol/l. Similarly, in spontaneously dopamine-sensitive preparations IBMX (1 mumol/l) or forskolin (0.01 mumol/l) produced only a 2-3-fold parallel shift to the left in the dopamine concentration-effect curves. However, higher concentrations of IBMX (10 mumol/l) or forskolin (0.1 mumol/l) produced 10-20-fold parallel shifts to the left in dopamine concentration-effect curves. Higher concentrations of IBMX (100 mumol/l) or forskolin (1 mumol/l) abolished the ability of the spasmogen to contract the preparations.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1987

Subclassification of peripheral dopamine receptors.

Dopamine receptors in peripheral tissues have been subclassified using agonists and antagonists. The vascular dopamine receptors in the dog and cat mesenteric vascular beds are similar; those in the rabbit isolated splenic artery are similar to those in the human isolated basilar artery, but appear to differ in some respects from those in the mesenteric vascular beds. The dopamine receptors in the chemoreceptor trigger zone of the dog and the neuronal dopamine receptors on the sympathetic nerve terminals supplying the cat heart and nictitating membrane and the dog femoral vascular bed seem to be the same. However they are all clearly different from the vascular dopamine receptors. The neuronal dopamine receptors on the cholinergic nerve terminals of the rabbit rectococcygeus muscle appear different from other neuronal receptors. The results suggest that sub-types of vascular and neuronal dopamine receptors may exist.

Animals↗
PubMed1985

Peripheral dopamine receptor blockade by SCH 23390 and domperidone in vitro.

The antagonist potencies of SCH 23390 and domperidone have been determined at vascular and neuronal dopamine receptors in the rabbit isolated splenic artery and rectococcygeus muscle, respectively. SCH 23390 was a potent, competitive antagonist at vascular (pA2 = 10.65) but not neuronal (pA2 less than 6.0) receptors. Domperidone was a potent, competitive antagonist at neuronal (pA2 = 7.9) but not vascular (pA2 less than 4.0) receptors. SCH 23390 and domperidone are, therefore, highly selective vascular and neuronal dopamine receptor antagonists respectively.

Animals↗
PubMed1984

Presynaptic alpha-adrenoceptors: do exogenous and neuronally released noradrenaline act at different sites?

The effects of dopamine receptor and alpha-adrenoceptor agonists and antagonists on the stimulation-evoked overflow of radioactivity from strips of dog saphenous vein previously loaded with [3H]-noradrenaline have been examined alone and in combination. In the presence of neuronal and extraneuronal catecholamine uptake inhibitors, noradrenaline (0.1-1 X 10(-6)M) and dopamine (0.01-1 X 10(-6)M) both inhibited the stimulation-evoked overflow of radioactivity. Sulpiride (1 X 10(-6)M) was without effect and prazosin (1 X 10(-7)M) had little effect on stimulation-evoked overflow but yohimbine enhanced it approximately 2 fold; the effect of yohimbine was similar at concentrations of 1 X 10(-7) and 1 X 10(-6)M. Sulpiride abolished the inhibitory effect of dopamine on stimulation-evoked overflow, but was without effect against noradrenaline. When allowance was made for the effects of yohimbine, alone, on overflow, yohimbine (1 X 10(-7)M) had no effect against dopamine and minimal effects against noradrenaline. A similar result was obtained when the concentration of yohimbine was increased to 1 X 10(-6)M. Prazosin did not antagonize the effect of noradrenaline. In the absence of the uptake inhibitors, clonidine (0.01-1 X 10(-5)M) inhibited stimulation-evoked overflow of radioactivity. Yohimbine (1 X 10(-6)M) was without effect on its own and antagonized the effects of clonidine at a concentration of 0.1 X 10(-5)M, but not at 0.01 or 1.0 X 10(-5)M. These findings suggest that dopamine inhibits overflow by stimulating presynaptic dopamine receptors on the terminals of the noradrenergic nerves supplying the dog saphenous vein. The interaction between yohimbine and noradrenaline is discussed in terms of the current concepts of control of transmitter release mediated via presynaptic alpha 2-adrenoceptors.

Animals↗
PubMed1984

Prejunctional dopamine receptors modulate twitch responses to parasympathetic nerve stimulation in the rabbit isolated rectococcygeus muscle.

Field stimulation of the parasympathetic nerves supplying the rabbit isolated rectococcygeus muscle produced individual twitch responses that were inhibited by dopamine (1 x 10(-8)-1 x 10(-5)M). The twitch-inhibitory effect of dopamine was reversed by haloperidol or sulpiride (1 x 10(-8)-1 x 10(-5)M for either) but not by phentolamine or yohimbine (up to 1 x 10(-4)M). Haloperidol and sulpiride were potent, specific, competitive antagonists of the twitch-inhibitory effect of dopamine; their pA2 values were 8.39 and 7.75, respectively. In contrast, cis alpha-flupenthixol, fluphenazine, bulbocapnine and thioridazine were weak or inactive against dopamine. Concentrations of dopamine that inhibited the twitch response to parasympathetic nerve stimulation had little or no effect on contractions elicited by carbachol or by direct muscle stimulation after abolition of neuronal conduction by tetrodotoxin. Thus, the effects of dopamine on responses elicited by parasympathetic nerve stimulation seem to be exerted at a prejunctional level rather than directly on the smooth muscle. The twitch-inhibitory effect of dopamine was mimicked by epinine, N,N-diethyldopamine, N,N-di-n-propyldopamine, 5,6-ADTN, N,N-di-n-propyl 5,6-ADTN, 6,7-ADTN, apomorphine and Sandoz 27-403. Sulpiride reversed the effects of all these agonists. N,N-di-n-propyl-6,7-ADTN and SK & F 82526 also inhibited the twitch response but their effects were not reversed by sulpiride. SK & F 38393 and DPI had little effect on the twitch response. The pharmacological characteristics of the presynaptic dopamine receptors in the rabbit rectococcygeus muscle show that they resemble those in the cat heart and rabbit ear artery in some respects but there are differences that suggest that the presynaptic dopamine receptors in the rabbit rectococcygeus muscle constitute a specific subgroup of receptors.

Adrenergic alpha-Agonists↗
PubMed1983

Dopamine receptors in human basilar arteries.

After phenoxybenzamine (10(-5) M), pretreatment, and in the presence of propranolol (10(-6) M) and indomethacin (2.8 X 10(-6) M), dopamine caused a marked concentration-dependent relaxation of isolated strips of human basilar artery contracted with PGF2 alpha. This effect was mimicked by apomorphine, 6,7-ADTN and SK&F 38393, but N,N-diethyl dopamine, N,N-di-n-propyl-dopamine and 5,6-ADTN caused only slight relaxation. (+)-Butaclamol, cis-alpha-flupenthixol, fluphenazine and haloperidol competitively antagonised the relaxant effects of dopamine, but sulpiride was ineffective in concentrations as high as 1.3 X 10(-4) M. These findings show that the dopamine receptors in the human basilar artery closely resemble those in the smooth muscle of the rabbit isolated mesenteric and splenic arteries, and the dog renal and mesenteric arteries in vivo, but differ from those located presynaptically on sympathetic nerve terminals.

Basilar Artery↗
PubMed1981

Characteristics of the dopamine receptors in the rabbit isolate splenic artery.

After blockade of alpha- and beta-adrenoceptors, the tension induced by PGF2alpha in splenic artery strips was relaxed by dopamine, 6, 7-ADTN, N-methyldopamine, apomorphine, N, N-di-n-propyl 5, 6-ADTN, N, N-di-n-propyl 6, 7-ADTN and Sandoz 27-403; their equipotent concentrations (relative to dopamine = 1) were 0.2: 0.3: 0.4: 1.1: 3.9 and 3.9 respectively. 5, 6 ADTN, N-methyl 5,6ADTN, N, N-diethyldopamine, N, N-di-n-propyldopamine and SKF 38393 were weakly active or inactive at relaxing the splenic artery strip. Bulbocapnine and cis-alpha-flupenthixol were specific, competitive, reversible antagonists of dopamine. Fluphenazine, clozapine, trifluoperazine, haloperidol and spiroperidol also antagonised dopamine, but were relatively weak antagonists and a small part of their action was non-specific. Sulpiride was inactive against dopamine. SKF 38393 selectively antagonised the effects of dopamine demonstrating that SKF 38393 has affinity, but little efficacy at the dopamine receptors in the splenic artery. The findings with both agonists and antagonists suggest that the vascular dopamine receptors in the rabbit splenic artery resemble those in the dog renal and mesenteric vascular beds.

Animals↗
PubMed1979

The relationships between the cardiovascular effects, alpha- and beta-adrenoceptor blocking actions and plasma concentration of labetalol in doca hypertensive rats.

The relationships between the cardiovascular effects, alpha- and beta-adrenoceptor blocking actions and plasma concentration of labetalol have been examined in conscious DOCA hypertensive rats. Labetalol (10, 30 and 100 mg/kg p.o.) reduced resting heart rate; blood pressure was reduced only by the two higher doses. The effects lasted 5-24 hours. There was a highly significant correlation between the plasma labetalol concentration and its cardiovascular effects. During the labetalol-induced hypotension and bradycardia the vasopressor responses to intra-arterial injections of phenylephrine were reduced; the tachycardia and vasodepressor responses produced by intra-arterial injections of isoprenaline were also reduced. It is concluded that alpha- and beta-adrenoceptor blockade probably account for the labetalol-induced decreases in resting blood pressure and heart rate respectively.

Adrenergic alpha-Antagonists↗
PubMed1978

Effect of labetalol on the uptake of [3H]-(-)-noradrenaline into the isolated vas deferens of the rat.

1 The effects of the combined alpha- and beta-adrenoceptor blocking drug, labetalol, on the uptake of [3H]-(-)-noradrenaline into the isolated vas deferens of the rat have been determined and compared with those of some other alpha-adrenoceptor blocking drugs and cocaine. 2 Labetalol, like cocaine, produced a simple competitive inhibition of [3H]-(-)-noradrenaline uptake and was about 4 times less potent than cocaine. It is concluded that labetalol is a potent inhibitor of uptake1. Phentolamine and thymoxamine also inhibited [3H]-(-)-noradrenaline uptake, and were respectively 8 and 14 times less potent than cocaine. Tolazoline, piperoxan and yohimbine were inactive in concentrations up to 30 microgram/ml. 3 The uptake1 blocking action of labetalol could explain, at least in part, the previously reported difference in its ability to block noradrenaline and phenylephrine vasopressor responses in the anaesthetized dog. 4 The possibility that uptake1 inhibitory concentrations of labetalol could be present in the blood of subjects receiving normal antihypertensive doses of the drug is discussed.

Animals↗
PubMedDate not supplied

Effects of dopamine receptor agonists and antagonists at peripheral neuronal and vascular dopamine receptors in the anaesthetised dog.

The interactions between several putative dopamine receptor agonists and antagonists have been examined at neuronal and vascular dopamine receptors in the femoral and mesenteric vascular beds, respectively, of anaesthetised dogs. N,N-di-n- propyldopamine (DPDA) and apomorphine caused vasodilatation in both vascular beds. Cis alpha-flupenthixol, fluphenazine, and sulpiride were much more potent at antagonising DPDA at neuronal than at vascular dopamine receptors. Fluphenazine and sulpiride were as potent against apomorphine as against DPDA at neuronal receptors, but cis alpha-flupenthixol was much less effective. Fluphenazine antagonised the vasodilator effect of apomorphine in the mesenteric vascular bed, but cis alpha-flupenthixol and sulpiride did not, even when used in doses much larger than were effective against DPDA. Further experiments, in dogs pretreated with phenoxybenzamine and propranolol, revealed that cis alpha-flupenthixol, fluphenazine, and sulpiride also antagonised the mesenteric vasodilator effects of dopamine, 2-amino-5,6-dihydroxy-1,2,3,4-tetrahydronaphthalene, 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene, and 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine, suggesting a common site of action of these drugs and DPDA. Only fluphenazine antagonised responses to apomorphine. The results support the view that neuronal and vascular dopamine receptors in the dog are different. They also show that apomorphine stimulates different receptors from DPDA in the mesenteric vascular bed and, perhaps, in the femoral vascular bed as well.

Anesthesia↗