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At least 19 recordsLinked to original sources
PubMed1992

Effects of 5-hydroxydopamine and 6-hydroxydopamine on the ultrastructure of type I cells in paraganglia of the rat recurrent laryngeal nerve.

The ultrastructure of the Type I cells in paraganglia of rat recurrent laryngeal nerve (RLN) was studied after the administration of 5-hydroxydopamine (5-OHDA) and 6-hydroxydopamine (6-OHDA). Normal Type I cells of RLN-paraganglia contained abundant organelles and their cytoplasm was characterized by the presence of numerous membrane-bounded dense-cored vesicles (DCVs). The DCVs were round in profile (diameter 107.67 +/- 0.06 nm, all values expressed as mean +/- s.e.m. in the present study) and possessed dense cores of moderate to low electron density. After 5-OHDA treatment (single injection, 100 mg/kg b.w., i.v.), the majority of DCVs were filled with a material of high electron density. No significant difference was observed between the profile diameter of the DCVs in 5-OHDA-treated rats (104.96 +/- 0.06 nm) and that in normal rats. After 6-OHDA treatment (three injections, 100 mg/kg b.w. each at 12 h intervals i.p.), no significant alteration in the electron density of the core was noted. However, most of the DCVs were enlarged and round, elliptical or irregular in profile (190.57 +/- 2.77 nm x 130.34 +/- 2.09 nm). The dense core of DCVs was centrally or eccentrically located in DCVs. The results of the present study indicate that: 1) there is only one type of granulated glomus cell (i.e., Type I cells) in the rat RLN-paraganglia under normal physiological condition; and 2) since the ultrastructural morphology of DCVs in Type I cells of rat RLN-paraganglia is altered after 5-OHDA or 6-OHDA treatment, these cells may possess mechanisms for the uptake of false adrenergic neurotransmitter and/or neurotoxin.

Animals↗
PubMed1976

Studies on the mechanisms of 6-hydroxydopamine cytotoxicity.

The uptake-accumulation and binding of radioactivity in mouse heart after administration of the catecholamine neurotoxin [3H]6-hydroxydopamine (6-OH-DA, 1 or 3 mg/kg, i.v.) has been investigated. It was confirmed that a substantial portion (8--20%) of the radioactivity taken up and retained by the heart could not be extracted with perchloric acid, in all probability representing covalently bound oxidation products of 6-OH-DA to tissue proteins. Pharmacological analysis showed that a large part of this fraction was associated with the adrenergic nerves. The time-course of the perchloric acid resistant binding to the adrenergic nerves was found to parallel that of the neurotoxic action of 6-hydroxydopamine as evaluated by monitoring the change in [3H]noradrenaline uptake. Calculation of the intranelronal 6-hydroxydopamine concentration (average) needed to induce degeneration showed it to be in the order of 50 mM. The binding ratio for tritium deriving from [3H]6-OH-DA between the intraneuronal and extraneuronal compartments was found to be 10,000 to 30,000, pointing to a very high neuronal specificity for 6-hydroxydopamine. The 'covalent' binding of oxidation products of [3H]6-OH-DA was considerably reduced after desipramine or 1-phenyl-3(2-thiazolyl)-2-thiourea administration, treatments both known to protect the adrenergic nerves from undergoing degeneration. Conversely it was found that the binding increased during conditions known to potentiate the neurotoxic action of 6-hydroxydopamine, e.g., after monoamine oxidase inhibition with nialamide. Subcellular fractionation studies indicated that the predominant site of interaction between 6-hydroxydopamine oxidation products and neuronal proteins is the cytoplasm and the axonal membrane. Analysis of the effect in vivo administration of 6-hydroxydopamine on the field-stimulated induced release of [3H]noradrenaline previously taken up in the adrenergic nerves showed a 6-hydroxydopamine indiced reduction in [3H]noradrenaline release which was approximately proportional to the reduction in the number of nerve terminals. These findings further support the view that 6-hydroxydopamine acts largely in an "all-or-none' fashion with respect to the neurodegenerative action. Administration of [3H]dopamine also resulted in a fraction which was not extractable with perchloric acid, although this fraction was very small compared to that found after an equal dose of [3H]6-hydroxydopamine. These data may indicate that oxidation products of dopamine can interact with tissue proteins. From the present results it can be concluded that there is a close relationship between 'covalent' binding of 6-hydroxydopamine oxidation products to neuronal elements and the cytotoxic action of 6-hydroxydopamine, indicating that this binding may play an important role in the neurodegenerative action of 6-hydroxydopamine on catecholamine neurons.

Adrenergic Fibers↗
PubMedDate not supplied

Control of hindlimb vascular resistance in rats chronically sympathectomized with 6-hydroxydopamine.

1. Vascular resistance was measured after acute surgical denervation in the blood-perfused hind limbs of adult normal rats and rats which had been treated with 6-hydroxydopamine in the first 2 weeks of postnatal life. Vascular resistance was significantly higher in the limbs of 6-hydroxydopamine treated rats. 2. No excess of vasoconstrictor materials was detected when blood from 6-hydroxydopamine treated rats was used to perfuse the hind limbs of untreated rats or other 6-hydroxydopamine treated rats. 3. Hind limb blood vessels of 6-hydroxydopamine treated rats showed increased sensitivity to normal amounts of circulating vasoconstrictors of adrenal origin and to intra-arterial infusions of noradrenaline and angiotensin. 4. Infusion of desipramine into the hindlimb blood vessels of 6-hydroxydopamine treated rats did not increase vasoconstrictor responses to infused noradrenaline. Infusion of desipramine into the limbs of untreated rats increased responses to noradrenaline but these never attained the magnitude and duration of responses seen in limbs of 6-hydroxydopamine treated rats. 5. The increased sensitivity to noradrenaline of hindlimb vessels from 6-hydroxydopamine treated rats could partly be accounted for by an absence of neuronal uptake sites and partly by the development of non-specific post-junctional supersensitivity.

Angiotensin II↗
PubMed1990

Effects on renal sympathetic axons in dog of acute 6-hydroxydopamine treatment in combination with selective neuronal uptake inhibitors.

1. In anaesthetized dogs, we have investigated the effect on renal responses to sympathetic nerve stimulation of acute treatment with the catecholaminergic neurotoxin 6-hydroxydopamine (2 mg kg-1 i.v.), administered alone or after blockade of neuronal catecholamine uptake pathways for noradrenaline (NA) or dopamine with desmethylimipramine or benztropine, respectively. 2. Under control conditions, renal nerve stimulation caused renal vasoconstriction, reduced glomerular filtration and sodium and water excretion and caused net efflux of NA and dopamine into the renal venous plasma. Two h after administration of 6-hydroxydopamine alone, there was abolition of both functional responses and catecholamine efflux during nerve stimulation. 3. In animals pretreated with desmethylimipramine (1 mg kg-1), 6-hydroxydopamine had no significant effect on functional responses to renal nerve stimulation and nerve-evoked efflux of NA was only moderately reduced. Efflux of dopamine was still markedly reduced by 6-hydroxydopamine, but more variably than occurred without desmethylimipramine treatment. 4. In animals pretreated with benztropine (0.2 mg kg-1), nerve-evoked efflux of dopamine, but not that of NA, was protected against reduction by 6-hydroxydopamine. A higher dose of benztropine (1 mg kg-1) protected efflux of both NA and dopamine against 6-hydroxydopamine. 5. We conclude that acute treatment with a low dose of 6-hydroxydopamine is an effective method of inactivating peripheral sympathetic nerves. The differential effects of desmethylimipramine and benztropine in preserving nerve-evoked efflux of NA and dopamine after 6-hydroxydopamine support the view that these catecholamines originate predominantly from different intrarenal axons. However, neither uptake blocker appears to be completely specific in its actions.

Animals↗
PubMed1975

Mechanisms of selective depletion of brain regional noradrenaline by systemic 6-hydroxydopamine in newborn rats.

6-Hydroxydopamine injected systemically into newborn rats caused permanent depletions of the noradrenaline content of only certain brain regions. When 6-hydroxydopamine was given i.p. on days 1 and 2 after birth only the cortex, hippocampus and spinal cord were permanently depleted. 6-Hydroxydopamine given on days 9 and 10 after birth caused a permenent depletion predominantly from the cerebellum. Other regions were unaffected or were depleted for 4 days or less. The hypothalamus showed a gradual recovery of noradrenaline levels over a period of more than 20 days after injection, suggesting that only in this region was the apparent lack of effect of 6-hydroxydopamine due to neuronal regrowth. 6-Hydroxydopamine appeared to gain access to all regions except the pons-medulla when injected up to 10 days after birth, since at least temporary effects on noradrenaline storage were observed. 3H-Noradrenaline after i.p. injection was found in similar relative amounts in all brain regions in rats up to 20 days old. Thus regional differences due to age in the ability of 6-hydroxydopamine to reach various brain regions apparently do not explain the selective susceptibility to permenent depletion. It is suggested that the selective depletion must be due to interactions between the maturity of the adrenergic neurones and other factors such as their ability to take up or retain the 6-hydroxydopamine.

Aging↗
PubMed1976

The effects of 6-hydroxydopamine on the appearance of granulated vesicles in glomus cells of the rat carotid body.

The glomus cells of the rat carotid body reveal an intense fluorescence after exposure to paraformaldehyde vapor and contain catecholamines. After initial fixation in glutaraldehyde, many granulated vesicles are seen in the glomus cells. After initial fixation in osmium tetroxide, most of the vesicles are depleted of their dense interiors and granulated vesicles occur infrequently. Administration of 6-hydroxydopamine followed by initial fixation in osmium tetroxide leads to the reapperance of dense interiors in virtually all vesicles. 6-Hydroxydopamine apparently is taken up by the membrane pump of the glomus cell and is incorporated into the amine storage granules, thereby displacing the endogenous monoamines. Osmium tetroxide does not dissolve the 6-hydroxydopamine from the vesicles, as it apparently does for the normal vesicular contents. The 6-hydroxydopamine does not fluoresce, hence 6-hydroxydopamine administration results in a decreased intensity of formaldehyde induced fluorescence in the glomus cells. Administration of reserpine after 6-hydroxydopamine treatment (and subsequent initial fixation in osmium tetroxide) depletes the previously restored dense material from the vesicles of the glomus cells. 6-Hydroxydopamine acts like a monoamine in that it is taken up by the glomus cell, incorporated into the vesicles, and can be depleted from the vesicles by reserpine.

Animals↗
PubMed1978

Nuclear magnetic resonance studies of 6-hydroxydopamine and its interactions with SH-containing model compounds. Evaluation of possible mechanism for neurocytotoxicity.

6-Hydroxydopamine (I) is a well-known neurocytotoxic agent which has become an important tool in many neurochemical studies in recent years. Biochemical investigations of the mechanism of action of 6-hydroxydopamine indicated that this amine binds covalently and irreversibly to proteins. In the present work, molecular properties of 6-hydroxydopamine in aqueous solution such as self-association, ionization, intramolecular conformations, and possible cyclization were investigated using 1H nuclear magnetic resonance spectroscopy. A model study for the interaction of 6-hydroxydopamine with proteins was undertaken by using SH-containing molecules: cysteine, glutathione, and bovine serum albumin. The binding of these compounds to 6-hydroxydopamine was found to cause labilization of the hydrogen attached to C2 of the amine aromatic ring. This effect was interpreted in terms of nucleophilic attack of RS- on C1 of 6-hydroxydopamine. A proposed model for neurocytotoxicity is discussed.

Cysteine↗
PubMed1991

Cholinergic stimulation of substantia nigra: abolition of carbachol-induced eating by unilateral 6-hydroxydopamine lesion of nigrostriatal dopamine neurones.

Microinjection of cholinergic agonists into the substantia nigra is known to elicit increases in eating, drinking and sexual behaviour under appropriate circumstances. It has been suggested that these effects are dependent on stimulation of nigrostriatal dopamine-containing neurones in the substantia nigra pars compacta, but no direct evidence has confirmed this. The present experiment was therefore undertaken to determine whether unilateral lesions of nigrostriatal dopamine neurones made by 6-hydroxydopamine would attenuate or abolish eating in satiated rats elicited by intranigral microinjection of the muscarinic agonist carbachol. Two groups of rats were tested: a 6-hydroxydopamine- and a sham-lesion group. Before lesions were made intranigral microinjection of 0.5 microgram/0.5 microliter carbachol stimulated significantly more eating than control microinjections in both groups. After 6-hydroxydopamine lesions, microinjection of carbachol elicited no more eating than vehicle alone. Rats given sham lesions (ascorbate-saline vehicle only) showed increased feeding to intra-nigral carbachol before and after sham-lesioning. Post-mortem analysis by HPLC was used to determine the concentration of dopamine, DOPAC, HVA, serotonin and 5-HIAA in the lesioned and non-lesioned hemispheres of both 6-hydroxydopamine- and sham-lesioned rats. In caudate-putamen there were significant reductions in the concentration of DA (to 50.03% of the level in control sides), DOPAC (to 49.34%) and HVA (to 63.98%) in the 6-hydroxydopamine-lesioned but not sham-lesioned rats. The concentration of dopamine, DOPAC and HVA were not affected in the nucleus accumbens. The turnover of dopamine (assessed by calculating the ratio of dopamine to DOPAC) in the caudate-putamen but not nucleus accumbens was also altered by the 6-hydroxydopamine lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Methylphenidate in 6-hydroxydopamine-treated developing rat pups. Effects on activity and maze performance.

In order to better devine the relationship between brain catecholaminergic mechanisms and the clinical syndrome of minimal brain dysfunction, we have developed an experimental model that has many of the features of the disorder seen in children. This model is effected by the preferential depletion of brain dopamine in 5-day-old rat pups following the intracisternal administration of 6-hydroxydopamine, and in the present investigation, we have examined the effects of methylphenidate hydrochloride (0.25 to 2.0 mg/kg) on activity levels and cognitive performance in normal and 6-hydroxydopamine treated animals. Methylphenidate therapy resulted in a significant increase in activity levels of normal rat pups 12 and 19 days of age; in contrast, methylphenidate administered to 6-hydroxydopamine-treated animals did not increase activity at 12 days of age and significantly reduced activity at 19 and 26 days. Methylphenidate had no effect on T-maze performance in normals, but significantly improved performance in 6-hydroxydopamine-treated animals. Our results suggest that the "paradoxical" response to methylphenidate found in 6-hydroxydopamine-treated rat pups may be the result of central denervation supersensitivity.

Age Factors↗
PubMed1976

6-Hydroxydopamine in treatment of open-angle glaucoma.

In patients with open-angle glaucoma, subconjunctival injection of 6-hydroxydopamine produced chemical sympathectomy and sensitization to topically applied epinephrine. Prior to entry into this study, all patients had intraocular pressures (IOPs) greater than 30 mm Hg and had not responded to maximal medical therapy. The 6-hydroxydopamine was prepared in an ascorbic acid-buffered solution and was well tolerated by the patients. After subconjunctival administration of 6-hydroxydopamine, the mean decrease in IOPs was 50% in the treated eyes and 5% in the contraleteral eyes. Topical administration of 1% epinephrine to eyes injected with 6-hydroxydopamine resulted in a mean fall of IOP of 40% that persisted for as long as three months. Repeated subconjunctival injections of 6-hydroxydopamine renewed the pressure-lowering effects and sensitization to topically applied epinephrine.

Conjunctiva↗
PubMed1977

Strain differences in responsiveness of norepinephrine-sensitive adenosine 3',5'-monophosphate-generating systems in rat brain slices after intraventricular administration of 6-hydroxydopamine.

The development of hyperresponsiveness in cyclic AMP-generating systems has been investigated in brain slices of Sprague-Dawley and F-344 rats following intraventricular administration of 6-hydroxydopamine. Hyperresponsiveness to adrenergic agonists in cerebral cortical slices of Sprague-Dawley rats pertained during the period 5-25 days after treatment with 6-hydroxydopamine. In contrast, hyperresponsiveness did not develop in cerebral cortical slices of F-344 rats. Reductions in norepinephrine levels of the cerebral cortex and hypothalamus following 6-hydroxydopamine treatment were comparable in the two rat strains. A hyperresponsiveness to norepinephrine and isoproterenol failed to develop in mesencephalic slices of either strain 12-14 days after treatment with 6-hydroxydopamine. The accumulation of cyclic AMP elicited by norepinephrine in cortical slices of F-344 rat is normally about 50% greater than the accumulation elicited in slices from Sprague-Dawley rats. However, after 6-hydroxydopamine treatment, there was no significant difference in the accumulations of cyclic AMP elicited in cortical slices from the two rat strains. These data indicate there may be a limit to the responsiveness of catecholamine-sensitive cyclic AMP generating systems which can develop following alterations in synaptic input.

Animals↗
PubMed1991

The effect of chronic L-dopa treatment on the recovery of motor function in 6-hydroxydopamine-lesioned rats receiving ventral mesencephalic grafts.

The effect of treatment for 5 weeks with L-DOPA (200 mg/kg/24 h) plus carbidopa (25 mg/kg/24 h) on the behavioral recovery produced by rat fetal ventral mesencephalon grafts implanted into the striatum of 6-hydroxydopamine-lesioned rats was assessed. Animals with unilateral 6-hydroxydopamine lesions of the nigrostriatal pathway and a sham graft (Group A) showed persistent high rates of rotation in response to the administration of apomorphine (0.5 mg/kg, s.c.) (contralateral rotation) or (+)-amphetamine (5 mg/kg, i.p.) (ipsilateral rotation). Treatment of sham-grafted animals with L-DOPA plus carbidopa had no effect on the rate of rotation to apomorphine or (+)-amphetamine (Group B). The proportion of animals showing marked stereotypy following apomorphine administration was greater in sham-grafted animals receiving L-DOPA and carbidopa than in sham-grafted animals alone. Animals receiving unilateral 6-hydroxydopamine lesions followed by a fetal graft (Group C) showed a reduction in apomorphine-induced contralateral rotation and a complete reversal of (+)-amphetamine-induced ipsilateral rotation when assessed 6 weeks later. The reductions in apomorphine- and (+)-amphetamine-induced rotational behaviour produced by the fetal graft in animals with a 6-hydroxydopamine lesion were not altered by treatment with L-DOPA plus carbidopa (Group D). The proportion of animals showing marked apomorphine-induced stereotypy did not change significantly in either group over time. In rats with a unilateral 6-hydroxydopamine lesion receiving fetal dopamine grafts, treatment with high doses of L-DOPA and carbidopa for 5 weeks does not have a detrimental effect on the functional activity of the grafts as assessed by reduction of apomorphine- and (+)-amphetamine-induced motor asymmetry. The continuation of L-DOPA therapy may not adversely affect fetal graft survival and growth in patients with Parkinson's disease.

Animals↗
PubMed1990

Studies on brain monoamine and neuropeptide systems after neonatal intracerebroventricular 6-hydroxydopamine treatment.

In order to study the effects of a neonatal dopamine lesion on dopaminergic, serotonergic and peptidergic systems, Sprague-Dawley rats were treated by intracerebroventricular administration of 6-hydroxydopamine (100 micrograms, days 3 and 6) following desipramine pretreatment (25 mg/kg s.c.). At 60-70 days postnatally a profound reduction of dopamine- and 3,4-dihydroxyphenylacetic acid levels was found in striatal and limbic forebrain regions concomitant with an extensive loss of tyrosine hydroxylase-immunoreactive fibers, while no significant alteration in noradrenaline levels was seen. A marked loss of tyrosine hydroxylase-immunoreactive cell profiles was also observed in the substantia nigra and ventral tegmental area in mesencephalon. In striatum, but not in other regions analysed, an almost 100% increase in serotonin levels and serotonin-immunoreactive fiber density was observed following 6-hydroxydopamine treatment. However, the number of serotonin-immunoreactive cell profiles in the median and dorsal raphe nuclei was not altered. The 6-hydroxydopamine treatment also led to reductions in substance P levels in striatum, nucleus accumbens and ventral mesencephalon. The cholecystokinin level in nucleus accumbens and neurotensin level in ventral mesencephalon were also reduced. A neonatal intracerebroventricular 6-hydroxydopamine treatment thus leads to a lesion of dopamine neurons in the mesencephalon with extensive loss of dopamine fibers in several forebrain areas, while localized serotonin fiber sprouting is induced in striatum. Furthermore, concomitant reductions of the levels of peptides related to the dopamine system occur following the 6-hydroxydopamine treatment. Behavioral disturbances such as hyperactivity and cognitive deficiencies occurring after a dopamine lesion early in life might therefore be due to plastic alterations in several different transmitter/neuromodulator systems as a direct or indirect consequence of the lesion.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Reduction of arginine vasopressin binding sites in mouse lateral septum by treatment with 6-hydroxydopamine.

The neuropeptide arginine vasopressin modulates neuroadaptive processes, including memory consolidation and functional tolerance to ethanol, by actions at CNS V1 receptors. Noradrenergic systems play a role in these actions of the peptide. To assess whether vasopressin may act presynaptically on catecholamine neurons, vasopressin receptors were measured by quantitative autoradiography in the lateral septum, an area that is innervated by catecholaminergic neurons and has a high density of V1 receptors, of control and 6-hydroxydopamine-treated mice. Vasopressin receptors were distributed non-uniformly throughout the lateral septum, with greater binding in the more caudal regions. Treatment with 6-hydroxydopamine lowered septal catecholamine levels and vasopressin binding, with a greater effect on binding in the intermediate and caudal portions of the lateral septum. Pretreatment with desmethylimipramine reversed the depletion of norepinephrine, and attenuated the effect of 6-hydroxydopamine on vasopressin binding in the intermediate region, but was less effective in the caudal region of the lateral septum. The results suggest that a portion of septal vasopressin receptors are localized on the terminals of noradrenergic and, possibly, dopaminergic neurons, consistent with the hypothesis that certain neuroadaptive responses to vasopressin could be mediated by modulation of neurotransmitter release. In contrast to the results with 6-hydroxydopamine, treatment of mice with 5,7-dihydroxytryptamine, to destroy serotonergic terminals, did not alter vasopressin binding in the lateral septum.

Animals↗
PubMed1978

The effect of 6-hydroxydopamine on the antinociceptive action of morphine.

The role of brain catecholamines in the antinociceptive action of morphine was investigated. Intraventricular 6-hydroxydopamine which depleted brain noradrenaline in the rat had no effect on morphine's antinociceptive action but combined treatment with pargyline and 6-hydroxydopamine to further deplete brain dopamine potentiated morphine's action. It was also shown that when dopamine receptors were blocked, the antinociceptive action of morphine was potentiated whereas alpha- and beta-adrenoceptor antagonists had no effect. 6-Hydroxydopamine had two effects in mice tested on the hot-plate. It produced a hyperalgesia and antagonized the antinociceptive action of morphine. This antagonism of morphine appeared to be the result of the depletion of noradrenaline rather than dopamine. Intraventricular injection of both catecholamines restored the antinociceptive action of morphine in 6-hydroxydopamine-treated mice but dopamine was ineffective in the presence of a dopamine beta-hydroxylase inhibitor. It is suggested that the antinociceptive action of morphine is expressed by noradrenergic neurones in the mouse and by both noradrenergic and dopaminergic neurones in the rat.

Analgesics↗
PubMedDate not supplied

Effect of various 6-hydroxydopamine treatments during development on growth and ingestive behavior.

Destruction of catecholamine-containing fibers in brain at 5 days of age with intracisternal injection of 6-hydroxydopamine reduced body growth, intake of a sucrose solution, and acquisition of an active avoidance response. Further characterization of behavioral deficits indicated that treated animals also showed reduced ingestion of saline solution when injected with desoxycorticosterone and a decreased eating response to insulin. In addition, all of these deficits produced by catecholamine depletion with 6-hydroxydopamine were observed in rats in which brain dopamine was preferentially reduced but not in rats having preferential destruction of noradrenergic fibers, suggesting that dopamine depletion amounts for the observed alterations in developing animals. Although animals treated with 6-hydroxydopamine at 14 days showed reduced intake of a sucrose solution, they did not have reduced growth. Since early malnourishment reduced growth, it seems possible that the reduced growth observed after destruction of dopaminergeic fibers may be related to an acute reduction of food intake which is perpetuated by persistent deficits in ingestive behavior. Evidence implicating malnourishment in other deficits produced by 6-hydroxydopamine could not be obtained.

Age Factors↗
PubMed1975

Role of saline consumption in the prevention of deoxycorticosterone hypertension in rats by central 6-hydroxydopamine.

1. The mechanism by which pretreatment of rats with intracisternal 6-hydroxydopamine prevents the onset of deoxycorticosterone hypertension has been studied. 2. Rats pretreated with central 6-hydroxydopamine increase their consumption of 0-17 mol/l sodium chloride--0-03 mol/l potassium chloride ('saline') less than normal rats when implanted with deoxycorticosterone. 3. Intact rats restricted to the equivalent consumption of saline of rats pretreated with 6-hydroxydopamine develop hypertension despite this restriction. 4. It is suggested that the prevention of deoxycorticosterone hypertension by central 6-hydroxydopamine does not depend on reduced saline consumption.

Animals↗