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PubMed1976

Increased plasma catecholamines in high renin hypertension.

Plasma catecholamines, indexes of sympathetic nervous tonicity, were measured simultaneously with renin both supine and after standing plus furosemide in patients with primary hypertension and normotensive volunteers. Seventy percent of hypertensive patients with high renin levels had increased catecholamines compared with a 14% incidence in the combined group with low and normal renin (P less than 0.001). Basal catecholamines were related directly to renin in the hypertensive patients and to blood pressure in the normal (P less than 0.05), but not in the high and low renin subgroups, and inversely to percent increase of catecholamines after standing plus furosemide in hypertensive and normotensive patients (P less than 0.01). Sympathetic nervous hypertonicity may be responsible for the elevation of blood pressure and for the activation of the renin-angiotensin system in patients with high renin hypertension.

Adolescent↗
PubMed1994

Efficacy of adenosine in terminating catecholamine-dependent supraventricular tachycardia.

The purpose of this study was to determine if adenosine is equally effective in terminating catecholamine-dependent and independent supraventricular tachycardia (SVT). The effect of adenosine on termination of SVT was studied in 21 patients: 12 with atrioventricular (AV) reciprocating tachycardia, and 9 with AV node reentrant tachycardia. Group 1 comprised 13 patients who had SVT induced in the absence of exogenous catecholamines, whereas group 2 comprised 8 who needed isoproterenol (1.6 +/- 0.4 micrograms/min) for induction. There was no statistical difference between the 2 groups regarding age, weight, mean arterial pressure during sinus rhythm and SVT, cycle length of SVT, or norepinephrine and epinephrine levels during sinus rhythm and SVT. Cycle length during sinus rhythm was significantly decreased in group 2. The mean dose of adenosine needed to terminate SVT was 52 +/- 6 micrograms/kg of body weight in group 1, and 61 +/- 12 micrograms/kg in group 2 (p > 0.05). In addition to isoproterenol not altering the minimal dose of adenosine necessary to terminate SVT, there was also no correlation between the dose of adenosine (mean 55 +/- 6 micrograms/kg) of each patient, and the corresponding endogenous epinephrine (273 +/- 59 pg/ml) (r = -0.19) and norepinephrine (400 +/- 58 pg/ml) (r = 0.01) levels during SVT, or cycle length of SVT (323 +/- 9 ms) (r = -0.35). The results show that adenosine is equally effective in terminating catecholamine-dependent and independent SVT; higher adenosine doses should not be needed to manage catecholamine-dependent SVT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1982

The effect of labor on maternal and fetal circulating catecholamines.

Maternal circulating catecholamines were determined in nonpregnant (n = 15) and antepartum (n = 15) subjects and at spontaneous vaginal (n = 20) and repeat cesarean section (n = 20) deliveries. Newborn levels of catecholamines were determined prior to the onset of respiration in the vaginal delivery (n = 20) and cesarean section (n = 20) groups. Maternal levels of norepinephrine at 36 to 38 weeks' gestation were lower than values in nonpregnant individuals, and did not increase at cesarean section but rose to nonpregnant levels at vaginal delivery. Antepartum levels of epinephrine were lower than levels in nonpregnant subjects and rose above nonpregnant levels in both delivery groups (P less than 0.02). Maternal levels of dopamine followed a similar pregnancy decline and rose above nonpregnant levels at delivery in both groups (P less than 0.02). Maternal levels of dopamine in the cesarean section group were significantly higher than those in vaginal delivery (P less than 0.05). Newborn levels of catecholamines demonstrated significant newborn secretion of norepinephrine, epinephrine, and dopamine at delivery in both groups. Umbilical arterial levels of norepinephrine and epinephrine were significantly greater after vaginal delivery than those after abdominal delivery (P less than 0.01). The significance of circulating catecholamines to, and their possible roles in, the parturient women and fetus are discussed.

Catecholamines↗
PubMed1983

Fetal catecholamines.

Experimental data from fetal human and animal research suggest that the fetal sympathoadrenal system, composed of the adrenal medulla, sympathetic neurons, and extra-adrenal chromaffin tissue functions from early fetal life to maintain fetal homeostasis. The extra-adrenal chromaffin tissue undergoes maturation at 9 to 11 weeks of gestation, whereas the adrenal medulla and sympathetic nervous system mature later in fetal life. The fetal catecholamine response to hypoxia, mediated predominantly by norepinephrine, is an important component of the fetal cardiovascular response to hypoxia, i.e., through alpha-receptor stimulation, fetal cardiac output redistribution occurs. Fetal catecholamine secretion in response to substrate availability, through alpha- and beta-receptor stimulation, provide a mechanism by which the fetus can utilize its own substrate stores. Pulmonary beta-receptor stimulation by catecholamines has been demonstrated to increase lecithin synthesis, increase surfactant secretion, and decrease lung fluid production near term. beta-Receptor stimulation has also been demonstrated to have trophic effects on the development of thermogenic brown adipose tissue. Although the exact stimulus for the initiation of parturition in the primate is unknown, fetal catecholamines, through direct myometrial alpha-adrenergic or dopaminergic receptor stimulation and/or through the stimulation of prostaglandin production, have the potential of facilitating the onset of parturition.

Adrenal Glands↗
PubMed1982

Studies on the mechanism by which tyrosine raises urinary catecholamines.

The source of urinary catecholamines and the mechanisms by which tyrosine administration raises these compounds were investigated in rats. Adrenalectomy blocked the tyrosine-induced rise in urinary epinephrine but not dopamine or norepinephrine. Following chemical sympathectomy with 6-hydroxydopamine (6-OHDA), the tyrosine-induced increase in urinary norepinephrine was diminished, but epinephrine and dopamine responses were unaffected. Cardiac norepinephrine, which is normally unchanged following tyrosine administration, became significantly elevated in 6-OHDA-pretreated animals. At the doses used in this study, tyrosine had no effect on the uptake or metabolic clearance of circulating catecholamines. We conclude that tyrosine augments the synthesis of the three catecholamines in sympathoadrenal cells by increasing the extent to which tyrosine hydroxylase is saturated with its amino acid substrate. Moreover, the effects of tyrosine on peripheral catecholamine synthesis may be enhanced under conditions of increased sympathetic activity.

Adrenal Glands↗
PubMed1983

Suppression by phospholipase A2 inhibitors of secretion of catecholamines from isolated adrenal medullary cells by suppression of cellular calcium uptake.

The involvement of phospholipase A2 in the secretion of catecholamines and cellular uptake of 45Ca2+ was investigated in isolated bovine adrenal medullary cells. In these cells, stimulation of cholinergic receptors by carbamylcholine causes the activation of receptor-linked Ca-channels and influx of Ca2+ is known to trigger the secretory process. Phospholipase A2 inhibitors, such as quinacrine, chloroquine, quinine and p-bromophenacyl bromide, all inhibited the secretion of catecholamines evoked by carbamylcholine in a dose-dependent manner. These phospholipase A2 inhibitors also inhibited the cellular uptake of 45Ca2+ evoked by carbamylcholine with similar dose-response curves to those for inhibition of catecholamine secretion. The inhibition by phospholipase A2 inhibitors was found to be distinct from inhibition by d-tubocurarine which competitively blocks acetylcholine receptors, and from inhibition by diltiazem which acts as a Ca-antagonist at Ca-channels. Phospholipase A2 inhibitors seem to suppress the secretion of catecholamines by interfering with the linkage between acetylcholine receptors and Ca-channels by the membrane effects including the inhibition of endogenous phospholipase A2 activity of the adrenal medullary cells.

Acetophenones↗
PubMed1987

Binding of catecholamines to alpha-1 acid glycoprotein, albumin and lipoproteins in human serum.

The binding of catecholamines in human serum was determined by equilibrium dialysis at 37 degrees. For serum concentrations of 10-15 nM the bound fractions were 28.8 +/- 2.2%, 25.7 +/- 1.7% and 22.2 +/- 2.2% for (+/-)-isoproterenol (IPR), (+/-)-norepinephrine (NE) and (+/-)-epinephrine (EPI), respectively. At higher serum concentrations saturation occurred. Alpha-1 acid glycoprotein (AAG) possessed one high affinity binding site and approximately 10 low affinity sites. The catecholamines were bound to AAG with the same order of potency for both classes of binding sites: IPR (Kd1: 100 microM Kd2: 2.2 mM) greater than NE (Kd1: 120 microM, Kd2: 6.5 mM) greater than EPI (Kd1: 140 microM, Kd2: 14 mM). Human serum albumin (HSA) and lipoproteins (SLP) interacted with the catecholamines in a non-saturable manner. IPR showed the strongest and EPI the weakest association to both of these serum protein fractions. (-)-Propranolol was able to inhibit the binding of IPR in serum and to isolated AAG, but not to HSA or to SLP. The present results show that AAG is an important catecholamine-binding protein in human serum. AAG, but not HSA or SLP, possesses binding sites shared by adrenergic receptor stimulators and blockers.

Binding Sites↗
PubMed1990

The effect of prenylamine and organic nitrates on the bioenergetics of bovine catecholamine storage vesicles.

We have compared the cardioprotective agents prenylamine and glyceryl trinitrate (GTN) with respect to their effects on the bioenergetics of catecholamine storage vesicles. Chromaffin granule ghosts, which have a well preserved ability to actively transport and store catecholamines, were used as a model for adrenergic synaptic vesicles due to their functional similarity. Prenylamine, which partially and reversibly deplete the endogenous stores of noradrenaline in adrenergic nerves and ganglia, was found to inhibit the generation of the transmembrane proton electrochemical gradient driven by a H(+)-ATPase, mainly by acting as an uncoupler of this ATPase. The inhibition of the energy dependent dopamine uptake (and noradrenaline biosynthesis) by prenylamine could be accounted for by its effect on the bioenergetics of the storage vesicles. The organic nitrates glyceryl trinitrate and isosorbide dinitrate also partly inhibited the catecholamine uptake in parallel with their effects on the proton electrochemical gradient. It is concluded that GTN is a weak catecholamine depletor. Experiments with 3-morpholinosydnonimin-hydrochloride, a source of nitric oxide (NO), opens up the possibility that the mechanism of inhibition of the bioenergetics of chromaffin granule ghosts by GTN is mediated by NO.

Animals↗
PubMed1994

Inhibition by ethaverine of catecholamine secretion through blocking L-type Ca2+ channels in PC12 cells.

Ethaverine, a derivative of papaverine, is used as a vasodilator and antispasmodic drug. We have investigated the effects of ethaverine on the secretion of [3H]norepinephrine from PC12 cells, of neuroendocrine origin. Treatment with ethaverine reduced catecholamine secretion in a concentration-dependent manner. The maximal inhibitory effect (90%) was achieved with 10 microM ethaverine, and the IC50 for secretion was approximately 2 microM. Ethaverine pretreatment for 1 min prior to stimulation by 70 mM K+ also decreased the level of intracellular Ca2+ in a concentration-dependent manner, as measured by fura-2 fluorescence. The IC50 for the inhibition of the increase in intracellular Ca2+ was approximately 2 microM. Nifedipine, a dihydropyridine L-type Ca2+ channel blocker, did not enhance the inhibitory effect of ethaverine on the 70 mM K(+)-induced increase in [Ca2+]i or catecholamine secretion. In contrast, the addition of the N-type voltage-sensitive Ca2+ channel antagonist omega-conotoxin with ethaverine resulted in further reductions in the increase in [Ca2+]i and catecholamine release. Maximally effective concentrations of ethaverine and nifedipine showed the same inhibitory effect on the 70 mM K(+)-evoked responses. However, ethaverine pretreatment did not inhibit the bradykinin-induced secretion and [Ca2+]i rise, which are known to be produced through the receptor-operated Ca2+ channels. We conclude that ethaverine reduces catecholamine secretion by blocking the L-type voltage-sensitive Ca2+ channel.

Animals↗
PubMed1996

Characterization of the catecholamine extraneuronal uptake2 carrier in human glioma cell lines SK-MG-1 and SKI-1 in relation to (2-chloroethyl)-3-sarcosinamide-1-nitrosourea (SarCNU) selective cytotoxicity.

Transport of (2-chloroethyl)-3-sarcosinamide-1-nitrosourea (SarCNU) and (-)-norepinephrine was investigated in SarCNU-sensitive SK-MG-1 and -resistant SKI-1 human glioma cell lines. [3H]SarCNU influx was inhibited by SarCNU, sarcosinamide, and (+/-)-epinephrine in SK-MG-1 cells with competitive inhibition observed by (+/-)-epinephrine (Ki = 140 +/- 12 microM) and (+/-)-norepinephrine (Ki = 255 +/- 41 microM). No effect on influx was detected in SKI-1 cells. [3H](-)-Norepinephrine influx was linear to 15 sec in both cell lines and temperature dependent only in SK-MG-1 cells. Influx of [3H](-)-norepinephrine was found to be saturable in SK-MG-1 (K(m) = 148 +/- 28 microM, Vmax = 1.23 +/- 0.18 pmol/microL intracellular water/sec) but not in SKI-1 cells. In SK-MG-1 cells, [3H](-)-norepinephrine influx was found to be inhibited competitively by (-)-epinephrine (Ki = 111 +/- 7 microM) and SarCNU (Ki = 1.48 +/- 0.22 mM). Ouabain and KCl were able to inhibit the [3H](-)-norepinephrine influx in SK-MG-1 cells, consistent with influx being driven by membrane potential. Several catecholamine uptake2 inhibitors were able to reduce significantly the influx of [3H](-)-norepinephrine and [3H]SarCNU with no inhibition by a catecholamine uptake1 inhibitor. These findings suggest that increased sensitivity of SK-MG-1 to SarCNU is secondary to enhanced accumulation of SarCNU mediated via the catecholamine extraneuronal uptake2 transporter, which is not detectable in SKI-1 cells. The introduction of SarCNU into clinical trials will confirm if increased uptake via the catecholamine extraneuronal uptake2 transporter will result in increased antitumor activity.

Antineoplastic Agents↗
PubMed1992

Sleep deprivation and impaired cognition. Possible role of brain catecholamines.

To assess the role of brain catecholamines in cognitive decline associated with sleep deprivation, 40 healthy male volunteers were randomized to conditions of total sleep deprivation or 40.5 h of rest. Within each sleep condition, subjects were further randomized to treatment with a 2-day regimen of placebo or alpha-methyl-para-tyrosine (AMPT), a catecholamine synthesis inhibitor. Cognitive performance was measured repeatedly over time using a computerized performance assessment battery. Treatment with AMPT or treatment with sleep deprivation increased sleepiness without producing marked or consistent deterioration in performance. By contrast, subjects who received both treatments reported greater sleepiness than those receiving either treatment alone, and developed severe cognitive impairment on a variety of tasks. These findings, along with previous evidence that catecholamine-enhancing drugs improve performance in sleep-deprived individuals, support the view that decline in cognitive performance during sleep deprivation may be mediated by brain catecholamines.

Adult↗
PubMed1979

Role of central catecholamines in the control of blood pressure and drinking behavior.

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.

Animals↗
PubMed1981

Serotonin-immunoreactive cells in the superior cervical ganglion of the rat. Evidence for the existence of separate serotonin- and catecholamine-containing small ganglionic cells.

Superior cervical ganglia of 8 adult male rats were examined by indirect immunofluorescence microscopy, using an antibody to a conjugate of bovine serum albumin and serotonin, and an antibody to a conjugate of bovine serum albumin and noradrenaline. The fixative used was 4% paraformaldehyde in 0.1 M phosphate buffer, pH 7.3. Consecutive cryostat sections of whole ganglia were alternately stained with these antibodies. Serotonin- as well as catecholamine-immunoreactive, small ganglionic cells were demonstrated, both arranged in clusters. Serotonin-immunoreactive cells were mostly located at the cranial or caudal side of the ganglia. Serotonin-immunoreactive cells provided with processes were easily observed. Only a few mast cells were seen. Catecholamine-immunoreactive cells were rounded without processes. This cell type did not seem to have a preferential position within the ganglia. Intermingling of both immunoreactive, small ganglionic cells was not observed. A considerable variety in the number of both immunoreactive cell types was established. Catecholamine-immunoreactive cells were absent in 3 our of 8 animals. Evidence is provided that the catecholamine-immunoreactive cells are storing noradrenaline. The presented data seem to indicate the presence of 3 different types of small, intensely fluorescent (SIF) cells in the superior cervical ganglion of the rat, viz. a dopamine-storing, a noradrenaline-storing, and a serotonin-storing SIF cell type.

Animals↗
PubMed1981

Effect of manipulating central catecholamines on puberty and the surge of luteinizing hormone and gonadotropin releasing hormone induced by pregnant mare serum gonadotropin in female rats.

We have investigated the effect of manipulating central catecholamines on the timing of puberty (as assessed by vaginal opening) in female rats and the surge of luteinizing hormone (LH) and gonadotropin releasing hormone (GnRH) induced by pregnant mare serum gonadotropin (PMSG) in immature female rats. Manipulation of the catecholamines was carried out with either 6-hydroxydopamine (6-OHDA) administered with or without either desipramine (DMI) or pargyline, or alpha-methyl-p-tyrosine (alpha-MPT). The neonatal administration of 6-OHDA delayed puberty, an effect which was potentiated by pretreatment with DMI and was associated with a reduction in the rate of body growth. Catecholamine fluorescence in animals aged 60--65 days that had been treated with DMI followed by 6-OHDA was diminished only in the caudatus--putamen; treatment with 6-OHDA alone resulted in diminished fluorescence in the hypothalamus and in the intermediate but not the external layer of the median eminence. The neonatal administration of alpha-MPT had no significant effect on either the growth rate or the timing of puberty. Regular oestrous cycle occurred after puberty in animals treated with either 6-OHDA or alpha-MPT. The PMSG-induced LH surge was significantly enhanced by 6-OHDA (administered i.v.) plus DMI, and reduced by 6-OHDA injected in to the lateral ventricle (v). The inhibitory effect of 6-OHDA (v) was reduced by DMI, but in animals given 6-OHDA (i.v.) after pargyline there was a marked reduction in the height of the LH surge. There was a good correlation between the changes in the concentrations of LH in peripheral plasma and the concentrations of GnRH in pituitary stalk plasma in that the PMSG-induced surge of GnRH was significantly increased by 6-OHDA (i.v.) plus DMI and reduced by 6-OHDA (v). In animals treated with 6-OHDA (i.v. plus DMI catecholamine fluorescence was reduced only in the external layer of the median eminence, while after 6-OHDA (v) plus DMI degeneration was seen in the medial forebrain bundle. These results demonstrate a marked difference between the long-term and acute effects of 6-OHDA on the gonadotropin control system. Neonatal treatment with 6-OHDA plus DMI significantly delays puberty and the rate of body growth, but does not affect cyclical gonadotropin release and has no persistent effect on the hypothalamic catecholaminergic systems. The acute administration of 6-OHDA, depending upon the route of administration and whether it is given after DMI, can either potentiate or inhibit the PMSG-induced surge of GnRH and consequently LH by mechanisms which involve destruction, respectively, of either dopaminergic terminals in the median eminence or catecholaminergic fibres in the dorsal hypothalamus.

Animals↗
PubMed1981

The contribution of brain stem catecholamine cell groups to the innervation of the sympathetic lateral cell column.

Data are presented on the quantitative distribution of individual catecholamines, noradrenaline (NA), dopamine (DA) and adrenaline (A) determined within specific microdissected areas of the third thoracic segment of the cat spinal cord, using a radioenzymatic assay. NA was found in much higher concentrations than the other catecholamines with highest levels in medial-ventral grey matter (754 +/- 56 ng/100 mg protein) and in dorsal and intermediolateral grey matter. DA was present in much smaller amounts, but was relatively concentrated in medial and dorsal grey matter (up to 76 +/- 1 ng/100 mg protein). Very little A was detected ( less than 17 ng/100 mg protein). Experiments were carried out to determine the contribution made by various brain stem cell groups to the catecholamine innervation of the spinal cord, and in particular the sympathetic lateral column. The concentrations of the catecholamines was determined in 5 groups of animals, 3-5 days after decerebration, or decerebration together with bilateral lesions of the A1, A2, A5 or A6 groups. A major and selective NA input to the sympathetic lateral column from the A1 cell group was revealed. There may also be a small contribution from the A2 and A6 groups, but none was shown from the A5 group. The A6 group was also shown to provide a selective noradrenergic input to the ventral horn. Some evidence is presented for the origin of noradrenergic inputs to other regions, e.g. dorsal horn. The possibility of a separate dopaminergic innervation to specific regions of the spinal cord is discussed.

Adrenergic Fibers↗
PubMed1982

The identification of specific brain nuclei in which catecholamine turnover is increased by left ventricular receptors during acute myocardial infarction in the rat.

Central catecholaminergic nerves have been shown to participate in the integration of cardio-cardiac reflexes induced by coronary artery ligation in the rat. In this study we measured the turnover of dopamine, norepinephrine and epinephrine in microdissected brain regions to identify some of the specific neural loci involved in this integration. Three groups of rats, treated with alpha-methyltyrosine, an inhibitor of catecholamine biosynthesis were examined: left coronary artery ligation, left coronary artery ligation with the left ventricle painted with lidocaine, and sham operation. An untreated group of resting rats was also examined. Dopamine, norepinephrine and epinephrine turnover was increased in ligated rats in nucleus tractus solitarius (right and left), nucleus commissuralis, A1-region, locus coeruleus, nucleus cuneatus, and area postrema in the pons-medulla and nucleus dorsomedialis in the hypothalamus. Norepinephrine and dopamine (but not epinephrine) turnover was increased in nucleus ambiguus in the brain stem and nucleus paraventricularis in the hypothalamus. A ligation-induced increase in norepinephrine turnover, alone, was exhibited by the A2-region and nucleus gigantocellularis in the medulla and nucleus supraopticus and nucleus hypothalamicus posterior in the hypothalamus. Dopaminergic nerves to the nucleus gigantocellularis appeared to be inhibited following coronary ligation. The catecholamine stores of 11 nuclear regions were not influenced by coronary artery occlusion. Topical lidocaine, applied to the ischemic left ventricle, only, of ligated rats, completely restored regional brain catecholamine turnover to that found in sham-operated animals. In conclusion, we have identified discrete loci in the brain in which catecholamine turnover (as measured by alpha-methyltyrosine induced disappearance) is increased by the stimulation of left ventricular receptors during acute myocardial ischemia in the rat.

Animals↗
PubMed1984

Differential effects of calcium on catecholamine synthesis regulation in olfactory tubercle and hypothalamic synaptosomes.

We have compared catecholamine synthesis regulation in rat brain olfactory tubercle and hypothalamic synaptosomes with regard to: calcium-dependency of stimulant drug-induced synthesis activation; tyrosine-dependency of amphetamine-induced synthesis stimulation, and the effects of the calcium chelator, ethylene glycol-bis-(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid (EGTA). Amphetamine-induced synthesis stimulation was markedly calcium-dependent in the olfactory tubercle, but was completely calcium-independent in the hypothalamus. The effect of amphetamine on catecholamine synthesis in the olfactory tubercle was dependent upon the concentration of tyrosine in the incubation buffer; amphetamine produced a biphasic response, inhibiting synthesis at low tyrosine concentrations and activating synthesis at higher tyrosine concentrations. In contrast to the olfactory tubercle, amphetamine-induced stimulation of synthesis in the hypothalamus was observed at both low and high tyrosine concentrations. Distinct tissue differences in drug responsiveness were also observed following exposure to EGTA; synthesis was stimulated by EGTA in the olfactory tubercle but not in the hypothalamus. These data provide evidence for regional differences in catecholamine regulation in the brain, and suggest that some of these differences may be related to differential effects of calcium on catecholamine formation.

Amphetamine↗
PubMed1988

Depletion of central catecholamines reduces pressor responses to arginine vasopressin.

Previous reports that central administration of arginine vasopressin (AVP) increases turnover of brain catecholamines raise the possibility that the pressor responses which follow central administration of AVP may be mediated, in part, by central catecholamines. To test this hypothesis, rats were given intraventricular injections of vehicle, or of the neurotoxin, 6-hydroxydopamine, which resulted in significant depletions of hypothalamic and medulla oblongata noradrenalin and hypothalamic dopamine, but not of medullary dopamine or of hypothalamic and medullary 5-hydroxytryptamine. Following a one week recovery, these conscious rats, fitted with indwelling arterial catheters, were given intraventricular injections of AVP; the increases in arterial pressure and heart rate were significantly reduced in the catecholamine-depleted animals. These data support the hypothesis that the pressor and tachycardia responses to intraventricular AVP are mediated, in part, by central catecholamine-containing neurons.

Animals↗