Biomedical subjects

A F Sved

Publications and source records attributed to A F Sved.

At least 73 records · Page 4Linked to original sources

PubMed1995

Local influence of endogenous norepinephrine on extracellular dopamine in rat medial prefrontal cortex.

Noradrenergic and dopaminergic projections converge in the medial prefrontal cortex and there is evidence of an interaction between dopamine (DA) and norepinephrine (NE) terminals in this region. We have examined the influence of drugs known to alter extracellular NE on extracellular NE and DA in medial prefrontal cortex using in vivo microdialysis. Local application of the NE uptake inhibitor desipramine (1.0 microM) delivered through a microdialysis probe increased extracellular DA (+149%) as well as NE (+201%) in medial prefrontal cortex. Furthermore, desipramine potentiated the tail shock-induced increase in both extracellular DA (stress alone, +64%; stress + desipramine, +584%) and NE (stress alone, +55%; stress + desipramine, +443%). In contrast, local application of desipramine did not affect extracellular DA in striatum, indicating that this drug does not influence DA efflux directly. Local application of the alpha 2-adrenoceptor antagonist idazoxan (0.1 or 5.0 mM) increased extracellular NE and DA in medial prefrontal cortex. Conversely, the alpha 2-adrenoceptor agonist clonidine (0.2 mg/kg; i.p.) decreased extracellular NE and DA in medial prefrontal cortex. These results support the hypothesis that NE terminals in medial prefrontal cortex regulate extracellular DA in this region. This regulation may be achieved by mechanisms involving an action of NE on receptors that regulate DA release (heteroreceptor regulation) and/or transport of DA into noradrenergic terminals (heterotransporter regulation).

Adrenergic Uptake Inhibitors↗

PubMed1994

Lithium chloride-induced anorexia, but not conditioned taste aversions, in rats with area postrema lesions.

Area postrema (AP) lesions were produced by vacuum aspiration in adult male Sprague-Dawley rats. Consistent with previous findings, when water-deprived rats were allowed to drink novel flavored fluids immediately before treatment with LiCl (3 mEq/kg, i.p.), sham-operated and non-operated control rats demonstrated a pronounced aversion to the fluids whereas rats with AP lesions did not decrease fluid consumption significantly. However, in a 30-min test period after overnight food deprivation, rats with AP lesions reduced food intake significantly and to an equivalent degree as control animals when pretreated with LiCl (3 mEq/kg, i.p. or i.v.). These and other results are consistent with the traditional view that AP mediates the sensation of nausea produced by LiCl treatment (hence the loss of conditioned taste aversions after AP lesions), but suggest that neither nausea nor AP is necessary for the marked disinclination to eat that is induced in rats by acute administration of LiCl.

Analysis of Variance↗

PubMed1994

Effect of atropine injected into the nucleus tractus solitarius on the regulation of blood pressure.

Previous experiments have demonstrated that stimulation of muscarinic cholinergic receptors in the nucleus tractus solitarius (NTS) of the rat decreases arterial blood pressure and heart rate. The present studies were designed to examine the role of cholinergic mechanisms in the NTS in the tonic regulation of arterial pressure and the baroreceptor reflex. Atropine injected into the NTS of chloralose-anesthetized rats produced a dose-dependent inhibition of cardiovascular responses elicited by injection of acetylcholine into the same site; 240 pmol atropine eliminated acetylcholine-evoked responses. Atropine also increased arterial blood pressure but only at higher doses. Even larger doses of atropine were required to alter cardiovascular responses elicited by electrical stimulation of the aortic depressor nerve. Methylatropine injected into the NTS also blocked acetylcholine-evoked responses but, in contrast to the actions of atropine, did not increase arterial pressure in the dose range required to block acetylcholine-evoked responses. Furthermore, a dose of methylatropine (1 nmol) capable of blocking acetylcholine-evoked cardiovascular responses did not alter aortic depressor nerve-evoked cardiovascular responses. This lack of an effect of methylatropine on arterial pressure and aortic depressor nerve-evoked responses was not due to limited diffusion of the drug within the NTS since 1 nmol methylatropine completely blocked acetylcholine-evoked responses even when injected 0.5 mm distant from the site of acetylcholine injection. These results suggest that cholinergic mechanisms in the NTS are not involved in the tonic regulation of cardiovascular function or the baroreceptor reflex. Furthermore, these results highlight the importance of characterizing doses of drugs used in microinjection studies.

Animals↗

PubMed1994

Stress-induced sensitization of dopamine and norepinephrine efflux in medial prefrontal cortex of the rat.

We examined whether prior exposure to chronic cold (17-28 days, 5 degrees C) alters basal or stress-evoked (30-min tail shock) catecholamine release in medial prefrontal cortex, nucleus accumbens, and striatum, using in vivo microdialysis. Basal norepinephrine (NE) concentrations in medial prefrontal cortex did not differ between chronically cold-exposed rats and naive control rats (2.7 +/- 0.3 vs. 2.5 +/- 0.2 pg/20 microliters respectively). Basal dopamine (DA) efflux in any of the brain regions was not significantly different between chronically cold-exposed rats and naive rats. However, a trend for lower basal DA efflux in the cold-exposed relative to naive rats was observed in medial prefrontal cortex (1.5 +/- 0.2 vs. 2.2 +/- 0.3 pg/20 microliters, respectively), nucleus accumbens (3.7 +/- 0.8 vs. 5.4 +/- 0.9 pg/20 microliters, respectively), and striatum (4.4 +/- 0.5 vs. 7.2 +/- 1.5 pg/20 microliters, respectively). In medial prefrontal cortex of rats previously exposed to cold, tail shock elicited a greater increase from baseline in both DA and NE efflux relative to that measured in naive rats (DA, 2.3 +/- 0.3 vs. 1.2 +/- 0.1 pg, respectively; NE, 3.8 +/- 0.4 vs. 1.4 +/- 0.2 pg, respectively). However, in nucleus accumbens or striatum of rats previously exposed to cold, the stress-induced increase in DA efflux was not significantly different from that of naive rats (nucleus accumbens, 1.8 +/- 0.7 vs. 1.5 +/- 0.3 pg, respectively; striatum, 1.9 +/- 0.4 vs. 2.6 +/- 0.7 pg, respectively). Thus, both cortical NE projections and cortically projecting DA neurons sensitize after chronic exposure to cold. In contrast, subcortical DA projections do not sensitize under these conditions.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

PNMT-containing neurons of the C1 cell group express c-fos in response to changes in baroreceptor input.

The immunocytochemical detection of Fos, the protein product of the immediate-early gene c-fos, was used as a marker for activated neurons to examine whether the C1 neurons in the rat rostral ventrolateral medulla (RVLM) respond to changes in baroreceptor afferent activity. After hydralazine-induced hypotension or sinoaortic denervation, two treatments that reduce baroreceptor afferent activity, numerous Fos-positive neurons were observed in the RVLM. The number of Fos-positive neurons in the RVLM was counted in brain stem sections from hydralazine-treated rats that had been previously injected with Fluorogold into the upper thoracic spinal cord to label spinally projecting RVLM neurons as well as stained for phenylethanolamine-N-methyltransferase (PNMT) as a marker of C1 neurons. The results indicate that approximately 80% of the C1 neurons expressed Fos in response to hydralazine injection; this was true of spinally projecting C1 neurons as well as those C1 neurons that were not labeled with Fluorogold. Furthermore, in hydralazine-treated rats, the majority of Fluorogold-labeled Fos-positive neurons contained PNMT. These results suggest that C1 neurons are sensitive to baroreceptor afferent input and support a role of these neurons in cardiovascular regulation.

Animals↗

PubMed1994

Use of sinoaortic denervation to study the role of baroreceptors in cardiovascular regulation.

To assess the role of arterial baroreceptors in cardiovascular regulation, many studies have used rats in which baroreceptor afferents have been surgically destroyed. However, interpretation of studies using sinoaortic-denervated (SAD) rats is complicated by variability in the extent of baroreceptor denervation. We have compared cardiovascular regulation in rats with total sinoaortic cardiovascular regulation in rats with total sinoaortic denervation, as assessed by the abolition of reflex changes in heart rate (HR) to increases and decreases in arterial pressure (AP), with rats that underwent the same denervation procedure but still had residual (although markedly blunted) reflex changes in HR to changes in AP. In totally SAD rats, the lability of AP was greatly exaggerated compared with sham-denervated rats, although the average AP was equivalent. In contrast, partially SAD rats had elevated AP, and although AP was more labile than in sham-denervated rats, it was less labile than in totally SAD rats. In addition, cardiovascular responses elicited by elimination of neural activity in the nucleus tractus solitarius (NTS) were qualitatively different between the two groups of rats; destruction of the NTS increased AP similarly in partially SAD rats and sham-denervated rats, whereas this treatment did not alter AP in totally SAD rats. Thus there are marked differences in SAD rats with no residual arterial baroreceptor reflex function compared with SAD rats with even a small degree of residual baroreceptor reflex function. These studies highlight the importance of carefully characterizing SAD rats used in studying the role of the baroreceptor reflex in cardiovascular regulation.

Animals↗

PubMed1994

Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats.

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.

Animals↗

PubMed1994

Locus coeruleus stimulation by corticotropin-releasing hormone suppresses in vitro cellular immune responses.

Previous studies have demonstrated that stressors alter cellular immune system function, and increase the activity of locus coeruleus neurons. Furthermore, stressors increase the release of corticotropin-releasing hormone (CRH) and locus coeruleus neurons are activated by CRH. Thus, the present study examined whether activation of the locus coeruleus by infusion of CRH modulates the function of blood and spleen lymphocytes assessed in vitro. CRH (100 ng) was administered into the region of the locus coeruleus in awake rats 1 hr before spleen and peripheral blood lymphocytes were collected for culture with nonspecific mitogens. Unilateral or bilateral microinfusion of CRH into the locus coeruleus produced a decrease in blood and spleen T-lymphocyte mitogenic responses to phytohemagglutinin, ConA, and an antibody to the T-lymphocyte antigen receptor. In contrast, infusion of saline into the locus coeruleus or CRH into the surrounding region of the dorsal pons did not alter spleen or blood lymphocyte responses. Plasma concentrations of adrenocorticotropic hormone, corticosterone, and IL-6 were increased by CRH infusion into the locus coeruleus. These results suggest that CRH-evoked activation of the locus coeruleus stimulates the hypophysial adrenal axis, possibly activates the sympathetic nervous system, and results in immunosuppression. Comparable changes in lymphocyte and hormone responses are produced by an aversive stimulus or a conditioned stressor, suggesting that activation of the locus coeruleus may be a component of stressor-induced immune alterations.

Adrenocorticotropic Hormone↗

PubMed1993

Quantitative autoradiography of alpha 1- and alpha 2-adrenergic receptors in the cerebral cortex of controls and suicide victims.

Alterations in both serotonergic and noradrenergic indices have been found in the brain of suicide victims. In order to better understand the role of the noradrenergic system in suicide, we carried out quantitative autoradiography of alpha 1- and alpha 2-adrenergic receptors using [3H]prazosin and [3H]-p-aminoclonidine respectively. We compared the distribution and relative density of these receptors in the prefrontal (PFC) and alpha 1-adrenergic receptors in the temporal cortex (TC) of suicide victims and controls matched for postmortem delay, age, side of brain and sex. We found that: (1) the laminar patterns of alpha 1-adrenergic receptors in the PFC (n = 20) and the TC (n = 16) were different (P = 0.022); (2) there was a 37% increase in alpha 1-adrenergic binding corresponding to layers IV-V of PFC of suicide victims compared to controls (P = 0.029); (3) the TC had a greater density of alpha 1-adrenergic binding sites than the PFC across all cortical layers (P = 0.006); (4) alpha 2-adrenergic binding sites had a specific laminar distribution in the PFC (n = 24) which did not differ in controls and suicide victims; (5) binding to alpha 2-adrenergic sites in the PFC of suicide victims did not differ from controls; and (6) norepinephrine concentrations in the same brain areas were elevated in the suicide group compared to controls, but did not correlate with binding to alpha 1- or alpha 2-adrenergic sites. The increase in [3H]prazosin (to alpha 1-adrenergic receptors) but not in [3H]-p-aminoclonidine (to alpha 2-adrenergic receptors), and in norepinephrine concentrations in the brain of suicide victims provides further evidence for an association between suicide and altered brain noradrenergic function. Future studies must determine whether these changes in brain noradrenergic function indicate increased or decreased transmission.

Adolescent↗

PubMed1993

Contrasting effects of the GABA transaminase inhibitors gamma-vinylGABA and aminooxyacetic acid on arterial pressure following injection into nucleus tractus solitarius.

The effect of injection of inhibitors of GABA-transaminase into the nucleus tractus solitarius (NTS) on arterial pressure was examined in anesthetized rats. Two typical GABA-transaminase inhibitors, gamma-vinylGABA (GVG) and aminooxyacetic acid (AOAA), increased arterial pressure when injected into the NTS, a response similar to that elicited by direct stimulation of GABA receptors in the NTS. However, with neither drug was the response consistent with the action of inhibiting GABA-T. The response elicited by GVG, despite GVG acting as an irreversible inhibitor of GABA-T, could be reproduced with subsequent injections. Still, the pressor response to GVG could be reversed by blockade of GABAB-receptors with CGP-35348, suggesting that GVG injection did increase GABA-mediated neural transmission. In contrast, the pressor response to AOAA could not be antagonized by blockade of either GABAA or GABAB receptors. These results suggest that acute inhibition of GABA-T does not necessarily result in an increase in GABA-mediated neural transmission.

4-Aminobutyrate Transaminase↗

PubMed1993

Amino acid neurotransmitters in nucleus tractus solitarius: an in vivo microdialysis study.

Amino acid neurotransmitters in the nucleus tractus solitarius (NTS) are thought to play a key role in the mediation of visceral reflexes and glutamate has been proposed as the neurotransmitter of visceral afferent nerves projecting to this region. The present studies sought to characterize the use of in vivo microdialysis to examine extracellular fluid levels of amino acids in the NTS of anesthetized rats. Using a microdialysis probe that was 450 microns in length and a sensitive HPLC assay for amino acids, amino acids could be measured in dialysate samples collected from the NTS. Perfusion of the microdialysis probe with 60 mM K+, to elicit depolarization of nerve terminals in the vicinity of the probe, resulted in increased dialysate fluid levels of aspartate, glutamate, glycine, taurine, and GABA. In contrast, glutamine and tyrosine were decreased and other amino acids were not significantly affected. Prior removal of the ipsilateral nodose ganglion did not alter the K(+)-evoked changes in dialysate levels of any of these amino acids. Electrical stimulation of the vagus nerves, using a variety of stimulus parameters, did not significantly alter dialysate levels of glutamate or any of the other amino acids that were measured. Blockade of glutamate uptake with dihydrokainate increased dialysate levels of glutamate, aspartate, and GABA, but in the presence of dihydrokainate vagal stimulation did not alter dialysate levels of these amino acids. The results show that in vivo microdialysis can be used to examine amino acid efflux in the rat NTS and provide further evidence for amino acidergic neural transmission in the NTS. However, these studies fail to support the hypothesis that vagal afferents release glutamate or aspartate.

Afferent Pathways↗

PubMed1993

Stress-induced dopamine release in the neostriatum: evaluation of the role of action potentials in nigrostriatal dopamine neurons or local initiation by endogenous excitatory amino acids.

It has been hypothesized that excitatory amino acids can initiate dopamine release in neostriatum. We examined whether the increase in extracellular dopamine in neostriatum produced by acute stress reflects presynaptic initiation of dopamine release by endogenous excitatory amino acids. Thirty minutes of intermittent tail-shock stress significantly elevated extracellular concentrations of dopamine, glutamate, aspartate, and gamma-aminobutyric acid in neostriatum of freely moving rats as measured with in vivo microdialysis. Local infusion of the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonovalerate or the non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione via the dialysis probe did not attenuate the stress-induced increase in extracellular dopamine. In fact, the increase was prolonged in rats treated with specific excitatory amino acid receptor antagonists. Infusion of tetrodotoxin into medial forebrain bundle increased extracellular glutamate and aspartate in neostriatum yet reduced basal dopamine in extracellular fluid to below the limit of detection of the assay and eliminated the stress-induced increase in extracellular dopamine. These findings fail to support the hypothesis that the stress-induced increase in extracellular dopamine in neostriatum is initiated locally by excitatory amino acids. Rather, the effects of stress on extracellular dopamine seem to be determined by impulse propagation in dopamine neurons.

2-Amino-5-phosphonovalerate↗

PubMed1993

Effect of serotonin on vasopressin release: a comparison to corticosterone, prolactin and renin.

Previously we reported that 5 min after intracerebroventricular (i.c.v.) injection, serotonin (5-HT, 2.5 micrograms) produced increases in blood pressure and decreases in heart rate in conscious rats that were blocked by LY 53857 (a selective 5-HT2/1C antagonist) and were sensitive to vasopressin antagonism. The present studies were performed to determine if this dose of 5-HT acts similarly to increase plasma vasopressin levels. In addition, the vasopressin responses were compared to prolactin, corticosterone, and plasma renin activity, three other neuroendocrine systems regulated in part by 5-HT. The administration of 5-HT (2.5 micrograms i.c.v.) produced a rapid (maximum response in less than 5 min) and brief (return to baseline by 15 min) increase in plasma vasopressin levels. The response was eliminated by the centrally acting 5-HT2/1C antagonist LY 53857 (100 micrograms/kg i.v.), but only attenuated by xylamidine (100 micrograms/kg i.v.), a 5-HT2/1C antagonist that reportedly does not cross the blood-brain barrier. 5-HT also increased plasma prolactin and corticosterone levels, but neither LY 53857 nor xylamidine altered these responses. In rats rendered chronically baroreceptor deficient by sinoaortic deafferentation, the vasopressin response to 5-HT was reduced, whereas the prolactin response was normal. 5-HT did not increase plasma renin activity in intact or baroreceptor-deficient rats, in contrast to the other neuroendocrine systems studied. Thus, the data demonstrate that vasopressin levels are elevated briefly following 5-HT i.c.v., consistent with the pharmacologic profile of the early cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)

Amidines↗

PubMed1993

Enhanced gamma-aminobutyric acid-mediated responses in nucleus tractus solitarius of hypertensive rats.

Previous studies demonstrated that stimulation of type B gamma-aminobutyric acid (GABAB) receptors but not type A (GABAA) receptors in the nucleus tractus solitarius of spontaneously hypertensive rats elicited a larger increase in arterial pressure compared with control rats of the Wistar-Kyoto strain. The present studies extended that observation by examining the cardiovascular response to injection into the nucleus tractus solitarius of a selective GABAB receptor antagonist, CGP 35348, in these strains as well as examining the cardiovascular responses to stimulation or blockade of GABAB receptors in the nucleus tractus solitarius in another model of hypertension, the rat treated with deoxycorticosterone acetate and salt. In both groups of hypertensive rats the pressor response to injection into the nucleus tractus solitarius of the GABA uptake blocking drug nipecotic acid was significantly greater compared with control rats (P < .01 in each model). Similarly, in both models of hypertension, the depressor response elicited by blockade of GABAB receptors in the nucleus tractus solitarius by injection of CGP 35348 was approximately 75% greater compared with control rats (P < .05 in each model). These results suggest that alterations in GABAB-mediated neural transmission in the nucleus tractus solitarius may contribute to the elevated arterial pressure observed in these models of hypertension.

4-Aminobutyrate Transaminase↗

PubMed1992

Tonic stimulation of GABAB receptors in the nucleus tractus solitarius modulates the baroreceptor reflex.

Previous studies have indicated that tonic stimulation of GABAB receptors in the nucleus tractus solitarius (NTS) contributes to the regulation of arterial blood pressure (AP). The present studies examined the hypotheses that (1) tonic stimulation of GABAB receptors in the NTS provides a tonic attenuation of the baroreceptor reflex and (2) enhanced stimulation of these GABAB receptors markedly attenuates the baroreceptor reflex resulting in an increase in AP. In chloralose-anesthetized rats electrical stimulation of the aortic depressor nerve elicited frequency-dependent decreases in AP and heart rate (HR). These responses were markedly attenuated, but not eliminated, by injection of the GABAB receptor agonist baclofen into the ipsilateral NTS. In contrast, the GABAA receptor agonist muscimol completely inhibited aortic depressor nerve-evoked responses. Blockade of GABAB receptors in the NTS by local injection of CGP-35348 elicited a dose-dependent decrease in AP, and a dose-dependent blockade of the pressor response elicited by injection of baclofen into the NTS. These results support the hypothesis that GABA acts tonically on GABAB receptors in the NTS to attenuate the baroreceptor reflex, thereby contributing to the regulation of AP.

Animals↗

PubMed1992

Neuroanatomical evidence that vagal afferent nerves do not possess a high affinity uptake system for glutamate.

The ability of vagal and glossopharyngeal afferent neurons to retrogradely transport 3H-D-aspartate from the nucleus tractus solitarius to the nodose and petrosal ganglia was examined. Injections of 3H-D-aspartate centered in the medial NTS at the rostral-caudal level of the area postrema failed to consistently label cells in the nodose and petrosal ganglia. In 5 of the 10 rats studied no retrogradely labeled neurons were observed in these ganglia ipsilateral to the injection site, while in the other 5 rats a small number of cells (less than 3%) were labeled. Injections of 3H-D-aspartate into the NTS consistently produced retrograde labeling of neurons in the ipsilateral paratrigeminal area. In addition, many heavily labeled neurons were observed in the injected as well as the contralateral NTS. Injections of 3H-D-asparate into the spinal trigeminal nucleus consistently labeled neurons in the trigeminal ganglion. Since the uptake and retrograde transport of 3H-D-aspartate appears to be characteristic of neurons that use glutamate or aspartate as a neurotransmitter, these results suggest that vagal and glossopharyngeal afferents are not glutamatergic or aspartatergic.

Afferent Pathways↗

PubMed1992

Gastric motility in conscious rats given oxytocin and an oxytocin antagonist centrally.

Previous experiments have shown that gastric motility is inhibited by microinjection of oxytocin (OT) into the dorsal motor nucleus of the vagus (DMN) in anesthetized rats, and that the inhibition of gastric motility after electrical stimulation of the hypothalamic paraventricular nucleus (PVN) is blocked by microinjection of an OT receptor antagonist directly into the DMN. As an extension of these observations, the present series of studies demonstrate that gastric motility in unanesthetized, freely moving rats was reduced both by intracerebroventricular (i.c.v.) administration of OT and by electrical stimulation of the PVN, and that both of these inhibitory effects were blocked by i.c.v. administration of an OT antagonist. Moreover, an OT antagonist administered i.c.v. alone caused an increase in baseline gastric motility. However, pretreatment with the same OT antagonist i.c.v. did not block the inhibitory effects of systemic LiCl or cholecystokinin on gastric motility in conscious rats. These results suggest that oxytocinergic neurons exert a tonic inhibitory effect on gastric motility in rats, but that the inhibitory effects of LiCl and cholecystokinin on gastric motility are not primarily mediated by parvocellular OT-containing neurons projecting from the PVN to the DMN.

Angiotensin Receptor Antagonists↗

PubMed1992

Stimulation of alpha 2-adrenergic receptors in nucleus tractus solitarius is required for the baroreceptor reflex.

Bilateral injection into the nucleus tractus solitarius (NTS) of the alpha 2-adrenergic receptor antagonist yohimbine produced a dose-related (10-500 pmol) increase in arterial pressure, with a maximal response of approximately 60 mm Hg. Idazoxan, also an alpha 2-adrenergic receptor antagonist, produced a similar response although idazoxan was less potent than yohimbine. The pressor response elicited by these drugs was attenuated by stimulation of adrenergic receptors in the NTS by local administration of either clonidine or tyramine. Doses of yohimbine (200 pmol) or idazoxan (5 nmol) that maximally increased arterial pressure also completely inhibited the depressor and bradycardic responses to electrical stimulation of the aortic depressor nerve. These results indicate that tonic stimulation of alpha 2-adrenergic receptors in the NTS is required for baroreceptor reflex function.

Adrenergic beta-Antagonists↗