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PubMed2006

The corticotropin-releasing factor system as a mediator of the appetite-suppressing effects of stress in fish.

A characteristic feature of the behavioural response to intensely acute or chronic stressors is a reduction in appetite. In fish, as in other vertebrates, the corticotropin-releasing factor (CRF) system plays a key role in coordinating the neuroendocrine, autonomic, and behavioural responses to stress. The following review documents the evidence implicating the CRF system as a mediator of the appetite-suppressing effects of stress in fish. Central injections of CRF or the related peptide, urotensin I (UI), or pharmacological treatments or stressors that result in an increase in forebrain CRF and UI gene expression, can elicit dose-dependent reductions in food intake that are at least partially reversed by pre-treatment with a CRF receptor antagonist. In addition, the appetite suppressing effects of various environmental, pathological, physical, and social stressors are associated with elevated levels of forebrain CRF and UI gene expression and with an activation of the hypothalamic-pituitary-interrenal (HPI) stress axis. In contrast, although stressors can also be associated with an increase in caudal neurosecretory system CRF and UI gene expression and an endocrine role for CRF-related peptides has been suggested, the physiological effects of peripheral CRF-related peptides on the gastrointestinal system and in the regulation of appetite have not been investigated. Overall, while CRF and UI appear to participate in the stress-induced changes in feeding behaviour in fish, the role of other know components of the CRF system is not known. Moreover, the extent to which the anorexigenic effects of CRF-related peptides are mediated through the hypothalamic feeding center, the HPI axis and cortisol, or via actions on descending autonomic pathways remains to be investigated.

Animals↗
PubMed1997

CNS sites involved in sympathetic and parasympathetic control of the pancreas: a viral tracing study.

The viral transneuronal tracing method was used to identify the CNS cell groups that regulate the parasympathetic and sympathetic outflow systems of the pancreas. Pseudorabies virus (PRV) was injected into the pancreas of vagotomized rats and after 6 days survival, the pattern of transneuronal labeling in the CNS sympathetic regulatory regions was determined. The converse experiment was performed in order to elucidate the central parasympathetic cell groups that regulate the pancreas. Immunohistochemical methods were used to identify putative neuropeptide- and catecholamine-containing CNS neurons involved in these regulatory circuits. The major finding of this study indicates that five brain regions, viz., paraventricular hypothalamic nucleus, perifornical hypothalamic region, A5 catecholamine cell group, rostral ventrolateral medulla, and lateral paragigantocellular reticular nucleus, contain a considerable amount of overlap in cell body labeling. In addition, the ventrolateral part of the periaqueductal gray matter and gigantocellular reticular nucleus, ventral part also showed a similar overlap, but the numbers of neurons found in these areas were considerably lower than the five major regions. These data suggest that these brain regions may provide parallel and possibly redundant, autonomic pathways affecting glucagon and adrenaline release.

Adrenal Medulla↗
PubMed1998

Attenuation of Fos expression to airpuff startle stimuli following tympanic membrane rupture.

The airpuff startle stimulus consists of two modalities, tactile and acoustic. Tympanic membrane rupture (TMR) effectively deafens a rat, thus preventing it from perceiving the acoustic component of the airpuff and permitting study of the tactile component in isolation. Previous studies have shown that the tactile modality is sufficient to drive the cardiovascular response to the airpuff, but cannot elicit the full behavioral startle response. In the present study Fos protein was used as a marker of neuronal activation to identify brain regions activated by the airpuff in both intact and TMR rats. Results show an attenuation of Fos expression following TMR in the dorsal and ventral cochlear nuclei, ventral nucleus of the lateral lemniscus and medial geniculate nucleus. In contrast, Fos expression following TMR was unchanged in the locus coeruleus, the laterodorsal tegmental nucleus, the supramammilary nucleus, and the ventromedial hypothalamic nucleus. Analysis of behavioral data confirmed that the startle response to the airpuff was diminished following TMR. These data are the first of which we know to employ an immediate early gene approach to discriminate between brain regions activated by the tactile and acoustic startle stimulus modalities. The results are discussed in terms of the classical acoustic startle circuit, and the central autonomic pathways activated by the tactile component of the airpuff.

Acoustic Stimulation↗
PubMed1998

Inositides in the nucleus: taking stock of PLC beta 1.

The nucleus was shown to be a site for inositol lipid cycle which can be affected by treatment of quiescent cells with growth factors such as IGF-I. In fact, the exposure of Swiss 3T3 cells to IGF-I results in a rapid and transient increase in nuclear PLC beta 1 activity. In addition, several other reports have shown the involvement of PLC beta 1 in nuclear signalling in different cell types. Indeed, PLC beta 1 differs from the PLC gamma and della isozymes in that it has a long COOH-terminal sequence which contains a cluster of lysine residues that are critical for association with the nucleus. Although the demonstration of PtInsP and PtdInsP2 hydrolysis by nuclear PLC beta 1 established the existence of nuclear PLC signalling, the significance of this autonomous pathway in the nucleus has yet to be thoroughly clarified. By inducing both the inhibition of PLC beta 1 expression by antisense RNA and its overexpression we show that this nuclear PLC is essential for the onset of DNA synthesis following IGF-I stimulation of quiescent Swiss 3T3 cells. Moreover, using a different cell system, i.e. Friend erythroleukemia cells induced to differentiate towards erythrocytes, it has been evidenced that there is a relationship between the expression and activity of nuclear PLC beta 1 and the association of PI-PT alpha with the nucleus in that, when PLC activity ceases, in differentiated and resting cells at the same time there is a dramatic decrease of the association of PI-PT alpha with the nucleus.

3T3 Cells↗
PubMed1997

Localization of NADPH diaphorase in the thoracolumbar and sacrococcygeal spinal cord of the dog.

The distribution of NADPH-d activity and NOS-immunoreactivity in the spinal cord of the dog was studied to evaluate the role of nitric oxide in lumbosacral afferent and spinal autonomic pathways. At all levels of the spinal cord examined, NADPH-d staining and NOS-immunoreactivity were present in neurons and fibers in the superficial dorsal horn, dorsal commissure and in neurons around the central canal. Sympathetic preganglionic neurons in the rostral lumbar segments identified by choline acetyl transferase (ChAT) immunoreactivity exhibited prominent NADPH-d and and NOS-immunoreactive staining; whereas the ChAT-immunoreactive parasympathetic preganglionic neurons in the sacral segments were not stained. The most prominent NADPH-d activity in the sacral segments occurred in fibers extending form Lissauer's tract through lamina I along the lateral edge of the dorsal horn to the region of the sacral parasympathetic nucleus. These fibers were prominent in the S1-S3 segments but not in adjacent segments (L5-L7 and Cx1 or in thoracolumbar segments. The NADPH-d fibers were not NOS-immunoreactive, but did overlap with a prominent fiber bundle containing vasoactive intestinal polypeptide immunoreactivity in the sacral spinal cord. These results indicate that nitric oxide may function as a transmitter in thoracolumbar sympathetic preganglionic neurons, but not in sacral parasympathetic preganglionic neurons. The functional significance of the NADPH-d positive, NOS-negative fiber bundle on the lateral edge of the sacral dorsal horn remains to be determined. However, based on anatomical studies in other species it seems reasonable to speculate that the fiber tract represents, in part, visceral afferent projections to the sacral parasympathetic nucleus.

Animals↗
PubMed1998

Autonomic brainstem projections to the pancreas: a retrograde transneuronal viral tracing study in the rat.

The present study describes brainstem nuclei that participate in the autonomic innervation of the pancreas, using a retrograde viral transneuronal tracing technique. It aimed at identifying the neuronal architecture of the parasympathetic, gustatory-induced insulin release by the endocrine pancreas (preabsorptive insulin response, PIR). Autonomic pathways organized for reflex adjustments of the end organ, as it happens in the PIR, involve relatively simple circuits. This implies a short brainstem circuit from the rostral gustatory nucleus of the solitary tract to the dorsal motor nucleus of the vagus. The present findings confirm projections to the pancreas, originating from preganglionic neurons in the dorsal motor nucleus of the vagus. Transneuronal labeling was detected in the medial, and to a lesser extent in the lateral nucleus of the solitary tract mainly at caudal and intermediate levels. Furthermore, infected neurons were seen in the brainstem in the dorsal and ventral part of the medullary reticular formation, in the area postrema and in the raphe nuclei. Sparse labeling was found in the gustatory zone of the nucleus tractus solitarius. These results indicate that a direct connection between the rostral nucleus tractus solitarius and the medial dorsal motor nucleus of the vagus is very unlikely, so that one or more intermediate stations may be involved. Candidates to complete this pathway are the intermediate or caudal nucleus tractus solitarius, the medullary reticular formation or the parabrachial nucleus.

Animals↗
PubMed1998

GABA- and glutamate-immunoreactive synapses on sympathetic preganglionic neurons projecting to the superior cervical ganglion.

Our previous work suggests that virtually all of the synapses on sympathetic preganglionic neurons projecting to the rat adrenal medulla are immunoreactive for either the inhibitory amino acid, gamma-aminobutyric acid (GABA) or the excitatory amino acid, L-glutamate. To investigate whether or not this is true for other groups of sympathetic preganglionic neurons, and to determine whether or not the proportion of inputs containing each type of amino acid neurotransmitter is the same for different groups of sympathetic preganglionic neurons, we retrogradely labelled rat and rabbit sympathetic preganglionic neurons projecting to the superior cervical ganglion and used post-embedding immunogold on ultrathin sections to localise GABA- and glutamate-immunoreactivity. The cell bodies and dendrites of both rat and rabbit sympathetic preganglionic neurons projecting to the superior cervical ganglion received synapses and direct contacts from nerve fibres immunoreactive for GABA and from nerve fibres immunoreactive for glutamate. In the rat, GABA was present in 48.9% of the inputs to sympathetic preganglionic neurons projecting to the superior cervical ganglion, and glutamate was present in 51.7% of inputs. Double immunogold labelling for glutamate and GABA on the same section, as well as labelling of consecutive serial sections for the two antigens, indicated that GABA and glutamate occur in separate populations of nerve fibres that provide input to rat sympathetic preganglionic neurons projecting to the superior cervical ganglion. We now have shown that GABA or glutamate is present in virtually all of the inputs to sympathetic preganglionic neurons projecting to the superior cervical ganglion and in essentially all of the inputs to sympathetic preganglionic neurons supplying the adrenal medulla. These findings are consistent with the hypothesis that all fast synaptic transmission in central autonomic pathways may be mediated by either excitatory or inhibitory amino acids. Furthermore, we showed a statistically significant difference in the proportion of glutamate-immunoreactive inputs between sympathetic preganglionic neurons projecting to the superior cervical ganglion and sympathoadrenal neurons (data from Llewellyn-Smith et al. [Llewellyn-Smith, I.J., Phend, K.D., Minson, J.B., Pilowsky, P.M., Chalmers, J.P., 1992. Glutamate immunoreactive synapses on retrogradely labelled sympathetic neurons in rat thoracic spinal cord. Brain Res. 581, 67-80]), with preganglionics supplying the adrenal medulla receiving more excitatory inputs than those supplying the superior cervical ganglion. This increased excitatory input to sympathoadrenal neurons may explain the predominant activation of these neurons following baroreceptor unloading.

Animals↗
PubMed2000

Bombesin and the brain-gut axis.

Bombesin is the first peptide shown to act in the brain to influence gastric function and the most potent peptide to inhibit acid secretion when injected into the cerebrospinal fluid (CSF) in rats and dogs. Bombesin responsive sites include specific hypothalamic nuclei (paraventricular nucleus, preoptic area and anterior hypothalamus), the dorsal vagal complex as well as spinal sites at T9-T10. The antisecretory effect of central bombesin encompasses a variety of endocrine/paracrine (gastrin, histamine) or neuronal stimulants. Bombesin into the CSF induces an integrated gastric response (increase in bicarbonate, and mucus, inhibition of acid, pepsin, vagally mediated contractions) enhancing the resistance of the mucosa to injury through autonomic pathways. The physiological significance of central action of bombesin on gastric function is still to be unraveled.

Animals↗
PubMed2003

Dispatch. Intercellular signaling: an elusive player steps forth.

Plasmodesmata play a central role in cell-to-cell communication in plants, allowing transport of regulatory proteins and mRNAs. A recent study has identified a specific protein that regulates the intercellular transport of macromolecules in plants, known as non-cell autonomous pathway protein 1.

Gene Expression Regulation↗
PubMed2003

Anorectic brainstem peptides: more pieces to the puzzle.

Eating a meal is a mechanical process involving autonomous pathways that relay sensory and motor information between the whole length of the digestive tract and the central nervous system. This circuitry is able to initiate and terminate the meal, primarily by gut-brainstem-gut reflex arcs, and is independent of the caloric content of a meal. However, as part of our ability to regulate body weight over time, we must be able to modulate the amount of energy that we take in as food and the amount of energy that we expend. Thus, the gut-brainstem axis must be coupled to other systems that take account of factors such as food availability and preference, changing energy requirements and our social habits. Here, we review the importance of the brainstem nucleus of the tractus solitarius as a site of integration and the routes by which it connects the gut-brainstem axis with regulatory neuronal and endocrine networks that allow for strict body weight management.

Animals↗
PubMed2000

Relationship between birth weight and body composition, energy metabolism, and sympathetic nervous system activity later in life.

OBJECTIVE: Epidemiological studies suggest that high birth weight might be associated with an increased risk of obesity later in life. Programming of metabolic, endocrine, and/or autonomic pathways during intrauterine development has been proposed to explain this association. RESEARCH METHODS AND PROCEDURES: To determine the relationship between birth weight and body composition and energy metabolism later in life, we measured fat mass and fat-free mass (hydrodensitometry or double-energy X-ray absorptiometry), 24-hour energy expenditure, sleeping metabolic rate, and 24-hour respiratory quotient (respiratory chamber) in 272 adult nondiabetic Pima Indians (161 males/ 111 females, age 25 +/- 5 years, mean +/- SD). In these subjects, birth weight varied over a wide range (2,000 to 5,000 g). Individuals known to be offspring of diabetic pregnancies were excluded. In 44 of the 272 subjects, muscle sympathetic nerve activity was assessed by microneurography. RESULTS: Birth weight was positively correlated with adult height (r = 0.20, p < 0.001) and fat-free mass (r = 0.21, p < 0.001), but not with fat mass (r = 0.01, not significant). Sleeping metabolic rate, adjusted for age, sex, fat-free mass, and fat mass, was negatively related to birth weight (r = -0.13, p < 0.05), whereas adjusted 24-hour energy expenditure (r = 0.07, not significant) and 24-hour respiratory quotient (r = -0.09, not significant) were not. There was no relationship between birth weight and muscle sympathetic nerve activity (r = 0.12, not significant, n = 44). DISCUSSION: In Pima Indians who are not offspring of diabetic pregnancies, high birth weight is associated with increased height and lean body mass, but not with increased adiposity later in life. Although high birth weight may be associated with relatively low resting energy expenditure, it is not associated with major abnormalities in 24-hour energy metabolism or with low muscle sympathetic nerve activity later in life.

Absorptiometry, Photon↗
PubMed2004

Neuropathology: the foundation for new treatments in spinal cord injury.

The first step essential in the search for a cure of human spinal cord injury (SCI) is to appreciate the complexity of the disorder. In this regard, it is not only the loss of ambulation but the sensory and autonomic changes that are equally important in recovery. In addition, there are the serious social emotional psychological and lifestyle effects of SCI which should also be taken into account. It is also true that no two SCI lesions are alike as each is the result of a SCI unique to that individual. Clinically of utmost importance is the segmental level of injury and whether it is complete, incomplete or discomplete (loss of all neurological functions below the injury but with physiological or anatomical continuity of Central nervous system tracts across the lesion). We are not concerned here with primary and secondary prevention or methods designed to limit the severity of the lesion after the event, important as they are, but with the requirements for a cure. Clearly, the greater the number of nerve fibers that can be preserved in the acute stage, the better will be the end result. Our focus at present is on the end-stage lesion with the aim of showing that a cure for SCI will depend upon establishing functionally useful central axonal regeneration and reestablishing physiological reconnections. Existing experimental methods are based on stimulating axonal regeneration by neutralizing inhibitory factors, adding positive trophisms and creating a permissive environment. Better results are obtained by bridging the gap with grafts of peripheral nerves or transplants of Schwann cells and genetically engineered fibroblasts. Recently, the potential for stem cells to enhance this process has created great interest. This is because of the ability of pluripotential cells to differentiate into neural tissue. A cure based on the physiopathology of SCI requires pyramidal, extrapyramidal, sensory, cerebellar and autonomic pathways to be regenerated with their appropriate neurotransmitters restored and reflexes integrated physiologically and in synchrony. In human SCI, there is a very long distance anatomically for axonal regrowth to occur in order to reach their relevant nuclei. This is because of continuing Wallerian degeneration. It also presumes that the target neurons are intact and that there has been no transneuronal degeneration above or below the lesion. Alternatively, in place of regenerated long axons, a multisynaptic pathway may be constructed from stem cells that have developed into neurons. Whether such a pathway would restore useful neurological functions is unknown. At present, the transplant and grafting research teams are exploring these possibilities in experimental animals. Moderate success in gaining axonal regeneration has been reported; however, it must be appreciated that the human lesion differs considerably from that of the experimental animal. In order to be successful, the neuropathology and neurophysiology of human SCI must be taken into account. The purpose of this review is to place the requirements for a cure, using stem cells, within the context of the neuropathology of human SCI.

Animals↗
PubMed2003

Central administration of neuropeptide FF causes activation of oxytocin paraventricular hypothalamic neurones that project to the brainstem.

Neuropeptide FF (NPFF), a morphine modulatory peptide, is emerging as an important neuromodulator in the context of central autonomic and neuroendocrine regulation. NPFF immunoreactivity and receptors have been identified in discrete autonomic regions within the brain and spinal cord, including the hypothalamic paraventricular nucleus (PVN). In this study, we examined the effects of intracerebroventricular (i.c.v.) administration of NPFF on activation of chemically identified PVN neurones that project to the brainstem nucleus of the solitary tract (NTS). In conscious rats, i.c.v. NPFF at a dose of 10 micro g, but not 8 micro g, caused an increase in arterial blood pressure. Immunohistochemical analysis revealed a dose-dependent increase in activated (Fos positive) PVN neurones following i.c.v. NPFF administration compared to controls receiving i.c.v. saline. Activated PVN neurones were located predominantly in the parvocellular compartment of the nucleus with relatively few Fos positive cells in the magnocellular subdivision. Chemical identification of activated neurones revealed significant number of activated cells to be oxytocin positive, whereas only few vasopressin, tyrosine hydroxylase (TH) or corticotrophin-releasing factor (CRF) neurones were double-labelled. Injection of the retrograde tracer fluorogold into the NTS resulted in labelling of significant numbers of parvocellular oxytocin, but not vasopressin, TH or CRF, PVN neurones. We conclude that centrally administered NPFF stimulates brainstem-projecting oxytocin PVN neurones. Oxytocin released from terminals within the NTS oxytocin thus modulate the activity of ascending visceral autonomic pathways that synapse initially within the NTS.

Animals↗
PubMed2003

AGL24 acts as a promoter of flowering in Arabidopsis and is positively regulated by vernalization.

MADS-domain-containing transcription factors comprise a large family of regulators that have diverse roles in plant development, including the regulation of flowering time. AGAMOUS-LIKE 20/SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1) and FRUITFUL act to promote flowering, whereas FLOWERING LOCUS C (FLC), FLOWERING LOCUS M/MADS AFFECTING FLOWERING1, and SHORT VEGETATIVE PHASE are inhibitors of flowering. Here we report that AGAMOUS-LIKE 24 (AGL24) also plays a role in the regulation of flowering time. agl24 mutants are late flowering and overexpression of AGL24 causes early flowering in wild-type and late-flowering-mutant backgrounds. The effect of AGL24 overexpression is most pronounced in autonomous-pathway-mutant and FRIGIDA-containing backgrounds. The behavior of AGL24 is most similar to that of SOC1. Like SOC1, AGL24 mRNA levels are upregulated by vernalization. Unlike SOC1, however, AGL24 mRNA levels are not affected by FLC, and therefore AGL24 may represent an FLC-independent target of the vernalization pathway. There is also evidence for cross-talk between AGL24 and SOC1. When overexpressed, SOC1 and AGL24 are able to upregulate each other's expression. Thus, AGL24 represents another component in a network of MADS-domain-containing transcription factors that regulate flowering time.

Arabidopsis↗
PubMed2004

Salicylic acid regulates flowering time and links defence responses and reproductive development.

Flowering relies on signaling networks that integrate endogenous and external cues. Normally, plants flower at a particular season, reflecting day length and/or temperature cues. However, plants can surpass this seasonal regulation and show precocious flowering under stress environmental conditions. Here, we show that UV-C light stress activates the transition to flowering in Arabidopsis thaliana through salicylic acid (SA). Moreover, SA also regulates flowering time in non-stressed plants, as SA-deficient plants are late flowering. The regulation of flowering time by SA seems to involve the photoperiod and autonomous pathways, but it does not require the function of the flowering time genes CONSTANS (CO), FCA, or FLOWERING LOCUS C (FLC).

Arabidopsis↗
PubMed2001

Effect of endogenous catecholamine on myocardial stunning in a simulated ischemia model.

During ischemia, large amounts of catecholamine are released to the myocardium from the sympathetic nerve endings in the heart. It has not been clearly shown whether the released catecholamine has detrimental or beneficial effects on postischemic myocardial contractile function. The aim of the present study was to investigate the effect of endogenous catecholamine released during ischemia on myocardial contractile function, using ferret papillary muscles in a stimulated ischemia model. Papillary muscles were excised and mounted in organ baths containing oxygenated physiological salt solution at 37 degrees C. In order to eliminate the effect of endogenous catecholamine, a subset of animals was reserpinized for 2 days prior to the experiments. Muscles were stabilized for 1 h, and stretched to the length at which maximal isometric tension developed. Ischemia was simulated by changing the solution to liquid fluorocarbon bubbled with 95% N2 and 5% CO2. After 20 min of ischemia, the bathing medium was replaced with oxygenated physiological salt solution and developed tension was measured for 60 min. Pharmacologic agents with specific effects on myocardial autonomic pathways were used to investigate the cellular mechanisms of the observed effects. Tension recovery of reserpinized muscles was significantly better than control muscles (65.5 +/- 2.8% vs. 54.9 +/- 5.0%, P < 0.01). Exogenously administered beta-adrenergic antagonists did not attenuate stunning in control muscles; whereas forskolin and carbachol exacerbated stunning. These results indicate that catecholamine released during ischemia exacerbates myocardial stunning and overrides the effect of clinically relevant concentrations of beta-adrenergic antagonists, which may limit their ability to protect myocardium from acute ischemic insult. The effect of endogenous catecholamine was simulated by forskolin, but not attenuated by carbachol, which suggests that changes in the contractile apparatus activated by excess cyclic AMP were relevant to the mechanical dysfunction that developed.

Adrenergic Uptake Inhibitors↗
PubMed1989

Marked blood pressure fluctuations during narcoleptic attacks alternating with abnormal wakefulness: effects of treatment with clonidine.

A middle-aged man was admitted to our department because of sleep-wake cycle disorders (alternating hypersomnia and sleeplessness), bipolar behavioural disturbances and marked fluctuations in blood pressure and heart rate. Neither evident precipitating stimuli nor an obvious cause for his illness were found. When tests that normally activate intrinsic autonomic responses were performed, two distinct circulatory patterns were recognized. During hypersomnia (phase A), cardiovascular reflex activity was blunted or abolished and orthostasis could not be maintained. The clinical, biochemical, behavioural pictures and the observed decrease in sympathetic outflow resembled the effects of clonidine administration. On the contrary, during sleeplessness (phase B) the autonomic pathways were functionally integral and orthostatic hypotension was not detected. The clinical, biochemical, behavioural features and cardiovascular overactivity closely mimicked the abrupt withdrawal syndrome encountered with clonidine. Three hypothetical mechanisms are advanced to explain this intriguing case as well as the acute and chronic relief of our patient's clinical problem following institution of clonidine therapy (phase C). The role played by central alpha adrenoceptors in integrating sleep-wake, cardiovascular and behavioural functions is also suggested.

Blood Pressure↗
PubMedDate not supplied

Effects of intracisternal and intravenous alpha-methyldopa and clonidine on haemodynamics and baroreceptor--heart rate reflex properties in conscious rabbits.

We determined the doses of intracisternal (i.c.) and intravenous (i.v.) clonidine and alpha-methyldopa (alpha-MD) that produced near-maximal falls in mean arterial pressure (MAP) in conscious rabbits. We then studied the haemodynamic mechanisms underlying the fall in MAP and changes in the properties of the baroreceptor-heart rate reflex. Intracisternal and intravenous administration of both drugs lowered MAP by approximately 25% of control, and the fall was about half due to the reduction in cardiac output and about half due to a fall in total peripheral resistance. Baroreceptor-heart rate reflex properties were studied by transiently inflating perivascular balloons to alter blood pressure and by deriving sigmoid curves relating MAP to heart period (HP, pulse interval). Both drugs produced very similar vagal facilitation during transient rises in MAP when given by the i.c. and i.v. routes; HP range (between upper and lower plateaus) increased to 145% of control, and gain rose to 190%. The effects of i.c. administration of both drugs on the cardiac sympathetic component of the baroreflex were studied in methscopolamine-treated rabbits. Clonidine produced more pronounced suppression of HP range and gain, while alpha-MD had little effect. These differences between drugs were still present with much larger i.c. doses. Our findings suggest that both drugs influence resting haemodynamics and the vagal component of the baroreflex through similar effects on the central autonomic pathways. But there are some differences in their central actions on cardiac sympathetic motoneurons.

Animals↗