Cardiovascular activation by serotonergic stimulation: role of corticotropin-releasing factor

1994 ◽  
Vol 267 (3) ◽  
pp. R859-R864 ◽  
Author(s):  
A. Dedeoglu ◽  
L. A. Fisher
Keyword(s):  
Receptor Agonist ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Corticotropin Releasing Factor ◽  
High Dose ◽  
Low Doses ◽  
Intracerebroventricular Administration ◽  
Central Administration ◽  
Pituitary Adrenal Axis

Serotonin (5-HT) and serotonergic agonists stimulate the release of corticotropin-releasing factor (CRF) from hypophysiotropic neurons and thereby activate the pituitary-adrenal axis. Studies were performed to test the hypothesis that the release of CRF into central nervous system (CNS) sites where it influences cardiovascular function is likewise stimulated by serotonergic mechanisms. Experiments were thus designed to examine whether the cardiovascular effects of central administration of low doses of 5-HT and the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), are secondary to the release of CRF. Intracerebroventricular administration of 5-HT (1 nmol) and 8-OH-DPAT (3 nmol) produced cardiovascular responses similar to those evoked by CRF (0.15 nmol), i.e., simultaneous elevations of arterial pressure and heart rate, in conscious unrestrained rats. Coadministration of the CRF receptor antagonist, alpha-helical CRF-(9-41) (9 nmol), significantly attenuated the pressor and tachycardic responses to 5-HT and 8-OH-DPAT as well as those to injection of CRF. In contrast, coadministration of alpha-helical CRF-(9-41) did not alter the pressor and bradycardic responses to a high dose (100 nmol) of serotonin. It is concluded that the cardiovascular effects of low doses of 5-HT and 8-OH-DPAT are mediated in part through the release of CRF within the CNS.

Cardiovascular effects of microinjection of low doses of serotonin into the NTS of unanesthetized rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1135-R1142 ◽  
Author(s):  
J. C. Callera ◽  
L. G. Bonagamba ◽  
C. Sevoz ◽  
R. Laguzzi ◽  
B. H. Machado
Keyword(s):  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Cardiovascular Reflexes ◽  
Low Doses ◽  
Reflex Bradycardia ◽  
Baseline Values ◽  
Dose Dependent Decrease ◽  
Baroreceptor Activation ◽  
Dose Dependent

In the present study, we analyzed in conscious rats the effects of microinjections of serotonin (5-HT; pmol range) into the nucleus of the solitary tract (NTS) on basal mean arterial pressure (MAP) and heart rate (HR) and also on the reflex bradycardia induced by the activation of the baro- and chemoreflex evaluated 1 min after 5-HT microinjection into the NTS. The data show that unilateral microinjection of 5-HT in the picomolar range into the NTS of unanesthetized rats produced a dose-dependent decrease in MAP and HR, which was blocked by previous microinjection of ketanserin (250 pmol/50 nl) into the NTS. The changes in MAP and HR induced by 5-HT were of very short duration, with a return to baseline values a few seconds later. The cardiovascular responses to baro- or chemoreflex activation 1 min after 5-HT microinjection into the NTS did not differ from the control, indicating that low doses of 5-HT produced no effect on the cardiovascular reflexes tested at that time. The present data show that, as also observed in anesthetized rats, the microinjection of picomolar doses of 5-HT into the NTS elicits the typical cardiovascular responses to baroreceptor activation. These effects, hypotension and bradycardia, seem to be mediated by 5-HT2 receptors because both were blocked by a selective 5-HT2 receptor antagonist. However, since microinjection of 5-HT (1 pmol) into the NTS produced no changes in the cardiovascular responses to the baro- and chemoreflex activated 1 min later, the role of 5-HT2 receptors in the processing of the cardiovascular afferent messages in the NTS remains to be elucidated.

Hypertension: Role of the Hypothalamic-Pituitary-Adrenal Axis

Physiology ◽  
1987 ◽  
Vol 2 (4) ◽  
pp. 132-135
Author(s):  
BA Scoggins
Keyword(s):  
Blood Pressure ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Factor ◽  
Pressure Regulation ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Central Actions ◽  
Prolonged Stress ◽  
Pituitary Adrenal Axis

Blood pressure regulation may be mediated by corticotropin-releasing factor and/or by adrenocorticotropic hormone, by adrenocortical steroids, or by adrenomedullary catecholamines. The interaction between these factors is complex. Catecholamines and central actions of the neuropeptides may be involved in rapid hemodynamic responses to "stress". In contrast, adrenocortical steroids are probably more important in longer-term adaptations of the circulation to prolonged stress.

The Potential Role of a Corticotropin-Releasing Factor Receptor-1 Antagonist in Psychiatric Disorders

CNS Spectrums ◽  
2008 ◽  
Vol 13 (6) ◽  
pp. 467-483 ◽  
Author(s):  
Stephen M. Stahl ◽  
Dana D. Wise
Keyword(s):  
Stress Response ◽  
Psychiatric Disorders ◽  
Stress Responses ◽  
Potential Role ◽  
Corticotropin Releasing Factor ◽  
Recovering Alcoholic ◽  
Mood And Cognition ◽  
Pituitary Adrenal Axis

The hypothalamic-pituitary-adrenal axis is a key mediator of the stress response in humans. The corticotropin-releasing factor (CRF) type 1 receptor (CRFR-1) in the pituitary gland is a gatekeeper for that response, and the CRFR-1 receptor is also present in many other mood- and cognition-related neural structures. Behaviorally, a number of relationships between stress and psychiatric disorders can be observed: chronic or repeated stress is associated with onset of depression; stressors can cause a recovering alcoholic to relapse; overactive stress responses mark many anxiety disorders; and insomnia can arise from an overactive stress response. Thus, a CRFR-1 antagonist could be useful for treating or preventing the consequences of CRF-mediated stress in depression, anxiety, insomnia, and substance abuse.

Cardiovascular responses to exercise in the rat: role of corticotropin-releasing factor

1990 ◽  
Vol 68 (2) ◽  
pp. 561-567 ◽  
Author(s):  
K. C. Kregel ◽  
J. M. Overton ◽  
D. R. Seals ◽  
C. M. Tipton ◽  
L. A. Fisher
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Treadmill Exercise ◽  
Cardiovascular Responses ◽  
Corticotropin Releasing Factor ◽  
Receptor Blockade ◽  
Conscious Rat ◽  
The Central Nervous System ◽  
Mesenteric Vascular Resistance

The effects of intracerebroventricular (icv) administration of a corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical CRF, on systemic and regional hemodynamic adjustments to exercise were studied in conscious rats. On consecutive days, rats received saline icv, alpha-helical CRF icv, and no treatment 30 min before treadmill exercise (TMX). Increases in heart rate (HR) and mean arterial pressure (MAP) in response to TMX (16.1-28.6 m/min) were similar after icv administration of saline or no treatment. In rats receiving saline icv or no treatment, estimated vascular resistance increased in the mesenteric and renal regions and declined in the iliac (hindlimb) region. After icv administration of alpha-helical CRF9-41, HR and MAP responses during TMX were significantly attenuated. In addition, TMX-induced elevations of estimated mesenteric vascular resistance and iliac blood flow velocity were blunted after CRF receptor blockade. These altered cardiovascular and hemodynamic responses were ultimately reflected in the animals' compromised ability to run. The results suggest that the central nervous system actions of endogenous CRF are necessary for the full expression of the cardiovascular adjustments to TMX in the conscious rat.

scholarly journals Cardiovascular Effects of Long-Term Central and Peripheral Administration of Urocortin, Corticotropin-Releasing Factor, and Adrenocorticotropin in Sheep

Endocrinology ◽  
2004 ◽  
Vol 145 (12) ◽  
pp. 5598-5604 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
P. Burns ◽  
D. A. Denton ◽  
B. Purcell ◽  
...  
Keyword(s):  
Stress Response ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Corticotropin Releasing Factor ◽  
Central Administration ◽  
Long Term Effects ◽  
Cardiovascular Actions ◽  
Term Administration

Abstract The neuroendocrine hormones ACTH and corticotropin- releasing factor (CRF), which are involved in the stress response, have acute effects on arterial pressure. New evidence indicates that urocortin (UCN), the putative agonist for the CRF type 2 receptor, has selective cardiovascular actions. The responses to long-term infusions of these hormones, both peripherally and centrally, in conscious animals have not been studied. Knowledge of the long-term effects is important because they may differ considerably from their acute actions, and stress is frequently a chronic stimulus. The present experiments investigated the cardiovascular effects of CRF, UCN, and ACTH in conscious sheep. Infusions were made either into the lateral cerebral ventricles (icv) or iv over 4 d at 5 μg/h. UCN infused icv or iv caused a prolonged increase in heart rate (HR) (P < 0.01) and a small increase in mean arterial pressure (MAP) (P < 0.05). CRF infused icv or iv progressively increased MAP (P < 0.05) but had no effect on HR. Central administration of ACTH had no effect, whereas systemic infusion increased MAP and HR (P < 0.001). In conclusion, long-term administration of these three peptides associated with the stress response had prolonged, selective cardiovascular actions. The striking finding was the large and sustained increase in HR with icv and iv infusions of UCN. These responses are probably mediated by CRF type 2 receptors because they were not reproduced by infusions of CRF.

Cardiovascular effects of treadmill exercise in physiological and pathological preclinical settings

2011 ◽  
Vol 300 (6) ◽  
pp. H1983-H1989 ◽  
Author(s):  
Cinzia Perrino ◽  
Giuseppe Gargiulo ◽  
Gianluigi Pironti ◽  
Anna Franzone ◽  
Laura Scudiero ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Multiple Organ ◽  
Organ Systems ◽  
Physiological Cardiac Hypertrophy ◽  
Models Of Disease ◽  
Acute Changes ◽  
Exercise In Humans

Exercise adaptations result from a coordinated response of multiple organ systems, including cardiovascular, pulmonary, endocrine-metabolic, immunologic, and skeletal muscle. Among these, the cardiovascular system is the most directly affected by exercise, and it is responsible for many of the important acute changes occurring during physical training. In recent years, the development of animal models of pathological or physiological cardiac overload has allowed researchers to precisely analyze the complex cardiovascular responses to stress in genetically altered murine models of human cardiovascular disease. The intensity-controlled treadmill exercise represents a well-characterized model of physiological cardiac hypertrophy because of its ability to mimic the typical responses to exercise in humans. In this review, we describe cardiovascular adaptations to treadmill exercise in mice and the most important parameters that can be used to quantify such modifications. Moreover, we discuss how treadmill exercise can be used to perform physiological testing in mouse models of disease and to enlighten the role of specific signaling pathways on cardiac function.

Cardiovascular effects of cadmium on intravenous and intracerebroventricular administration in rats

1983 ◽  
Vol 61 (11) ◽  
pp. 1430-1432 ◽  
Author(s):  
V. N. Puri ◽  
R. N. Sur
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Cadmium Acetate ◽  
Cardiovascular Responses ◽  
Cadmium Exposure ◽  
Intracerebroventricular Administration

Cardiovascular responses to the intravenous (i.v.) and the intracerebroventricular (i.c.v.) administration of cadmium acetate were evaluated in rats anaesthetized with urethane. Cadmium acetate (1 mg/kg i.v.) caused an initial fall followed by a persistent rise in blood pressure. Cadmium acetate (1 μg i.c.v.) produced a more marked hypertensive effect. In the spinal-transected rat, the effect of intravenous cadmium was reduced but the effect of intraventricularly administered cadmium was completely abolished. It is, therefore, suggested that both central and peripheral mechanisms are involved in the pressor response to cadmium exposure.

Integrated autonomic and behavioral responses to L/N Ca2(+)-channel blocker omega-conotoxin in conscious rats

1990 ◽  
Vol 259 (3) ◽  
pp. R427-R438
Author(s):  
S. Shapira ◽  
O. M. Adeyemo ◽  
G. Feuerstein
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Motor Deficits ◽  
Channel Blockers ◽  
Gamma Aminobutyric Acid ◽  
Central Administration ◽  
Arterial Blood ◽  
Behavioral Variables ◽  
Ca2 Channels

omega-Conotoxin (omega-ctx) was used as a probe for studying the putative role of brain L/N-type Ca2+ channels in regulation of autonomic functions. Rats were injected intracerebroventricularly (icv) with omega-ctx, and hemodynamic, biochemical and behavioral variables were monitored. omega-Ctx (0.032-10 nmol/kg) caused a persistent, dose-dependent shaking behavior, complex thermoregulatory changes, and motor deficits lasting up to 48 h. Cardiovascular responses to omega-ctx included tachycardia (+71 +/- 16%, P less than 0.01) and elevated arterial blood pressure (+16 +/- 1%, P less than 0.05) associated with increased circulating levels of norepinephrine and epinephrine. Higher doses, 1 or 10 nmol/kg, resulted in circulatory shock and death. Central administration of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), diltiazem (100 or 1,000 nmol/kg), neomycin (100 nmol/kg, each), nifedipine (10 nmol/kg), and CdCl2 (100 nmol/kg), which represent intracellular, non-specific N-, L-, and L/N-type Ca2(+)-channel blockers, respectively, did not cause any behavioral or hemodynamic effects, whereas the L-channel agonist BAY K 8644 (100 nmol/kg icv) caused a mild transient pressor response. Pretreatment with the gamma-aminobutyric acid (GABA) agonist muscimol (icv) or a combined intravenous pretreatment with propranolol and N-methylatropine blocked the omega-ctx effects. Our data suggest that omega-ctx actions in the brain involve central GABAergic mechanisms modulated by yet a different type of Ca2+ channels not characterized by any of the known voltage-operated Ca2+ channels.

Cardiovascular responses to hypoxia and hypercapnia in barodenervated rats

1990 ◽  
Vol 68 (2) ◽  
pp. 678-686 ◽  
Author(s):  
B. R. Walker ◽  
B. L. Brizzee
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Conscious Rat ◽  
Hypercapnic Hypoxia ◽  
Intact Rats

Experiments were performed to examine the role of the arterial baroreceptors in the cardiovascular responses to acute hypoxia and hypercapnia in conscious rats chronically instrumented to monitor systemic hemodynamics. One group of rats remained intact, whereas a second group was barodenervated. Both groups of rats retained arterial chemoreceptive function as demonstrated by augmented ventilation in response to hypoxia. The cardiovascular effects to varying inspired levels of O2 and CO2 were examined and compared between intact and barodenervated rats. No differences between groups were noted in response to mild hypercapnia (5% CO2); however, the bradycardia and reduction in cardiac output observed in intact rats breathing 10% CO2 were eliminated by barodenervation. In addition, hypocapnic hypoxia caused a marked fall in blood pressure and total peripheral resistance (TPR) in barodenervated rats compared with controls. Similar differences in TPR were observed between the groups in response to isocapnic and hypercapnic hypoxia as well. It is concluded that the arterial baroreflex is an important component of the overall cardiovascular responses to both hypercapnic and hypoxic stimuli in the conscious rat.

Sign in / Sign up

Export Citation Format

Share Document