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.

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 hypocretin-1 in nucleus of the solitary tract

2003 ◽  
Vol 284 (4) ◽  
pp. H1369-H1377 ◽  
Author(s):  
Cleusa V. R. de Oliveira ◽  
M. Patricia Rosas-Arellano ◽  
L. Pastor Solano-Flores ◽  
John Ciriello
Keyword(s):  
Cardiovascular Effects ◽  
Receptor Blocker ◽  
Vagal Activity ◽  
Solitary Tract ◽  
Neuronal Circuits ◽  
Reflex Bradycardia ◽  
Male Wistar Rats ◽  
Dose Dependent Decrease ◽  
Dose Dependent ◽  
Hypocretin 1

Experiments were done in male Wistar rats to investigate the effects of microinjection of hypocretin-1 (Hcrt-1) into the nucleus of the solitary tract (NTS) on mean arterial pressure (MAP), heart rate (HR), and the baroreflex. In the first series, the distribution of Hcrt-1-like immunoreactivity (Ir) was mapped within the region of NTS. Hcrt-1 Ir was found throughout the NTS region, predominantly within the caudal dorsolateral (Slt), medial (Sm), and interstitial subnuclei of the NTS. In the second series, in α-chloralose or urethane-anesthetized rats, microinjection of Hcrt-1 (0.5–5 pmol) into the caudal NTS elicited a dose-dependent decrease in MAP and HR. A mapping of the caudal NTS region showed that the largest depressor and bradycardia responses elicited by Hcrt-1 were from sites in the Slt and Sm. In addition, doses >2.5 pmol at a small number of sites localized to the caudal commissural nucleus of NTS elicited pressor and tachycardia responses. Intravenous administration of the muscarinic receptor blocker atropine methyl bromide abolished the bradycardia response and attenuated the depressor response, whereas subsequent administration of the nicotinic receptor blocker hexamethonium bromide abolished the remaining MAP response. Finally, microinjection of Hcrt-1 into the NTS significantly potentiated the reflex bradycardia to activation of arterial baroreceptors as a result of increasing MAP by systemic injections of phenylephrine (2–4 μg/kg). These results suggest that Hcrt-1 in the NTS activates neuronal circuits that increases vagal activity to the heart, inhibits sympathetic activity to the heart and vasculature, and alters the excitability of NTS neuronal circuits that reflexly control the circulation.

The Effects of Branchial Denervation and Pseudobranch Ablation on Cardioventilatory Control in an Air-Breathing Fish

1991 ◽  
Vol 161 (1) ◽  
pp. 347-365 ◽  
Author(s):  
DAVID J. McKENZIE ◽  
MARK L. BURLESON ◽  
DAVID J. RANDALL
Keyword(s):  
Cardiovascular Responses ◽  
Sodium Cyanide ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
Reflex Bradycardia ◽  
Afferent Information ◽  
Gill Ventilation ◽  
Air Ventilation ◽  
Amia Calva

Present address and address for reprint requests: Istituto di Scienze Farmacologiche, via Balzaretti 9, Università di Milano, Milano 20133, Italy. The role of sensory afferent information from the gills of Amia calva in cardiovascular and ventilatory control was investigated by bilateral branchial denervation and pseudobranch ablation. Aquatic hypoxia or 1 mg of sodium cyanide (NaCN) in the water flowing over the gills stimulated bradycardia, and gill and air ventilation in sham-operated fish. Sodium cyanide, noradrenaline (NA) and adrenaline (A) infusion into the dorsal aorta increased gill ventilation, and NA and A infusion also stimulated tachycardia and an increase in blood pressure. Following denervation and pseudobranch ablation, O2 consumption (V·OO2), airbreathing frequency (fAB) and arterial O2 tension (PaOO2) declined, and circulating NA levels increased, as compared with sham-operated fish. Cardiovascular and air-breathing responses to hypoxia were abolished and gill ventilatory responses attenuated. All ventilatory and cardiovascular responses to NaCN were abolished and gill ventilatory responses to NA and A were attenuated in animals following denervation and pseudobranch ablation. These results demonstrate that O2-sensitive chemoreceptors in the gills and pseudobranch control reflex bradycardia and air-breathing responses in Amia, but that gill ventilatory responses to hypoxia, NA and A are partially mediated by extrabranchial mechanisms. Plasma NA levels increased during hypoxia in shamoperated and denervated animals, indicating that circulating NA may have mediated gill ventilatory responses in denervated animals.

Hemodynamic effects of low-dose atipamezole in isoflurane-anesthetized cats receiving an infusion of dexmedetomidine

2017 ◽  
Vol 20 (6) ◽  
pp. 571-577 ◽  
Author(s):  
Manuel Martin-Flores ◽  
Daniel M Sakai ◽  
Juhana Honkavaara ◽  
Luis Campoy
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Low Dose ◽  
Healthy Adult ◽  
Cardiovascular Effects ◽  
Low Doses ◽  
Arterial Blood ◽  
Target Plasma ◽  
Target Plasma Concentration ◽  
Baseline Values

Objectives The objective of this study was to evaluate the cardiovascular effects of low-dose atipamezole administered intravenously to isoflurane-anesthetized cats receiving dexmedetomidine. We hypothesized that atipamezole would increase heart rate (HR) and reduce arterial blood pressure in isoflurane-anesthetized cats receiving dexmedetomidine. Methods Six healthy adult domestic shorthair cats were anesthetized with isoflurane and instrumented for direct arterial pressures and cardiac output (CO) measurements. The cats received a target-controlled infusion of dexmedetomidine (target plasma concentration 10 ng/ml) for 30 mins before administration of atipamezole. Two sequential doses of atipamezole (15 and 30 μg/kg IV) were administered at least 20 mins apart, during dexmedetomidine administration. The effects of dexmedetomidine and each dose of atipamezole on HR, mean arterial blood pressure (MAP), CO and systemic vascular resistance (SVR) were documented. Results Dexmedetomidine reduced the HR by 22%, increased MAP by 78% (both P ⩽0.01), decreased CO by 48% and increased SVR by 58% (both P ⩽0.0003). Administration of atipamezole 15 and 30 μg/kg intravenously increased HR by 8% ( P = 0.006) and 4% ( P = 0.1), respectively. MAP decreased by 39% and 47%, respectively (both P ⩽0.004). Atipamezole 30 μg/kg returned CO and SVR to baseline values. Conclusions and relevance Low doses of atipamezole (15 and 30 μg/kg) administered intravenously to anesthetized cats decreased arterial blood pressure with only marginal increases in HR. Atipamezole 30 μg/kg restored CO and SVR to baseline values before dexmedetomidine administration.

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.

scholarly journals The Cardiovascular Effects of Central Hydrogen Sulfide Are Related to KATP Channels Activation

2011 ◽  
pp. 729-738 ◽  
Author(s):  
W.-Q. LIU ◽  
C. CHAI ◽  
X.-Y. LI ◽  
W.-J. YUAN ◽  
W.-Z. WANG ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hydrogen Sulfide ◽  
Katp Channel ◽  
Channel Blocker ◽  
Cardiovascular Effects ◽  
Katp Channels ◽  
Channel Activation ◽  
The Central Nervous System ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Hydrogen sulfide (H2S), an endogenous “gasotransmitter”, exists in the central nervous system. However, the central cardiovascular effects of endogenous H2S are not fully determined. The present study was designed to investigate the central cardiovascular effects and its possible mechanism in anesthetized rats. Intracerebroventricular (icv) injection of NaHS (0.17~17 μg) produced a significant and dose-dependent decrease in blood pressure (BP) and heart rate (HR) (P<0.05) compared to control. The higher dose of NaHS (17 μg, n=6) decreased BP and HR quickly of rats and 2 of them died of respiratory paralyse. Icv injection of the cystathionine beta-synthetase (CBS) activator s-adenosyl-L-methionine (SAM, 26 μg) also produced a significant hypotension and bradycardia, which were similar to the results of icv injection of NaHS. Furthermore, the hypotension and bradycardia induced by icv NaHS were effectively attenuated by pretreatment with the KATP channel blocker glibenclamide but not with the CBS inhibitor hydroxylamine. The present study suggests that icv injection of NaHS produces hypotension and bradycardia, which is dependent on the KATP channel activation.

scholarly journals Low Doses of Imidacloprid Induce Oxidative Stress and Neural Cell Disruption in Earthworm Eisenia fetida

2021 ◽  
Vol 84 ◽  
pp. 1-11
Author(s):  
Artem Huslystyi ◽  
Victor Nedzvetsky ◽  
Serhii Yermolenko ◽  
Viktor Gasso ◽  
Vladyslav Petrushevskyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Neuron Specific Enolase ◽  
Stress Generation ◽  
Low Doses ◽  
Neuronal Marker ◽  
Dose Dependent Decrease ◽  
Species Production ◽  
Dose Dependent

Imidacloprid is a widely used pesticide that belongs to the class of neonicotinoids. There is a piece of rising evidence that neonicotinoids exert cytotoxic effects in non-target organisms including vertebrate species such as mammals. Nevertheless, dose-limiting toxicity and molecular mechanisms of neonicotinoids' deleterious effects are still poorly understood. In accord to imidacloprid fate in the environment, the most of used pesticide is absorbed in the soil. Therefore, earthworms, which are prevailing soil organisms, could be considered as a target of neonicotinoids toxicity. The earthworm’s simple nervous system is a prospective model for neurotoxicological studies. We exposed earthworms to imidacloprid in a paper contact test with a doses range of 0.1‑0.4 µg/cm2 for 14 days. In the present work, we studied the imidacloprid effect on oxidative stress generation and neuronal marker neuron-specific enolase (NSE) expression. The exposure to imidacloprid induced a dose-dependent decrease in NSE. Both reactive oxygen species production and lipid peroxidation level were upregulated as well. Observed NSE decline suggests imidacloprid-caused disturbance in earthworm neuron cells. Obtained data have shown that relatively low doses of imidacloprid are potent to induce cytotoxicity in neurons. Furthermore, neurotoxicity could be recognized as one of an individual scenario of the general imidacloprid toxicity. Thus, presented results suggest the cytotoxicity of imidacloprid low doses in non-target organisms and hypothesize that NSE downregulation could be estimated as a biomarker of neonicotinoid cytotoxicity in a nervous system of non-insect species.

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.

Enhanced pressor responses to ICV vasopressin after pretreatment with oxytocin

1994 ◽  
Vol 266 (2) ◽  
pp. R592-R598 ◽  
Author(s):  
P. Poulin ◽  
A. Komulainen ◽  
Y. Takahashi ◽  
Q. J. Pittman
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Effects ◽  
Intracerebroventricular Injection ◽  
Central Administration ◽  
Cardiovascular Actions ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Dose Dependent ◽  
Higher Doses

The role of oxytocin (OT) in the modulation of arginine vasopressin (AVP)-induced cardiovascular effects within the central nervous system was investigated in urethan-anesthetized rats. Intracerebroventricular injection of AVP (1-10 pmol) produced dose-dependent increases in mean arterial pressure (MAP) and heart rate (HR). These responses were enhanced in rats pretreated 24 h earlier with OT (10 pmol icv). The enhanced cardiovascular effects of AVP in OT-pretreated animals were dose dependent, blocked by the V1 antagonist d(CH2)5Tyr(Me)AVP, not evoked by OT alone, and occurred in the absence of changes in basal (nonstimulated) MAP and HR. In addition, central administration of AVP in OT-pretreated rats, but not in saline-pretreated controls, caused dose-dependent oscillations of the MAP and HR responses and, at higher doses, death of the animals. The enhanced cardiovascular actions of centrally injected AVP in OT-pretreated rats do not appear to be secondary to skeletal muscle contractions or the result of cerebral ischemia. Our data point to an interaction between the central oxytocinergic and vasopressinergic systems in cardiovascular control.

Abated cardiovascular responses to chronic oral lisinopril treatment in conscious elderly rats

1999 ◽  
Vol 276 (5) ◽  
pp. R1408-R1415 ◽  
Author(s):  
Ruben Buñag ◽  
Jennifer Mellick ◽  
Brandy Allen
Keyword(s):  
Baroreflex Sensitivity ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Male Rats ◽  
Adrenergic Blockade ◽  
Reflex Bradycardia ◽  
Age Related ◽  
Pressor Responses ◽  
Mean Pressure ◽  
Old Rats

To determine whether the cardiovascular effects of chronic treatment with lisinopril are age related, we compared baroreflex sensitivity and pressor responsiveness in 4-mo- and 21-mo-old male rats that had been given oral lisinopril daily for 4 wk. Reflex bradycardia elicited by elevating blood pressure with phenylephrine was stronger in 4-mo-old rats than it was in 21-mo-old rats and also stronger in lisinopril-treated rats than it was in untreated rats of the same age. Pressor responses to angiotensin or norepinephrine were recorded after combined cholinergic and β-adrenergic blockade and then analyzed not only as absolute but also as percent increases in mean pressure. Although pressor responses seemed to be slightly reduced by lisinopril when expressed as absolute increases in mean pressure, corresponding percent increases were always larger in 4-mo-old rats than they were in 21-mo-old rats and were clearly enhanced by lisinopril more in younger rats. The stronger overall enhancement of pressor responsiveness and reflex bradycardia in younger rats suggests that the cardiovascular effects of lisinopril diminish with advancing age.

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