Neuronal and cardiovascular responses to ANF microinjected into nucleus ambiguous

1991 ◽  
Vol 260 (6) ◽  
pp. R1089-R1094 ◽  
Author(s):  
R. Ermirio ◽  
P. Ruggeri ◽  
C. E. Cogo ◽  
C. Molinari ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Factor ◽  
Cardiovascular Responses ◽  
Atropine Sulfate ◽  
The Other ◽  
Neuronal Activation ◽  
Muscle Paralysis ◽  
Before And After ◽  
Cardiac Slowing ◽  
Bilateral Vagotomy

Effects of microinjection of atrial natriuretic factor (ANF) into cardioinhibitory sites in the nucleus ambiguous (NA) or on single vagal cardioinhibitory neurons (VCN) were investigated in urethan-anesthetized rats. Sites containing cardioinhibitory neurons were identified by observing a marked and reproducible bradycardia in response to microiontophoretically applied (20-40 nA) or microinjected (20 nl) 0.1 M L-glutamate. In 35 of the 40 (87.5%) cardioinhibitory sites identified by microinjection of glutamate, ANF (20 nl of 10(-7) M) decreased heart rate (HR; -47.1 +/- 2.5 beats/min). No responses were elicited in the other five sites. In animals paralyzed and artificially ventilated, the HR effects of ANF were not significantly different before and after muscle paralysis. Microinjections of 10 nl of 10(-7) M ANF caused excitation of 19 of 21 VCN (90%), which was followed by a decrease in HR (-20.8 +/- 2.3 beats/min); no neuronal or cardiovascular responses were elicited by ANF in the remaining two VCN. Bilateral vagotomy or atropine sulfate (1 mg/kg iv) abolished cardiac slowing without affecting neuronal activation, whereas propranolol (2 mg/kg iv) did not affect either response to ANF. These results suggest that ANF is a neuromediator involved in the excitation of cardioinhibitory neurons in the NA.

Cardiovascular effects of microinjection of ANF and brain natriuretic peptide into ventrolateral medulla

1990 ◽  
Vol 259 (1) ◽  
pp. R32-R37 ◽  
Author(s):  
R. Ermirio ◽  
G. L. Avanzino ◽  
P. Ruggeri ◽  
M. Bergaglio ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic Factor ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
The Other ◽  
Ventrolateral Medulla ◽  
Lateral Aspect ◽  
Cardiovascular Neurons

Cardiovascular effects of microinjection of atrial natriuretic factor (ANF) into 77 sites of the ventrolateral medulla (VLM) were investigated in urethan-anesthetized rats. Changes in mean arterial pressure (MAP) and heart rate (HR) in response to injections of glutamate into these sites were used to determine that they contained cardiovascular neurons. ANF (20 nl of 10(-7) M) decreased MAP [-8.9 +/- 1.5 (SE) mmHg] and HR [-9.0 +/- 2.8 (SE) beats/min] in 5 of 36 vasopressor sites identified by glutamate located in the more rostral and lateral aspect of the rostral VLM (RVLM); no effect was elicited in the other 31 RVLM sites. ANF decreased MAP (-10.4 +/- 2.4 mmHg) and HR (-9.8 +/- 3.0 beats/min) in 25 of 41 depressor sites distributed throughout the caudal VLM (CVLM); no response was observed in the other 16 CVLM sites. Brain natriuretic peptide (BNP) was microinjected (20 nl of 10(-7) M) in 21 VLM sites, before or after microinjection of ANF. BNP and ANF elicited similar results in 17 sites, a decline in MAP and HR in 10 sites, and no effect in 7 sites. In the remaining four cases ANF caused a decline in MAP and in HR, whereas BNP had minimal or no effect. Cardiovascular responses to ANF microinjection into the RVLM and CVLM support the hypothesis that ANF is involved in the transmission of baroreceptor information from the nucleus tractus solitarii to these medullary regions. The similarity of the results obtained with BNP and ANF suggests that these peptides may serve similar roles in medullary pathways involved in the control of the cardiovascular system.

Bradycardia during stimulation of the septum and somatic afferents in the rabbit

1979 ◽  
Vol 236 (3) ◽  
pp. R225-R230 ◽  
Author(s):  
A. L. Brickman ◽  
F. R. Calaresu ◽  
G. J. Mogenson
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Cardiovascular Responses ◽  
Lateral Septum ◽  
Afferent Fibers ◽  
Cardiac Slowing ◽  
Bilateral Vagotomy ◽  
The Individual ◽  
Alpha Chloralose ◽  
Stimulation Of

Experiments were done in paralyzed rabbits anesthetized with either pentobarbital sodium or alpha-chloralose to test the possibility that the septum may alter the cardiovascular responses elicited by stimulation of somatic afferent fibers. Electrical stimulation of the lesser saphenous nerve (LSN), a branch of the sciatic nerve, at certain parameters elicited bradycardia, which could be abolished by bilateral vagotomy or intravenous injection of atropine methylbromide. Distinct and characteristic changes in mean arterial pressure and heart rate were elicited by electrical stimulation of histologically localized sites in five septal areas. Septal sites from which stimulation elicited bradycardia were chosen for the study of interaction between the septum and LSN. The cardiac slowing elicited by combined stimulation of the lateral septum and LSN was significantly greater than the sum of the responses elicited by separate stimulation of the two different structures. In contrast, the bradycardia elicited by combined stimulation of medial septal structures and LSN was significantly smaller than the sum of the individual responses. These experiments demonstrate that the magnitude of heart rate responses elicited by stimulation of somatic afferent fibers may be modified by the septum.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

Effect of sleep restriction on orthostatic cardiovascular control in humans

2000 ◽  
Vol 88 (3) ◽  
pp. 966-972 ◽  
Author(s):  
N. K. Muenter ◽  
D. E. Watenpaugh ◽  
W. L. Wasmund ◽  
S. L. Wasmund ◽  
S. A. Maxwell ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Lower Body Negative Pressure ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Sleep Restriction ◽  
Orthostatic Tolerance ◽  
Arterial Baroreflex ◽  
Finger Arterial Pressure ◽  
Before And After

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction ( P > 0.3). Systolic pressure was greater at −60 mmHg LBNP after sleep restriction than before sleep restriction (110 ± 6 and 124 ± 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 ± 8 and 99 ± 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

Reflex cardiovascular response to exercise is modulated by circulating vasopressin

1992 ◽  
Vol 263 (5) ◽  
pp. R1104-R1109 ◽  
Author(s):  
C. L. Stebbins
Keyword(s):  
Heart Rate ◽  
Receptor Antagonist ◽  
Cardiovascular Response ◽  
Regional Blood Flow ◽  
Plasma Concentrations ◽  
Cardiovascular Responses ◽  
Vascular Effect ◽  
Ganglionic Blockade ◽  
Hindlimb Muscles ◽  
Before And After

Peripheral vasopressin (AVP) can act centrally to sensitize the arterial baroreflex and/or peripherally to attenuate regional blood flow by a direct vascular effect. Because plasma concentrations of AVP increase during exercise, this study examined the possibility that AVP is capable of modulating the reflex cardiovascular response to static muscle contraction. Thus, in anesthetized cats, the pressor [mean arterial pressure (MAP)], myocardial contractile (dP/dt), and heart rate responses to 30-45 s of electrically induced static contraction of the hindlimb muscles were compared before and after intravenous injection of the V1 receptor antagonist d[CH2)5Tyr(Me)]-AVP (V1-x, n = 7), V1-x plus the V2 receptor antagonist [d(CH2)5,D-Phe2,Ile4,Arg8,Ala9]vasopressin (V2-x, n = 5), or the ganglionic blocker hexamethonium chloride (n = 5). In three additional cats, the contraction-induced cardiovascular response was monitored before and after injection of V1-x + V2-x and after hexamethonium. Subsequent to treatment with V1-x, the MAP and dP/dt responses to contraction were augmented by 18 +/- 5 and 22 +/- 10%, respectively (P < 0.05). After injection of V1-x + V2-x, the MAP and dP/dt responses were augmented to a similar extent (32 +/- 6 and 40 +/- 17%, respectively; P < 0.05). However, there was no difference in the magnitude of augmentation of these responses between the two conditions. The heart rate response was not altered by either treatment. Ganglionic blockade eliminated the cardiovascular responses to contraction. Last, when the pressor and contractile responses to contraction were initially augmented by administration of V1-x + V2-x, subsequent ganglionic blockade abolished the entire cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)

Dose-response effects of atropine on pancreatic response to secretin before and after truncal vagotomy

1985 ◽  
Vol 248 (5) ◽  
pp. G532-G538
Author(s):  
M. V. Singer ◽  
W. Niebel ◽  
K. H. Uhde ◽  
D. Hoffmeister ◽  
H. Goebell
Keyword(s):  
Heart Rate ◽  
Atropine Sulfate ◽  
Truncal Vagotomy ◽  
Before And After ◽  
Pancreatic Fistulas ◽  
Effective Doses ◽  
High Doses ◽  
Protein Output ◽  
Higher Doses ◽  
Intravenous Atropine

In dogs with gastric and pancreatic fistulas, we studied the effect of intravenous atropine in doses ranging from 0.9 to 58 nmol X kg-1 X h-1 on the pancreatic secretory response to secretin before and after truncal vagotomy. Truncal vagotomy did not alter the incremental bicarbonate response to secretin. Before and after truncal vagotomy, 7 nmol X kg-1 X h-1 and all higher doses of atropine sulfate significantly decreased the bicarbonate response to low doses (5.2 and 10.3 pmol X kg-1 X h-1) of secretin but had no significant effect on responses to high doses (20.5 and 41 pmol X kg-1 X h-1). The inhibitory potency of the effective doses of atropine did not differ significantly. Secretin did not stimulate pancreatic protein output above basal. Truncal vagotomy reduced protein output basally and during secretin by about 50%. Before and after truncal vagotomy, 7 nmol X kg-1 X h-1 and all higher doses of atropine significantly decreased protein output basally and during secretin. Secretin and truncal vagotomy did not alter basal heart rate. Only the three highest doses (14, 29, and 58 nmol X kg-1 X h-1) of atropine significantly increased heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of blood pressure, heart rate, age, and sex on concentrations of atrial natriuretic factor and cyclic GMP in 124 volunteers.

1989 ◽  
Vol 35 (7) ◽  
pp. 1519-1523 ◽  
Author(s):  
M Wencker ◽  
S Hauptlorenz ◽  
W Moll ◽  
B Puschendorf
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Confidence Interval ◽  
Atrial Natriuretic Factor ◽  
Blood Donation ◽  
Healthy Individuals ◽  
Natriuretic Factor ◽  
Before And After ◽  
Age And Sex ◽  
Atrial Natriuretic

Abstract The significance of increased atrial natriuretic factor (ANF) in relation to blood pressure and age is still controversial. We investigated the influence of blood pressure, age, and some other variables on ANF and its putative second messenger, cGMP. Samples for ANF and cGMP detection were taken from 124 ostensibly healthy individuals who were donating blood. Samples were also collected from 27 volunteers before and after blood donation, to study the influence of bleeding. During blood donation, ANF increased from 78.9 to 87.4 ng/L (P = 0.0035), whereas cGMP remained unchanged. ANF concentrations in 124 healthy individuals, corrected for the influence of bleeding, were 61.5 (SD 26.1) ng/L, with a 95% confidence interval of 10.0 to 112.1 ng/L. Mean cGMP concentrations in plasma were 2.9 (SD 1.45) nmol/L, with a 95% confidence interval of 0.4 to 5.75 nmol/L. Multivariance analysis revealed no significant influence of blood pressure, age, heart rate, or sex on concentrations of either ANF or cGMP in plasma.

Neuronal and cardiovascular responses to ANF microinjected into the solitary nucleus

1989 ◽  
Vol 256 (2) ◽  
pp. R577-R582 ◽  
Author(s):  
R. Ermirio ◽  
P. Ruggeri ◽  
C. E. Cogo ◽  
C. Molinari ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Unit Activity ◽  
Atrial Natriuretic Factor ◽  
Single Unit ◽  
Cardiovascular Responses ◽  
Firing Frequency ◽  
Neuronal Firing ◽  
Single Unit Activity

The effect on single-unit activity, arterial pressure, and heart rate of a microinjection of atrial natriuretic factor (ANF) into 78 histologically verified sites in the nucleus tractus solitarii (NTS) was investigated in rats. Injections of 50 nl of 10(-7) M ANF excited 34 neurons (44%), mainly localized at the level of the obex, inhibited 15 (19%), and had no effect on the remaining 29 (37%). The increase in firing frequency of the 34 excited neurons was always followed by a decline in mean arterial pressure [MAP, -10.6 +/- 1.8 (SE) mmHg; P less than 0.01] and heart rate [HR, -9.6 +/- 3.1 (SE) beats/min; P less than 0.05]. When injections of ANF caused either no effect or inhibition of single-unit activity, no changes in either MAP or HR were observed. Single units excited by injections of ANF were also excited by activation of arterial baroreceptors and inhibited by baroreceptor unloading. Control injections of an inactive peptide analogue of ANF or of vehicle never produced any effects on neuronal firing frequency or on MAP and HR. Similar results were obtained from animals paralyzed and artificially ventilated. These results support the hypothesis that ANF plays a role in the chemical transmission of baroreceptor information within the NTS.

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction

1997 ◽  
Vol 272 (6) ◽  
pp. H2774-H2781 ◽  
Author(s):  
T. Kobayashi ◽  
D. Caringi ◽  
D. J. Mokler ◽  
A. Ally
Keyword(s):  
Heart Rate ◽  
Muscle Contraction ◽  
Ampa Receptors ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Contrast Administration ◽  
Tibial Nerve Stimulation ◽  
Before And After

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

scholarly journals Perturbations of Adjuvant Chemotherapy on Cardiovascular Responses and Exercise Tolerance in Patients with Early-Stage Breast Cancer

Biology ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 910
Author(s):  
Hsin-Fu Lin ◽  
Ching-Ying Tseng ◽  
Toby Mündel ◽  
Yi-Yuan Lin ◽  
Chung-Chi Lin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Heart Rate ◽  
Exercise Tolerance ◽  
Early Stage ◽  
Heart Rate Recovery ◽  
Cardiovascular Responses ◽  
Early Stage Breast Cancer ◽  
Exercise Heart Rate ◽  
Post Exercise ◽  
Before And After

Background: Adjuvant chemotherapies are commonly used for treating early-stage breast cancer. However, whether chemotherapeutic regimens affect exercise tolerance and cardiovascular responses remains unclear. Therefore, we investigated the effects of receiving CAF and AC-T on exercise tolerance and cardiovascular responses in patients with early-stage breast cancer. Methods: Thirty-four patients with breast cancer (age: 44 ± 1 years; stage I-II) received either CAF (n = 15) or AC-T (n = 19), depending on clinical decisions. Their step-exercise tolerance and cardiovascular responses were assessed before and after chemotherapy. Results: After chemotherapy, there were no differences in baseline measurements between patients receiving CAF or AC-T. The increases in resting heart rate (RHR) of those receiving AC-T was significantly greater than that of those receiving CAF. CAF and AC-T did not result in increased pulse wave velocity (PWV), yet the subendocardial viability ratio (SEVR) in patients receiving AC-T was significantly lower than the baseline. Greater change in post-exercise heart rate recovery (recovery HR) after chemotherapy was observed in those who had received AC-T; the Recovery HR in AC-T patients was significantly higher during post-exercise period than that in CAF patients. Conclusions: AC-T chemotherapy increases RHR and impairs exercise tolerance after chemotherapy more than CAF. Moreover, AC-T also lowers myocardial perfusion more than CAF after chemotherapy.

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