Autonomic influences on heart rate and blood pressure in the toad, Bufo marinus, at rest and during exercise

1988 ◽  
Vol 134 (1) ◽  
pp. 377-396 ◽  
Author(s):  
I. Wahlqvist ◽  
G. Campbell

Blood pressure (PA) and heart rate (HR) were measured in the conscious, resting toad, Bufo marinus. Treatment with bretylium (an adrenergic neurone blocking agent), alone or in combination with phentolamine and propranolol (adrenoceptor antagonists) did not alter PA or HR significantly. Atropine caused a small but significant increase in HR but had no effect on PA. The experiments indicate a cholinergic cardio-inhibitory tone but give no evidence for an adrenergic pressor tone at rest. Treadmill exercise caused a rapid increase in PA and HR which was sustained throughout the exercise period. This response was partly psychogenic. The concentration of plasma catecholamines increased during exercise and was high enough to affect organs that were included in an extracorporeal blood circuit with the exercising animal. Bretylium treatment revealed an initial hypotension, presumably due to work hyperaemia, followed by a hypertension which was reduced compared to controls. The tachycardia was delayed but HR eventually reached control levels. Additional treatment with phentolamine and propranolol did not further affect the PA response, but significantly reduced the tachycardia reached during exercise. It is concluded that the cardiovascular responses to exercise involve adrenergic nerve fibres causing hypertension and an initial rapid tachycardia. Circulating catecholamines seem to be the major cause of the sustained tachycardia.

1991 ◽  
Vol 261 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Smith

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.


1989 ◽  
Vol 67 (4) ◽  
pp. 269-275 ◽  
Author(s):  
Colleen L. Riphagen ◽  
Quentin J. Pittman

Vasopressinergic pathways within the spinal cord have been implicated in the control of cardiovascular function. This study was undertaken to determine the mechanisms whereby intrathecally administered arginine vasopressin (AVP) increases blood pressure and heart rate in anesthetized rats. The cardiovascular responses to intrathecal AVP administration were significantly attenuated after intravenous administration of the ganglionic blocking agent, chlorisondamine chloride, as were the pressor responses following α-adrenergic receptor blockade with phentolamine and the heart rate responses following β-receptor blockade with propranolol. Intrathecal administration of the V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP completely blocked the cardiovascular responses to intrathecal AVP injections, but did not significantly alter the responses to intrathecal substance P injections. There was no evidence for the involvement of the rennin–angiotensin system in the pressor responses to intrathecal AVP, as (i) an angiotensin II receptor blocking agent, [Sar1, Val5, Ala8]angiotensin, failed to significantly alter the responses to intrathecal AVP, and (ii) plasma renin levels did not change following administration of the peptide. Intrathecal injections of [3H]AVP suggest that only small amounts of the peptide may cross into the plasma during the time in which the cardiovascular variables are changing. These data provide evidence that intrathecally administered AVP discretely activates the sympathetic outflow to the heart and vasculature, and confirm the neurally mediated nature of the response.Key words: blood pressure, spinal cord, peptides, autonomic nervous system, neurotransmitter.


1981 ◽  
Vol 241 (5) ◽  
pp. R307-R311
Author(s):  
D. G. Smith ◽  
P. J. Berger ◽  
B. K. Evans

Perivascular balloons were used to elicit heart rate (HR) responses to imposed changes in mean arterial pressure (Pa) in conscious unrestrained toads (Bufo marinus). It is clear that functional baroreceptors lie in the pulmocutaneous arteries of B. marinus, and that these can elicit compensatory heart rate responses to perturbations of blood pressure. Functional baroreceptors were not present in the carotid circulation and are probably absent from the lateral aortae and conus arteriosus as well. Normalized gain of the baroreceptor-heart rate reflex (delta HR%/delta Pa) in five toads was 13%/kPa, which is considerably less than that found in other vertebrates to date.


1979 ◽  
Vol 47 (6) ◽  
pp. 1207-1211 ◽  
Author(s):  
J. LeBlanc ◽  
J. Cote ◽  
M. Jobin ◽  
A. Labrie

Plasma epinephrine (E) and norepinephrine (NE) as well as blood pressure and heart rate variations were measured in 12 male subjects before, during, and after a cold hand test (5 degrees C for 2 min), a mental arithmetic test, and a combination of both these tests. Although the cold and mental tests had comparable effects on blood pressure, the heart rate response was greater than the mental test. The mental test produced a greater increase of E than the cold test, but the effect of the cold test was greater on NE than on E. Changes in heart rate were significantly correlated with E variations but not with NE, whereas changes in blood pressure were correlated with NE. Resting NE was correlated with resting blood pressure and resting E with resting heart rate. Finally the levels of basal E were positively correlated with the increase in E during the test. Cardiovascular changes were shown to be differently modified by a mental and a cold test. Evidence was given indicating that these changes are related to differences in E and NE responses in the presence of these tests.


1989 ◽  
Vol 257 (4) ◽  
pp. R901-R908 ◽  
Author(s):  
L. Marson ◽  
J. A. Kiritsy-Roy ◽  
G. R. Van Loon

The effects of mu- and delta-opioid receptor activation on sympathoadrenal and cardiovascular responses to stress were examined in conscious rats. The mu-selective agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO) or the delta-selective agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) was injected into a lateral cerebral ventricle, then rats were stressed by restraint. Plasma catecholamines were measured, and arterial blood pressure and heart rate were recorded continuously. Restraint stress evoked increases in plasma catecholamines and heart rate in saline-pretreated rats. Both DAGO and DPDPE increased basal plasma levels of catecholamines and blood pressure, and DAGO, 5 nmol, produced bradycardia. DAGO, 5 nmol, but not DPDPE, potentiated the plasma catecholamine responses to restraint. However, the presence of DAGO or DPDPE during restraint resulted in decreases in heart rate and blood pressure. The effects of DAGO and DPDPE on plasma catecholamines, heart rate, and blood pressure were blocked by a mu-selective dose of naloxone but were not reversed by the delta-selective antagonist ICI 174864. These results indicate that mu-receptor stimulation during restraint stress facilitates sympathoadrenal and parasympathetic outflow and results in vasodilatation of some peripheral vascular beds.


Author(s):  
Ewan Thomas ◽  
Marianna Bellafiore ◽  
Ambra Gentile ◽  
Antonio Paoli ◽  
Antonio Palma ◽  
...  

AbstractThe aim of this study will be to review the current body of literature to understand the effects of stretching on the responses of the cardiovascular system. A literature search was performed using the following databases: Scopus, NLM Pubmed and ScienceDirect. Studies regarding the effects of stretching on responses of the cardiovascular system were investigated. Outcomes regarded heart rate(HR), blood pressure, pulse wave velocity (PWV of which baPWV for brachial-ankle and cfPWV for carotid-femoral waveforms), heart rate variability and endothelial vascular function. Subsequently, the effects of each outcome were quantitatively synthetized using meta-analytic synthesis with random-effect models. A total of 16 studies were considered eligible and included in the quantitative synthesis. Groups were also stratified according to cross-sectional or longitudinal stretching interventions. Quality assessment through the NHLBI tools observed a “fair-to-good” quality of the studies. The meta-analytic synthesis showed a significant effect of d=0.38 concerning HR, d=2.04 regarding baPWV and d=0.46 for cfPWV. Stretching significantly reduces arterial stiffness and HR. The qualitative description of the studies was also supported by the meta-analytic synthesis. No adverse effects were reported, after stretching, in patients affected by cardiovascular disease on blood pressure. There is a lack of studies regarding vascular adaptations to stretching.


1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963


2016 ◽  
Vol 29 (3) ◽  
pp. 543-552
Author(s):  
João Douglas Alves ◽  
Jorge Luiz de Brito Gomes ◽  
Caio Victor Coutinho de Oliveira ◽  
José Victor de Miranda Henriques Alves ◽  
Fabiana Ranielle de Siqueira Nogueira ◽  
...  

Abstract Introduction: Tai-Chi-Chuan and Yoga have becoming popular practices. However is unclear the cardiovascular effects, and if they present similar behavior to aerobic and resistance sessions. Objective: To evaluate the cardiovascular responses during the session and post-exercise hypotension (PEH) of Tai Chi Chuan (TS) and Yoga (YS) in comparison to aerobic (AS) and resistance (SR) exercises. Methods: Fourteen young women (22.3 ± 2 years) apparently healthy performed four sessions (AS, RS, TS and YS). The heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP) were recorded at resting, during (every 10 minutes) and until 50 minutes of recovery. Results: AS, RS, TS e YS showed significant increase in HR compared to resting.AS at 10, 30 e 50 minutes in relation to RS, TS e YS. The RS in relation to TS and YS at 10, 30 and 50 minutes. No significant difference between TS and YS. SBP was significantly increased in AS, RS, TS e YS at 10, 30 e 50 minutes during the session, in relation to rest. AS was significantly higher at 30 e 50 minutes than RS and higher than TS and YS at 10, 30 e 50 minutes. No significant difference in DBP. For PEH, AS, RS and TS significantly reduced at 10, 30 and 50 minutes. YS reduced at 50 minutes. No significant diastolic PEH. Conclusion: TS and YS showed as safe alternatives of exercising in the normotensive young adult woman, despite having lower values, they promote similar hemodynamic behavior to AS and RS.


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