scholarly journals Respiratory modulation of barareceptor and chemoreceptor reflexes affecting heart rate and cardiac vagal efferent nerve activity.

1976 ◽  
Vol 259 (2) ◽  
pp. 523-530 ◽  
Author(s):  
N S Davidson ◽  
S Goldner ◽  
D I McCloskey
Keyword(s):  
Heart Rate ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Respiratory Modulation ◽  
Vagal Efferent Nerve

Effects of CGRP on baroreflex control of heart rate and renal sympathetic nerve activity in rabbits

1992 ◽  
Vol 263 (4) ◽  
pp. R874-R879 ◽  
Author(s):  
H. Okamoto ◽  
S. Hoka ◽  
T. Kawasaki ◽  
M. Sato ◽  
J. Yoshitake
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Afferent Nerve ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Efferent Nerve ◽  
Induced Hypotension ◽  
Calcitonin Gene ◽  
Alpha Chloralose ◽  
Renal Sympathetic

We examined the effects of intravenous infusion of calcitonin gene-related peptide (CGRP) and sodium nitroprusside (SNP) on baroreceptor afferent nerve activity, renal sympathetic efferent nerve activity (RSNA), and heart rate in alpha-chloralose-anesthetized rabbits. Baroreceptor afferent nerve activity was measured from aortic nerves during CGRP- and SNP-induced hypotension. Decreases in aortic nerve activity in response to decreases in mean arterial pressure were not different during CGRP and SNP infusion. Progressive infusion of CGRP (12-120 pmol.kg-1.min-1) increased RNSA by 83 +/- 14 (mean +/- SE), 175 +/- 26, 246 +/- 36, and 343 +/- 41%, and heart rate by 8 +/- 2, 24 +/- 3, 37 +/- 4, and 47 +/- 6 beats/min during falls of blood pressure of 5, 10, 15, and 20 mmHg, respectively. These increases in RSNA and heart rate produced by CGRP were significantly greater than those produced by SNP. The alterations in heart rate and RSNA with CGRP were reversed by restoring blood pressure with phenylephrine HCl. In rabbits with sinoaortic and vagal deafferentation, the responses of heart rate and RSNA to a fall of blood pressure were abolished during both CGRP and SNP infusion. Therefore, it is suggested that the facilitated responses of heart rate and RSNA during CGRP infusion occurred by way of the arterial baroreflex arc.

scholarly journals Abnormal cardiovascular response to exercise in hypertension: contribution of neural factors

2017 ◽  
Vol 312 (6) ◽  
pp. R851-R863 ◽  
Author(s):  
Jere H. Mitchell
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiovascular Response ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Functional Sympatholysis ◽  
Neural Factors ◽  
Response To Exercise

During both dynamic (e.g., endurance) and static (e.g., strength) exercise there are exaggerated cardiovascular responses in hypertension. This includes greater increases in blood pressure, heart rate, and efferent sympathetic nerve activity than in normal controls. Two of the known neural factors that contribute to this abnormal cardiovascular response are the exercise pressor reflex (EPR) and functional sympatholysis. The EPR originates in contracting skeletal muscle and reflexly increases sympathetic efferent nerve activity to the heart and blood vessels as well as decreases parasympathetic efferent nerve activity to the heart. These changes in autonomic nerve activity cause an increase in blood pressure, heart rate, left ventricular contractility, and vasoconstriction in the arterial tree. However, arterial vessels in the contracting skeletal muscle have a markedly diminished vasoconstrictor response. The markedly diminished vasoconstriction in contracting skeletal muscle has been termed functional sympatholysis. It has been shown in hypertension that there is an enhanced EPR, including both its mechanoreflex and metaboreflex components, and an impaired functional sympatholysis. These conditions set up a positive feedback or vicious cycle situation that causes a progressively greater decrease in the blood flow to the exercising muscle. Thus these two neural mechanisms contribute significantly to the abnormal cardiovascular response to exercise in hypertension. In addition, exercise training in hypertension decreases the enhanced EPR, including both mechanoreflex and metaboreflex function, and improves the impaired functional sympatholysis. These two changes, caused by exercise training, improve the muscle blood flow to exercising muscle and cause a more normal cardiovascular response to exercise in hypertension.

Splenic afferents and some of their reflex responses

1982 ◽  
Vol 242 (3) ◽  
pp. R247-R254 ◽  
Author(s):  
N. L. Herman ◽  
D. R. Kostreva ◽  
J. P. Kampine
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Venous Pressure ◽  
Systemic Blood Pressure ◽  
Contractile Force ◽  
Afferent Nerve ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
C Fibers ◽  
Stimulation Period

Afferent nerve activity was recorded from the distal ends of cut splenic nerves in pentobarbital- (35 mg/kg) anesthetized mongrel dogs (15-20 kg). Increases in splenic venous pressure (SVP) produced either by manual compression of discrete portions of the spleen or splenic contraction produced by injection of epinephrine (100 micrograms) into the splenic artery or vein of an occluded spleen produced significant increases in SVP and splenic afferent nerve activity. Increases in splenic afferent nerve activity were linearly related to increases in SVP. Histological sections of nerves from which afferent recordings were obtained demonstrated that all afferents were unmyelinated C-fibers. Electrical stimulation of the cut central end of splenic nerves resulted in marked reflex increases in both renal and cardiopulmonary sympathetic efferent nerve activity that remained elevated throughout the stimulation period. Reflex increase in cardiopulmonary sympathetic efferent nerve activity was associated with increases in right (22-45%) and left (11-19%) ventricular contractile force measured with Brodie-Walton strain gauge transducers, in heart rate (5-15 beats/min), and in blood pressure (5-10 mmHg). This study is the first to demonstrate both the existence of low-pressure baroreceptors in the spleen and that these splenic afferents can reflexly alter cardiopulmonary and renal sympathetic efferent nerve activity, heart rate, ventricular contractile force, and systemic blood pressure.

Reflex effects of renal afferents on the heart and kidney

1981 ◽  
Vol 241 (5) ◽  
pp. R286-R292 ◽  
Author(s):  
D. R. Kostreva ◽  
J. L. Seagard ◽  
A. Castaner ◽  
J. P. Kampine
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Renal Vein ◽  
Contractile Force ◽  
Renal Vascular Resistance ◽  
Afferent Activity ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Vein Occlusion ◽  
Renal Vascular

The reflex effects of renal afferents on the heart and kidney were studied in dogs anesthetized with pentobarbital sodium. Renal afferent and efferent nerve activity recorded from the renal nerves during occlusion of a single renal vein resulted in increases in nontonically firing renal afferent activity and decreases in tonically firing afferent activity. Renal efferent nerve activity from the contralateral kidney was always inhibited during single renal vein occlusion. This decrease in nerve activity was associated with a decrease in renal vascular resistance. Denervation of the congested kidney eliminated the reflex changes in renal vascular resistance. Cardiopulmonary sympathetic efferent nerve activity from the ansae subclavia was always reflexly inhibited by single renal vein occlusion. Although heart rate and left ventricular contractile force were not altered during renal vein occlusion, right ventricular contractile force decreased by -6 to -25%. This reflex decrease in contractile force was eliminated by denervation of the congested kidney. These studies demonstrate that renal afferents, activated by increases in renal venous pressure, can reflexly inhibit contralateral renal and cardiopulmonary sympathetic efferent nerve activity, decrease contralateral renal vascular resistance, and decrease right ventricular contractile force, without altering heart rate.

scholarly journals Exogenous cholecystokinin-8 reduces vagal efferent nerve activity in rats through CCKA receptors

2000 ◽  
Vol 129 (8) ◽  
pp. 1649-1654 ◽  
Author(s):  
Violeta Bucinskaite ◽  
Mieko Kurosawa ◽  
Thomas Lundeberg
Keyword(s):  
Nerve Activity ◽  
Efferent Nerve ◽  
Ccka Receptors ◽  
Vagal Efferent Nerve

Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man

1995 ◽  
Vol 133 (6) ◽  
pp. 723-728 ◽  
Author(s):  
Ettore C degli Uberti ◽  
Maria R Ambrosio ◽  
Marta Bondanelli ◽  
Giorgio Transforini ◽  
Alberto Valentini ◽  
...  
Keyword(s):  
Heart Rate ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Heart Rate Response ◽  
Statistical Significance ◽  
Inhibitory Effect ◽  
Amino Acid Residues ◽  
Nerve Activity ◽  
Receptor Stimulation

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643 Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function. Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy

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