Temporal relationships of barosensory attenuation in conscious rabbits

1976 ◽  
Vol 230 (6) ◽  
pp. 1480-1486 ◽  
Author(s):  
MP Gimpl ◽  
AL Brickman ◽  
MP Kaufman ◽  
N Schneiderman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Hypothalamic Stimulation ◽  
Aortic Nerve ◽  
Temporal Relationships ◽  
Train Stimulation ◽  
Posterior Hypothalamic Stimulation ◽  
Simple Summation ◽  
Stimulation Of

Electrical stimulation of anterior or posterior hypothalamus with 10-s trains elicited heart rate and blood pressure decreases. Presentation of anterior hypothalamic stimulation coincident with or 5, 10, or 15 s prior to 5-s train stimulation of aortic nerve (AN) summated with depressor-decelerator responses to AN stimulation. The summating effect was more pronounced for heart rate than for blood pressure. Simultaneous onset of AN and posterior hypothalamic stimulation did not influence AN responses. In contrast, when AN stimulation was delayed until 5, 10, or 15 s after onset of posterior hypothalamic stimulation, small, moderate, and full attenuation of AN responses occurred, respectively. Since AN and posterior hypothalamic stimulation each led to depressor-decelerator responses, attenuation of AN responses cannot be attributed to simple summation of cardiovascular responses elicited by intracranial and aortic nerve stimulation.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Nervous control of heart rate: activity in the cardiac vagus of the dogfish

1982 ◽  
Vol 53 (6) ◽  
pp. 1330-1335 ◽  
Author(s):  
E. W. Taylor ◽  
P. J. Butler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Action Potentials ◽  
Sympathetic Innervation ◽  
Nervous Control ◽  
Temporal Relationships ◽  
Maximum Water ◽  
External Stimuli ◽  
Neurophysiological Basis ◽  
Stimulation Of

In the absence of any sympathetic innervation to the heart, nervous control of heart rate in the dogfish is solely attributable to inhibitory parasympathetic input from the vagus nerve. Action potentials can be recorded from the cardiac vagus of the dogfish following its exposure in the anterior cardinal sinus. The rates of heartbeat and ventilation, blood pressure, hematocrit, and responses to external stimuli such as hypoxia, which include a bradycardia, remained typical of fish with their nervous and circulatory systems virtually intact. The recordings included sporadically active units that accelerated during hypoxia, possibly inducing the bradycardia, and regular bursts of action potentials synchronous with ventilatory movements that appeared to arise reflexly from stimulation of pharyngeal proprioceptors. These bursts may loosely couple the respiratory and cardiac pumps, increasing the probability of concurrence between periods of maximum water and blood flow. The preparation enables detailed study of the temporal relationships between the pumps and its neurophysiological basis.

Rabbit cardiovascular responses to aortic nerve stimulation at fixed carotid pressure

1979 ◽  
Vol 236 (5) ◽  
pp. H769-H774
Author(s):  
H. O. Stinnett ◽  
D. F. Peterson ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Equilibrium Pressure ◽  
Aortic Nerve ◽  
Before And After ◽  
State Changes ◽  
Pressure Changes ◽  
Central Stimulation ◽  
Stimulation Of

In pentobarbital-anesthetized rabbits with aortic nerves cut, reflex heart rate and mean arterial pressure (MAP) changes were quantified in response to maximal central stimulation of the left aortic nerve (LANS) before and during steady-state changes in isolated carotid intrasinus pressure (ISP). To distinguish possible vagally mediated cardiopulmonary influences, responses were measured before and after vagotomy. Changes in MAP observed by altering ISP within +/- 15 mmHg of the equilibrium pressure (EP) were linear and inversely correlated to changes in ISP, with a slope of approximately 3 both before and after vagotomy (r greater than or equal to 0.929, P less than 0.05). The peak fall in MAP during LANS was dependent upon ISP. The change in the MAP responses to LANS for each mmHg change in ISP ranged from 1.7 with vagi intact to 1.3 after vagotomy. Heart rate was unaltered by isolation of the carotid sinus and was independent of the small changes in ISP between +/- 15 mmHg of EP. These results indicate that blood pressure changes elicited by the aortic baroreflex are extremely sensitive to the degree of carotid sinus compensation. Thus, to assess the sensitivity of any arterial reflex area, the existing level of compensation by other barosensitive areas must be known.

scholarly journals Reflex cardiovascular responses originating in exercising muscles of mice

2001 ◽  
Vol 90 (2) ◽  
pp. 579-585 ◽  
Author(s):  
Jeffery M. Kramer ◽  
Arthur Aragones ◽  
Tony G. Waldrop
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Muscle Contraction ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Dependent Manner ◽  
Direct Stimulation ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Stimulation Of

The cardiovascular responses induced by exercise are initiated by two primary mechanisms: central command and reflexes originating in exercising muscles. Although our understanding of cardiovascular responses to exercise in mice is progressing, a murine model of cardiovascular responses to muscle contraction has not been developed. Therefore, the purpose of this study was to characterize the cardiovascular responses to muscular contraction in anesthetized mice. The results of this study indicate that mice demonstrate significant increases in blood pressure (13.8 ± 1.9 mmHg) and heart rate (33.5 ± 11.9 beats/min) to muscle contraction in a contraction-intensity-dependent manner. Mice also demonstrate 23.1 ± 3.5, 20.9 ± 4.0, 21.7 ± 2.6, and 25.8 ± 3.0 mmHg increases in blood pressure to direct stimulation of tibial, peroneal, sural, and sciatic hindlimb somatic nerves, respectively. Systemic hypoxia (10% O2-90% N2) elicits increases in blood pressure (11.7 ± 2.6 mmHg) and heart rate (42.7 ± 13.9 beats/min), while increasing arterial pressure with phenylephrine decreases heart rate in a dose-dependent manner. The results from this study demonstrate the feasibility of using mice to study neural regulation of cardiovascular function during a variety of autonomic stimuli, including exercise-related drives such as muscle contraction.

Pressoceptive and chemoceptive aortic reflexes in decorticate and in decerebrate cats

1965 ◽  
Vol 208 (4) ◽  
pp. 708-714 ◽  
Author(s):  
G. Baccelli ◽  
M. Guazzi ◽  
A. Libretti ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Cardiovascular Responses ◽  
Decrease Blood Pressure ◽  
Aortic Nerve ◽  
Decerebrate Cats ◽  
Sham Rage ◽  
Stimulation Of

Graded electrical stimulation of three different components of the aortic nerve has been performed in decorticate cats, and later repeated after intercollicular decerebration. Threshold stimuli, involving only the largest fibers probably originating from pressoceptors, slightly decrease blood pressure and respiration both in quiet decorticate and in decerebrate cats. However, in decorticate animals during "spontaneous" fits of sham rage, inhibition of all somatic and visceral components of rage behavior is observed. When aortic nerve stimuli also involve intermediate-threshold fibers presumably of chemoceptive origin, excitation of rage behavior accompanied by strong hypertension and hyperventilation is seen in decorticate preparations, while after decerebration reflex hyperpnea is accompanied by hypotension or by no consistent pressor change. Stronger stimuli activating smaller fibers of probable pressoceptive origin still have conspicuous excitatory effects in decorticate animals, as shown by appearance of rage activity and pressor reactions, whereas after decerebration prominent hypotension with hyperpnea is observed. The predominance of excitatory cardiovascular responses to aortic nerve stimuli in decorticate animals, and of inhibitory reactions after decerebration, is discussed.

scholarly journals Corticotropin-releasing hormone projections from the paraventricular nucleus of the hypothalamus to the nucleus of the solitary tract increase blood pressure

2019 ◽  
Vol 121 (2) ◽  
pp. 602-608 ◽  
Author(s):  
Lei A. Wang ◽  
Dianna H. Nguyen ◽  
Steve W. Mifflin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Cardiovascular Responses ◽  
Solitary Tract ◽  
Increase Blood Pressure ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Optogenetic Stimulation ◽  
Stimulation Of

Activation of corticotropin-releasing hormone (CRH) type 2 receptors (CRHR2) in the nucleus of the solitary tract (NTS) contributes to the development of hypertension, but the source of CRH inputs to the NTS that increases blood pressure remains unknown. This study tested the hypothesis that activation of CRH-containing projections from the paraventricular nucleus of the hypothalamus (PVN) to the NTS increase blood pressure. We expressed channelrhodopsin 2 (ChR2), a light-sensitive ion channel, into CRH-containing neurons in the PVN. This was achieved by injecting Cre-inducible virus expressing ChR2 into the PVN of CRH-Cre mice. CRH-Cre mice are genetically modified mice expressing Cre recombinase only in neurons producing CRH. We found that optogenetic stimulation of CRH-containing somas in the PVN or CRH-containing fibers in the NTS originating from the PVN significantly increased blood pressure and heart rate. Microinjection of K-41498 (CRHR2 antagonist) into the NTS attenuated the pressor and tachycardiac responses induced by optogenetic stimulation of CRH-containing somas in the PVN. In vitro loose-patch recordings revealed that optogenetic stimulation of CRH-containing fibers in the NTS originating from the PVN significantly increased the discharge frequency of NTS neurons. This effect was attenuated by pretreatment of K-41498 and was abolished by pretreatment of kynurenic acid (nonselective glutamate receptor antagonist). These results suggest that activation of PVN-NTS CRH-containing projections increases blood pressure and heart rate. The cardiovascular responses may be mediated at least in part by the corelease of CRH and glutamate from NTS CRH-containing axons originating from the PVN. NEW & NOTEWORTHY Optogenetic stimulation of paraventricular nucleus of the hypothalamus (PVN) corticotropin-releasing hormone (CRH)-containing somas or nucleus of the solitary tract (NTS) CRH-containing fibers originating from the PVN increased blood pressure and heart rate. Corelease of CRH and glutamate from NTS CRH-containing axons originating from the PVN may contribute to the pressor and tachycardiac responses elicited by optogenetic stimulation of PVN CRH-containing somas.

Cardiovascular responses to electrocardiogram-coupled stimulation of rabbit aortic nerve

1976 ◽  
Vol 230 (5) ◽  
pp. 1374-1378 ◽  
Author(s):  
HO Stinnett ◽  
DF Peterson ◽  
VS Bishop
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Cardiovascular Responses ◽  
Initial Slope ◽  
Peripheral Vasculature ◽  
Arterial Blood ◽  
Aortic Nerve ◽  
Reflex Control ◽  
Sympathetic Efferent Activity ◽  
Stimulation Of

Electrical stimulation of the rabbit's aortic nerve during one or more cardiac cycles resulted in a reflex fall in heart rate and mean arterial blood pressure (MAP). The onset of bradycardia and of fall in MAP were independent of the number of beats stimulated. The initial slope of the heart rate and MAP responses increased as the number of beats stimulated increased, reaching a maximum at five beats of stimulation. Bradycardia peaked 8 and 10 beats after the end of one and two cycles of stimulation, respectively, while the peak response occurred at, or prior to, the end of stimulation when 12 or more beats were involved. Onset and recovery of both responses were consistent, and seldom did MAP indicate a return toward control during stimulation. Thus, central nervous system modulation of sympathetic activity to the peripheral vasculature was sustained as long as the aortic nerve input was maintained. However, reflex control of heart rate was more complex, involving simultaneous alteration in both vagal and sympathetic efferent activity.

Posterior hypothalamic influences on cardiovascular effects of aortic nerve stimulation

1989 ◽  
Vol 257 (6) ◽  
pp. H1994-H2000 ◽  
Author(s):  
J. K. Smith ◽  
K. W. Barron
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Posterior Hypothalamus ◽  
Hypothalamic Stimulation ◽  
Bipolar Electrode ◽  
Aortic Depressor Nerve ◽  
Aortic Nerve ◽  
Posterior Hypothalamic Stimulation ◽  
Stimulation Of

The purpose of this study was to examine the influence of stimulation of the posterior hypothalamus on the baroreflex responses produced by stimulation of the aortic depressor nerve. Animals were initially anesthetized and implanted with a bipolar electrode in the posterior hypothalamus. Three to 5 days later, animals were anesthetized with urethan, and the left aortic depressor nerve was dissected and placed on a bipolar platinum-iridium electrode. The effects of electrical stimulation of the posterior hypothalamus (0, 160, and 280 microA) were examined in baroreflex-intact and acutely sinoaortic baroreceptor-denervated animals, and the responses to aortic nerve stimulation (2, 8, 16, and 32 Hz) were examined during each level of hypothalamic stimulation. The first set of experiments was performed in baroreceptor-intact animals; e.g., in animals with arterial baroreceptor inputs intact from both carotid sinus regions in addition to intact right aortic baroreceptor afferent pathways. In that group, stimulation of the posterior hypothalamus attenuated the bradycardia and depressor effects of aortic nerve stimulation. When influences from other baroreceptor inputs were removed with acute sinoaortic baroreceptor denervation, posterior hypothalamic stimulation interrupted the reflex bradycardia due to aortic nerve stimulation; however, the depressor response to aortic nerve stimulation was not attenuated. Similar to the arterial pressure response, hypothalamic stimulation did not attenuate the decreases in mesenteric and iliac vascular resistance produced by aortic nerve stimulation in the baroreflex-denervated group. We conclude that posterior hypothalamic stimulation attenuates baroreflex-mediated bradycardia but does not alter baroreflex control of arterial pressure and peripheral vascular resistance.

Vagal inhibition of cardiovascular activity in the decerebrate cat

1962 ◽  
Vol 203 (3) ◽  
pp. 449-452 ◽  
Author(s):  
Richard L. Glasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Cardiovascular Activity ◽  
Decerebrate Cat ◽  
Arterial Blood ◽  
Rostral Portion ◽  
The Brain ◽  
Decerebrate Animal ◽  
Stimulation Of

Cardiovascular responses after decerebration at three levels of the central neuraxis and subsequent vagotomy were studied in the cat. Midpontile decerebration produced a marked, transient depression in heart rate and arterial blood pressure, from which recovery to and sometimes above pretransection levels usually occurred within 30 min. Subsequent vagotomy in the midpontile decerebrate animals produced marked tachycardia and hypertension. This cardiovascular hyperactivity, particularly hypertension, was conspicuously diminished by stimulation of the central ends of the sectioned vagi. In distinct contrast to the dramatic augmentation of cardiovascular activity after vagotomy in the midpontile animals, vagotomy in midmesencephalic and medullary animals typically produced moderate and transient elevations in heart rate and blood pressure. These data support the concept of a cardiovascular-augmenter area in the caudal pons and a cardiovascular-depressor area in a more rostral portion of the brain stem. These data suggest that the vagal system antagonizes and masks a potential cardiovascular hyperactivity in the midpontile decerebrate animal.

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