scholarly journals Electrical stimulation of the midbrain increases heart rate and arterial blood pressure in awake humans

2002 ◽  
Vol 539 (2) ◽  
pp. 615-621 ◽  
Author(s):  
Judith M. Thornton ◽  
Tipu Aziz ◽  
David Schlugman ◽  
David J. Paterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Stimulation Of

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.

Beta2-mediated hypotension and myocardial injury

1982 ◽  
Vol 60 (8) ◽  
pp. 1144-1148 ◽  
Author(s):  
Alison Brown-Lukacsko ◽  
Peter Lukacsko
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Elevated Serum ◽  
Blocking Agent ◽  
Arterial Blood ◽  
Ganglionic Blocking ◽  
Elevated Heart Rate ◽  
Stimulation Of

This study was designed to investigate the importance of beta2 receptor mediated hypotension in the pathogenesis of myocardial injury. The effect of isoproterenol and the putative beta2 agonist albuterol on arterial blood pressure, heart rate, the myocardial content of ATP and cAMP, and the serum content of MB-CPK was examined in conscious rats. Isoproterenol (5.25 mg/kg, s.c.) and albuterol (45 mg/kg, s.c.) lowered blood pressure and elevated heart rate to the same extent. Also, both agonists increased the myocardial content of cAMP, decreased the myocardial content of ATP, and elevated serum MB-CPK. The beta1 antagonist practolol, but not the ganglionic blocking agent chlorisondamine, attenuated the elevation in heart rate to albuterol without reducing its effect on blood pressure. Practolol, but not chlorisondamine, abolished the effects of albuterol on cAMP, ATP, and MB-CPK. These data suggest that the myocardial injury which is associated with an increased heart rate and changes in cAMP, ATP, and MB-CPK following the administration of albuterol is not the result of beta2-mediated hypotension, but is due to stimulation of myocardial beta1 receptors.

Cerebral blood flow and behavior during brain stimulation in the goat

1977 ◽  
Vol 232 (5) ◽  
pp. H495-H499
Author(s):  
M. Manrique ◽  
E. Alborch ◽  
J. M. Delgado
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Maxillary Artery ◽  
Internal Maxillary Artery ◽  
Arterial Blood ◽  
And Behavior ◽  
Stimulation Of

Cerebral blood flow, heart rate, arterial blood pressure, and behavior were studied in conscious goats during electrical stimulation of the diencephalon and mesencephalon. Stimulation of the subthalamic area produced a considerable increase in ipsilateral cerebral blood flow and heart rate, accompanied by either a small or a large increase in systemic arterial blood pressure. Cardiovascular effects were associated with changes in alertness. The increase in cerebral blood flow was partially abolished by previous administration of atropine directly into the internal maxillary artery. Stimulation of the mesencephalic reticular formation caused a marked increase in blood pressure with no change or with some decrease in cerebral blood flow. After administration of phentolamine into the internal maxillary artery, stimulation produced increase in cerebral blood flow. The behavioral response consisted of restlessness and attempted flight. These results suggest the existence of cholinergic vasodilator and adrenergic vasoconstrictor pathways to cerebral blood vessels that may be stimulated electrically.

PREFERENTIAL RELEASE OF OXYTOCIN FROM THE NEUROHYPOPHYSIS AFTER ELECTRICAL STIMULATION OF THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN OF THE GUINEA-PIG

1968 ◽  
Vol 40 (2) ◽  
pp. 205-214 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Arterial Blood Pressure ◽  
Pituitary Stalk ◽  
Milk Ejection ◽  
Arterial Blood ◽  
Milk Ejection Reflex ◽  
The Brain ◽  
Stimulation Of

SUMMARY Discrete portions of the afferent path of the milk-ejection reflex have been explored in the brain of the lactating guinea-pig. Both intramammary pressure and arterial blood pressure were recorded to detect release of oxytocin and vasopressin. It was found that the milk-ejection responses which occurred after electrical stimulation of the pathway in the midbrain and hypothalamus were caused by the release of oxytocin without detectable release of vasopressin. A mixture of oxytocin and vasopressin, in the ratio of approximately 3:1, was released only after electrical stimulation of the rostral tuberal region of the hypothalamus adjacent to the pituitary stalk. It is concluded that the afferent path in the brain of the guinea-pig studied is concerned with the preferential release of oxytocin from the neurohypophysis and that it is the pathway of the milk-ejection reflex.

Medullary sympathoexcitatory neurons are inhibited by activation of the medial prefrontal cortex in the rat

1996 ◽  
Vol 270 (4) ◽  
pp. R713-R719 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Arterial Blood Pressure ◽  
Medial Prefrontal Cortex ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Stimulation Of ◽  
Nerve Discharge

Electrical stimulation of the medial prefrontal cortex (MPFC) reduces arterial blood pressure. To investigate the mechanism of this response, the effects of electrical and chemical stimulation of the MPFC on splanchnic and lumbar sympathetic nerve discharge and on the discharges of barosensitive neurons of the rostral ventrolateral medulla (RVLM) were studied in halothane-anesthetized rats. Electrical stimulation (20 Hz, 1 ms, 100 and sympathoinhibitory responses (reduced discharge of the splanchnic sympathetic nerve). Microinjection of glutamate (10 nmol/100 nl) into the MPFC also reduced arterial blood pressure and sympathetic discharge. Electrical stimulation (0.5 Hz, 1-ms pulse pairs, 3-ms interval, 150-300 microA) produced distinct patterns of splanchnic and lumbar sympathetic nerve discharge. A clear sympathoinhibitory phase with an onset latency of 146 +/- 14 ms was observed only in the case of the splanchnic sympathetic nerve activity. Electrical stimulation at depressor sites within the MPFC also inhibited the discharge of 10 of 21 RVLM barosensitive neurons tested. RVLM neurons were never excited by MPFC stimulation. These results indicate that the MPFC contains neurons that form part of a central sympathoinhibitory pathway.

Cuneiform nucleus stimulation produces activation of medullary sympathoexcitatory neurons in rats

1995 ◽  
Vol 268 (3) ◽  
pp. R752-R758 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Ventrolateral Medulla ◽  
Onset Latency ◽  
Thoracic Spinal Cord ◽  
Arterial Blood ◽  
Thoracic Spinal ◽  
Cuneiform Nucleus ◽  
Stimulation Of

Activation of the cuneiform nucleus (CNF) of the midbrain produces elevation of arterial blood pressure. This study examined the influence of the CNF on arterial blood pressure, sympathetic vasomotor outflow, and the discharges of barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) in halothane-anesthetized, paralyzed rats. Electrical stimulation (50 Hz, 25-75 microA, 10 s) of the CNF elicited intensity-dependent elevations in arterial blood pressure associated with excitation of the sympathetic vasomotor discharge (elevated discharge of the lumbar sympathetic nerve). Intermittent paired-pulse electrical stimulation of the CNF elicited an excitatory response in the discharge of the lumbar sympathetic outflow that consisted of an early peak (onset latency 84 +/- 4 ms) and a smaller late peak (onset latency 217 +/- 6 ms). Seventeen of 22 RVLM sympathoexcitatory neurons tested were excited by stimulation of the CNF. Twelve of 14 units tested projected to the thoracic spinal cord, and of these, 10 units were excited by CNF stimulation with an onset latency of 16 +/- 1 ms. These findings support the hypothesis that the sympathoexcitatory and pressor responses elicited by activation of the CNF are mediated by RVLM sympathoexcitatory neurons.

Area postrema stimulation induced cardiovascular changes in the rat

1988 ◽  
Vol 255 (5) ◽  
pp. R855-R860 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Marcus
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Control ◽  
Control Mechanisms ◽  
Arterial Blood

The studies described here have utilized electrical stimulation techniques to examine the effects of activation of neural elements within the area postrema (AP) on cardiovascular control mechanisms. A total of 45 urethananesthetized male Sprague-Dawley rats were used in these experiments. Low-frequency electrical stimulation (10 Hz, 200 microA) in the AP resulted in rapid onset (less than 2 s), short-lasting (less than 5 s after end of stimulation) decreases in mean arterial blood pressure (-34.8 +/- 2.7 mmHg, n = 17 rats). In contrast, similar stimulation in the adjacent nucleus tractus solitarius (NTS) caused similarly timed increases in blood pressure (+43.1 +/- 6.7 mmHg, n = 5 rats). Activation of neural elements within the AP was found to significantly (Student's t test, P less than 0.01) reduce heart rate, an effect that was also specific to the AP site as similar stimulation in the NTS was without effect. These data support an important role for AP in cardiovascular control mechanisms. They demonstrate that stimulation in AP results in rapid reversible decreases in mean arterial blood pressure and heart rate. Such findings further emphasise the potential roles of this circumventricular structure in autonomic control mechanisms.

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