Interdependence of rostral and caudal ventrolateral medullary areas in the control of blood pressure

R. N. Willette, S. Punnen, A. J. Krieger, Hreday Sapru

Research output: Contribution to journalArticle

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Abstract

Pharmacologic experiments were carried out to test the degree of interdependence of rostral vasopressor and caudal vasodepressor neuron pools in the ventrolateral medulla (VLPA and VLDA, respectively). In two groups of urethane-anesthetized rats, the γ-aminobutyric acid (GABA) agonist muscimol (10 ng/site) was bilaterally microinjected into both the VLPA and VLDA to inhibit neuronal activity at these sites. In one group of experiments, muscimol was microinjected first into the VLPA and then into the VLDA. Following muscimol microinjection in the VLPA the mean arterial pressure (MAP) and heart rate (HR) decreased to 40 ± 6 mm Hg and 310 ± 21 beats/min (bpm) from a control level of 90 ± 3 mm Hg and 403 ± 23 bpm. Subsequent microinjection of muscimol in the VLDA had no significant effect on BP or HR. This lack of response was not due to severe fall in BP caused by microinjection of muscimol into the VLPA. In the second group of experiments muscimol was first injected into the VLDA followed by muscimol microinjection into the VLPA. In the VLDA muscimol significantly increased MAP and HR to 139 ± 4 mm Hg and 427 ± 4 bpm from a control level of 87 ± 2 mm Hg and 356 ± 23 bpm. The aortic depressor nerve response (-37 ± 1 mm Hg and -47 ± 4 bpm) was converted to an aortic 'pressor' response (+20 ± 1 mm Hg and -13 ± 6 bpm). Subsequent microinjection of muscimol into the VLPA caused MAP and HR to fall to 43 ± 5 mm Hg and 338 ± 17 bpm. The aortic 'pressor' response was also abolished (2 ± 2 mm Hg). These results indicate that neuronal activity in the rostral VLPA is an important determinant for changes in BP and its reflex regulation mediated by the VLDA. However, BP changes mediated by the rostral VLPA are independent of the level of neuronal activity in the VLDA. Sites of VLPA and VLDA interaction are discussed.

Original languageEnglish (US)
Pages (from-to)169-174
Number of pages6
JournalBrain research
Volume321
Issue number1
DOIs
StatePublished - Oct 29 1984

Fingerprint

Muscimol
Blood Pressure
Microinjections
Heart Rate
Arterial Pressure
GABA Agonists
Aminobutyrates
Urethane
Reflex
Neurons

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Developmental Biology
  • Clinical Neurology

Cite this

Willette, R. N. ; Punnen, S. ; Krieger, A. J. ; Sapru, Hreday. / Interdependence of rostral and caudal ventrolateral medullary areas in the control of blood pressure. In: Brain research. 1984 ; Vol. 321, No. 1. pp. 169-174.
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abstract = "Pharmacologic experiments were carried out to test the degree of interdependence of rostral vasopressor and caudal vasodepressor neuron pools in the ventrolateral medulla (VLPA and VLDA, respectively). In two groups of urethane-anesthetized rats, the γ-aminobutyric acid (GABA) agonist muscimol (10 ng/site) was bilaterally microinjected into both the VLPA and VLDA to inhibit neuronal activity at these sites. In one group of experiments, muscimol was microinjected first into the VLPA and then into the VLDA. Following muscimol microinjection in the VLPA the mean arterial pressure (MAP) and heart rate (HR) decreased to 40 ± 6 mm Hg and 310 ± 21 beats/min (bpm) from a control level of 90 ± 3 mm Hg and 403 ± 23 bpm. Subsequent microinjection of muscimol in the VLDA had no significant effect on BP or HR. This lack of response was not due to severe fall in BP caused by microinjection of muscimol into the VLPA. In the second group of experiments muscimol was first injected into the VLDA followed by muscimol microinjection into the VLPA. In the VLDA muscimol significantly increased MAP and HR to 139 ± 4 mm Hg and 427 ± 4 bpm from a control level of 87 ± 2 mm Hg and 356 ± 23 bpm. The aortic depressor nerve response (-37 ± 1 mm Hg and -47 ± 4 bpm) was converted to an aortic 'pressor' response (+20 ± 1 mm Hg and -13 ± 6 bpm). Subsequent microinjection of muscimol into the VLPA caused MAP and HR to fall to 43 ± 5 mm Hg and 338 ± 17 bpm. The aortic 'pressor' response was also abolished (2 ± 2 mm Hg). These results indicate that neuronal activity in the rostral VLPA is an important determinant for changes in BP and its reflex regulation mediated by the VLDA. However, BP changes mediated by the rostral VLPA are independent of the level of neuronal activity in the VLDA. Sites of VLPA and VLDA interaction are discussed.",
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Interdependence of rostral and caudal ventrolateral medullary areas in the control of blood pressure. / Willette, R. N.; Punnen, S.; Krieger, A. J.; Sapru, Hreday.

In: Brain research, Vol. 321, No. 1, 29.10.1984, p. 169-174.

Research output: Contribution to journalArticle

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T1 - Interdependence of rostral and caudal ventrolateral medullary areas in the control of blood pressure

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N2 - Pharmacologic experiments were carried out to test the degree of interdependence of rostral vasopressor and caudal vasodepressor neuron pools in the ventrolateral medulla (VLPA and VLDA, respectively). In two groups of urethane-anesthetized rats, the γ-aminobutyric acid (GABA) agonist muscimol (10 ng/site) was bilaterally microinjected into both the VLPA and VLDA to inhibit neuronal activity at these sites. In one group of experiments, muscimol was microinjected first into the VLPA and then into the VLDA. Following muscimol microinjection in the VLPA the mean arterial pressure (MAP) and heart rate (HR) decreased to 40 ± 6 mm Hg and 310 ± 21 beats/min (bpm) from a control level of 90 ± 3 mm Hg and 403 ± 23 bpm. Subsequent microinjection of muscimol in the VLDA had no significant effect on BP or HR. This lack of response was not due to severe fall in BP caused by microinjection of muscimol into the VLPA. In the second group of experiments muscimol was first injected into the VLDA followed by muscimol microinjection into the VLPA. In the VLDA muscimol significantly increased MAP and HR to 139 ± 4 mm Hg and 427 ± 4 bpm from a control level of 87 ± 2 mm Hg and 356 ± 23 bpm. The aortic depressor nerve response (-37 ± 1 mm Hg and -47 ± 4 bpm) was converted to an aortic 'pressor' response (+20 ± 1 mm Hg and -13 ± 6 bpm). Subsequent microinjection of muscimol into the VLPA caused MAP and HR to fall to 43 ± 5 mm Hg and 338 ± 17 bpm. The aortic 'pressor' response was also abolished (2 ± 2 mm Hg). These results indicate that neuronal activity in the rostral VLPA is an important determinant for changes in BP and its reflex regulation mediated by the VLDA. However, BP changes mediated by the rostral VLPA are independent of the level of neuronal activity in the VLDA. Sites of VLPA and VLDA interaction are discussed.

AB - Pharmacologic experiments were carried out to test the degree of interdependence of rostral vasopressor and caudal vasodepressor neuron pools in the ventrolateral medulla (VLPA and VLDA, respectively). In two groups of urethane-anesthetized rats, the γ-aminobutyric acid (GABA) agonist muscimol (10 ng/site) was bilaterally microinjected into both the VLPA and VLDA to inhibit neuronal activity at these sites. In one group of experiments, muscimol was microinjected first into the VLPA and then into the VLDA. Following muscimol microinjection in the VLPA the mean arterial pressure (MAP) and heart rate (HR) decreased to 40 ± 6 mm Hg and 310 ± 21 beats/min (bpm) from a control level of 90 ± 3 mm Hg and 403 ± 23 bpm. Subsequent microinjection of muscimol in the VLDA had no significant effect on BP or HR. This lack of response was not due to severe fall in BP caused by microinjection of muscimol into the VLPA. In the second group of experiments muscimol was first injected into the VLDA followed by muscimol microinjection into the VLPA. In the VLDA muscimol significantly increased MAP and HR to 139 ± 4 mm Hg and 427 ± 4 bpm from a control level of 87 ± 2 mm Hg and 356 ± 23 bpm. The aortic depressor nerve response (-37 ± 1 mm Hg and -47 ± 4 bpm) was converted to an aortic 'pressor' response (+20 ± 1 mm Hg and -13 ± 6 bpm). Subsequent microinjection of muscimol into the VLPA caused MAP and HR to fall to 43 ± 5 mm Hg and 338 ± 17 bpm. The aortic 'pressor' response was also abolished (2 ± 2 mm Hg). These results indicate that neuronal activity in the rostral VLPA is an important determinant for changes in BP and its reflex regulation mediated by the VLDA. However, BP changes mediated by the rostral VLPA are independent of the level of neuronal activity in the VLDA. Sites of VLPA and VLDA interaction are discussed.

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