Intrathecal bombesin is sympathoexcitatory and pressor in rat

2011 ◽  
Vol 301 (5) ◽  
pp. R1486-R1494 ◽  
Author(s):  
Branimir Zogovic ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Phrenic Nerve ◽  
Nerve Activity ◽  
Thoracic Spinal Cord ◽  
Phrenic Nerve Activity ◽  
Amino Acid Peptide ◽  
Arterial Blood ◽  
Thoracic Spinal

Bombesin, a 14 amino-acid peptide, is pressor when administered intravenously in rat and pressor and sympathoexcitatory when applied intracerebroventricularly. To determine the spinal effects of bombesin, the peptide was administered acutely in the intrathecal space at around thoracic spinal cord level six of urethane-anesthetized, paralyzed, and bilaterally vagotomized rats. Blood pressure, heart rate, splanchnic sympathetic nerve activity (sSNA), phrenic nerve activity, and end-tidal CO2 were monitored to evaluate changes in the cardiorespiratory systems. Bombesin elicited a long-lasting excitation of sSNA associated with an increase in blood pressure and tachycardia. There was a mean increase in arterial blood pressure of 52 ± 5 mmHg (300 μM; P < 0.01). Heart rate and sSNA also increased by 40 ± 4 beats/min ( P < 0.01) and 162 ± 33% ( P < 0.01), respectively. Phrenic nerve amplitude (PNamp, 73 ± 8%, P < 0.01) and phrenic expiratory period (+0.16 ± 0.02 s, P < 0.05) increased following 300 μM bombesin. The gain of the sympathetic baroreflex increased from −2.8 ± 0.7 to −5.4 ± 0.9% ( P < 0.01), whereas the sSNA range was increased by 99 ± 26% ( P < 0.01). During hyperoxic hypercapnia (10% CO2 in O2, 90 s), bombesin potentiated the responses in heart rate (−25 ± 5 beats/min, P < 0.01) and sSNA (+136 ± 29%, P < 0.001) but reduced PNamp (from 58 ± 6 to 39 ± 7%, P < 0.05). Finally, ICI-216,140 (1 mM), an in vivo antagonist for the bombesin receptor 2, attenuated the effects of 300 μM bombesin on blood pressure (21 ± 7 mmHg, P < 0.01). We conclude that bombesin is sympathoexcitatory at thoracic spinal segments. The effect on phrenic nerve activity may the result of spinobulbar pathways and activation of local motoneuronal pools.

Role of the ventral surface of medulla in the generation of Mayer waves

1989 ◽  
Vol 257 (4) ◽  
pp. R804-R809 ◽  
Author(s):  
M. A. Haxhiu ◽  
E. van Lunteren ◽  
E. C. Deal ◽  
N. S. Cherniack
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Phrenic Nerve ◽  
Pressure Oscillation ◽  
Nerve Activity ◽  
Intermediate Area ◽  
Mayer Waves ◽  
Phrenic Nerve Activity ◽  
Arterial Blood ◽  
Cyclic Changes

The regions adjacent to the ventrolateral medullary surface (VMS) play critical roles in the regulation of respiratory and cardiovascular function. Furthermore, these areas seem to be important sites for the integration of afferent inputs from certain sensory organs and the source of excitatory inputs to preganglionic sympathetic and parasympathetic neurons. To determine whether the VMS contributes to the generation of nonrespiratory-related periodic oscillations of arterial blood pressure (Mayer waves), excitatory substances, such as N-methyl-D-aspartate (NMDA), cholinergic agonists, and neuropeptides (substance P, neurokinin A, neurotensin), were applied topically to the intermediate area of VMS in anesthetized cats. In addition, the effects of application of lidocaine and inhibitory substances (benzodiazepines) on Mayer waves were studied. After application of excitatory substances to the VMS, we observed oscillations of arterial blood pressure, recurring with a period of 17.8 +/- 10 (SE) s, which had similar characteristics as the Mayer waves recorded during hypercapnia or hypoxia. In addition, cyclic changes in phrenic nerve activity and tracheal tone occurred with the same periodicity as arterial blood pressure oscillation. Application of lidocaine or benzodiazepines on the intermediate area of the VMS abolished Mayer waves observed during hypercapnia, hypoxia, or application of excitatory substances. These findings show for the first time that the VMS can be considered as one of several synaptic relays involved in the generation of arterial blood pressure oscillation, as well as the cyclic changes in phrenic nerve activity and tracheal smooth muscle tone that occur simultaneously.

Chemical activation of group I and II muscle afferents has no cardiorespiratory effects

1984 ◽  
Vol 56 (5) ◽  
pp. 1223-1228 ◽  
Author(s):  
T. G. Waldrop ◽  
K. J. Rybicki ◽  
M. P. Kaufman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Phrenic Nerve ◽  
Gastrocnemius Muscle ◽  
Chemical Activation ◽  
Muscle Afferents ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Cardiorespiratory Function ◽  
Group I

Although stimulation of group III and IV muscle afferents is known to cause reflex changes in cardiorespiratory function, it has not been resolved whether group I and II afferents contribute to this reflex activation. Therefore, we measured the effects of intra-arterial nonparalyzing doses of succinylcholine (50–100 micrograms/kg) on the firing of muscle afferents from the gastrocnemius muscle in one group of cats, and heart rate, blood pressure, and integrated phrenic nerve activity in a second group of cats. In nonparalyzed cats, succinylcholine injections caused muscular fasciculations and firing of all four groups of muscle afferents. However, succinylcholine stimulated only group I and II afferents after paralysis with gallamine triethiodide. Succinylcholine caused increases in blood pressure, heart rate, and phrenic nerve activity before paralysis. After paralysis, succinylcholine had no effects on any of the cardiorespiratory measures. We conclude that activation of only group I and II afferent fibers from the gastrocnemius muscle has no reflex effects on blood pressure, heart rate, or phrenic nerve activity. These afferents, therefore, are unlikely to play a role in increasing cardiorespiratory function during exercise.

Measurement of sympathetic nerve activity in the unanesthetized rat

1989 ◽  
Vol 67 (1) ◽  
pp. 250-255 ◽  
Author(s):  
J. P. Fluckiger ◽  
G. Gremaud ◽  
B. Waeber ◽  
A. Kulik ◽  
A. Ichino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Reduction ◽  
Response Curves ◽  
Nerve Activity ◽  
Dose Dependent

A new system was developed in our laboratory to continuously monitor intra-arterial pressure, heart rate, and sympathetic nerve activity in unanesthetized rats. The animals were prepared 24 h before the start of the experiments. Sympathoneural traffic was measured at the level of splanchnic nerve. The amplitude of the spikes recorded at this level was utilized to express sympathetic nerve activity. The amplitude of the residual electroneurogram signal present 30 min after the rats were killed was 32 +/- 2 mV (mean +/- SE; n = 11). For analysis, these background values were subtracted from values determined in vivo. The nerve we studied contains postganglionic fibers, since electrical activity decreased in response to ganglionic blockade with pentolinium (1.25 mg/min iv for 4 min). The amplitude of spikes fell by 43 +/- 4% (n = 4). Sympathetic nerve activity was highly reproducible at a 24-h interval (104 +/- 26 vs. 111 +/- 27 mV for the amplitude of spikes; n = 11). Dose-response curves to the alpha 1-stimulant methoxamine and to bradykinin were established in four rats. The increase in blood pressure induced by methoxamine caused a dose-dependent fall in sympathetic nerve activity, whereas the blood pressure reduction resulting from bradykinin was associated with a dose-dependent activation of sympathetic drive. These data therefore indicate that it is possible with out system to accurately measure sympathetic nerve activity in the awake rat, together with intra-arterial pressure and heart rate.

Oscillations in Blood Pressure associated with Phrenic Nerve Activity

Nature ◽  
1967 ◽  
Vol 214 (5084) ◽  
pp. 206-207 ◽  
Author(s):  
NEIL S. CHERNIACK ◽  
MARK HEYMANN ◽  
JOSEPH C. CHISHOLM
Keyword(s):  
Blood Pressure ◽  
Phrenic Nerve ◽  
Nerve Activity ◽  
Phrenic Nerve Activity

Baroreflex control of muscle sympathetic nerve activity during skin surface cooling

2007 ◽  
Vol 103 (4) ◽  
pp. 1284-1289 ◽  
Author(s):  
Jian Cui ◽  
Sylvain Durand ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Skin Surface ◽  
Surface Cooling ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Arterial Blood

Skin surface cooling improves orthostatic tolerance through a yet to be identified mechanism. One possibility is that skin surface cooling increases the gain of baroreflex control of efferent responses contributing to the maintenance of blood pressure. To test this hypothesis, muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate were recorded in nine healthy subjects during both normothermic and skin surface cooling conditions, while baroreflex control of MSNA and heart rate were assessed during rapid pharmacologically induced changes in arterial blood pressure. Skin surface cooling decreased mean skin temperature (34.9 ± 0.2 to 29.8 ± 0.6°C; P < 0.001) and increased mean arterial blood pressure (85 ± 2 to 93 ± 3 mmHg; P < 0.001) without changing MSNA ( P = 0.47) or heart rate ( P = 0.21). The slope of the relationship between MSNA and diastolic blood pressure during skin surface cooling (−3.54 ± 0.29 units·beat−1·mmHg−1) was not significantly different from normothermic conditions (−2.94 ± 0.21 units·beat−1·mmHg−1; P = 0.19). The slope depicting baroreflex control of heart rate was also not altered by skin surface cooling. However, skin surface cooling shifted the “operating point” of both baroreflex curves to high arterial blood pressures (i.e., rightward shift). Resetting baroreflex curves to higher pressure might contribute to the elevations in orthostatic tolerance associated with skin surface cooling.

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

2002 ◽  
Vol 282 (1) ◽  
pp. R252-R258 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Arterial Blood ◽  
The Relationship

To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature ( P < 0.01), MSNA ( P < 0.01), heart rate ( P< 0.01), and skin blood flow ( P < 0.001), whereas mean arterial blood pressure did not change significantly ( P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (−128.3 ± 13.9 U · beats−1 · mmHg−1) was similar ( P = 0.31) with normothermia (−140.6 ± 21.1 U · beats−1 · mmHg−1). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating.

Hypoxia-mediated in vivo release of dopamine in nucleus tractus solitarii of rabbits

1991 ◽  
Vol 70 (6) ◽  
pp. 2395-2400 ◽  
Author(s):  
M. Goiny ◽  
H. Lagercrantz ◽  
M. Srinivasan ◽  
U. Ungerstedt ◽  
Y. Yamamoto
Keyword(s):  
Phrenic Nerve ◽  
High Performance ◽  
Nucleus Tractus Solitarii ◽  
Severe Hypoxia ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
In Vivo Release ◽  
Bilateral Carotid ◽  
Da Release

A wide variety of neuroactive substances have been suggested to be involved in the respiratory depression observed in response to severe hypoxia. By use of the technique of microdialysis, the release of dopamine (DA) was measured in the nucleus tractus solitarii during severe hypoxic provocations (6% O2 in N2) in the adult pentobarbital-anesthetized rabbit. DA release was analyzed by high-performance liquid chromatography with electrochemical detection. Such hypoxic provocations caused pronounced phase of depression in the phrenic nerve activity and enhanced release of DA. After bilateral carotid sinus nerve denervation, acute severe hypoxia did not give rise to enhanced release of DA or to phrenic nerve depression. Mild hypoxic (9% or 12% O2 in N2) or hypercapnic (6% CO2) stimuli resulted in an increased phrenic nerve activity without any concomitant changes in DA release. Decerebration at the midcollicular level in rabbits prevented an enhanced release of DA in the nucleus tractus solitarii during severe hypoxia. The results suggest that 1) DA is involved in the central ventilatory response to severe hypoxia, 2) not only the initial excitatory but also the second depressive phase in response to severe hypoxia is mediated partially by the peripheral chemoreceptors, and 3) the depressive phase is dependent on intact connections from suprapontine structures.

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