Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits

1994 ◽  
Vol 77 (5) ◽  
pp. 2449-2455 ◽  
Author(s):  
L. B. Wilson ◽  
C. K. Dyke ◽  
J. A. Pawelczyk ◽  
P. T. Wall ◽  
J. H. Mitchell
Keyword(s):  
Blood Pressure ◽  
Muscle Contraction ◽  
Arterial Blood Pressure ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Subsequent Increase ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Blood Pressure Responses

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

Activation of Spinobulbar Lamina I Neurons by Static Muscle Contraction

2002 ◽  
Vol 87 (3) ◽  
pp. 1641-1645 ◽  
Author(s):  
L. B. Wilson ◽  
D. Andrew ◽  
A. D. Craig
Keyword(s):  
Muscle Contraction ◽  
Small Diameter ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Ventrolateral Medulla ◽  
Antidromic Activation ◽  
Lamina I ◽  
Arterial Blood ◽  
Autonomic Reflexes ◽  
Blood Pressure Responses

Spinal lamina I neurons are selectively activated by small-diameter somatic afferents, and they project to brain stem sites that are critical for homeostatic control. Because small-diameter afferent activity evoked by contraction of skeletal muscle reflexly elicits exercise-related cardiorespiratory activation, we tested whether spinobulbar lamina I cells respond to muscle contraction. Spinobulbar lamina I neurons were identified in chloralose-anesthetized cats by antidromic activation from the ipsilateral caudal ventrolateral medulla. Static contractions of the ipsilateral triceps surae muscle were evoked by tibial nerve stimulation using parameters that avoid afferent activation, and arterial blood pressure responses were recorded. Recordings were maintained from 13 of 17 L7 lamina I spinobulbar neurons during static muscle contraction, and 5 of these neurons were excited. Three were selectively activated only by muscle afferents and did not have a cutaneous receptive field. Spinobulbar lamina I neurons activated by muscle contraction provide an ascending link for the reflex cardiorespiratory adjustments that accompany muscular work. This study provides an important first step in elucidating an ascending afferent pathway for somato-autonomic reflexes.

scholarly journals Influence of endurance training on central sympathetic outflow to skeletal muscle in response to a mixed meal

2010 ◽  
Vol 108 (4) ◽  
pp. 882-890 ◽  
Author(s):  
Colin N. Young ◽  
Shekhar H. Deo ◽  
Areum Kim ◽  
Masahiro Horiuchi ◽  
Catherine R. Mikus ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endurance Training ◽  
Arterial Blood Pressure ◽  
Plasma Insulin ◽  
Muscle Sympathetic Nerve Activity ◽  
Insulin Response ◽  
Sympathetic Outflow ◽  
Mixed Meal ◽  
Arterial Blood ◽  
Central Sympathetic Outflow

Nutrient intake is accompanied by increases in central sympathetic outflow, a response that has been mainly attributed to insulin. Insulin-mediated sympathoexcitation appears to be blunted in insulin-resistant conditions, suggesting that aside from peripheral insulin insensitivity, such conditions may also impair the central action of insulin in mediating sympathetic activation. What remains unclear is whether an insulin-sensitive state, such as that induced by chronic endurance training, alters the central sympathetic effects of insulin during postprandial conditions. To examine this question plasma insulin and glucose, muscle sympathetic nerve activity (MSNA), heart rate, and arterial blood pressure were measured in 11 high-fit [HF; peak oxygen uptake (V̇o2peak) 65.9 ± 1.4 ml·kg−1·min−1] and 9 average-fit (AF; V̇o2peak 43.6 ± 1.3 ml·kg−1·min−1) male subjects before and for 120 min after ingestion of a mixed meal drink. As expected, the insulin response to meal ingestion was lower in HF than AF participants (insulin area under the curve0–120: 2,314 ± 171 vs. 4,028 ± 460 μIU·ml−1·120−1, HF vs. AF, P < 0.05), with similar plasma glucose responses between groups. Importantly, following consumption of the meal, the HF subjects demonstrated a greater rise in MSNA compared with the AF subjects (e.g., 120 min: Δ21 ± 1 vs. 8 ± 3 bursts/100 heart beats, HF vs. AF, P < 0.05). Furthermore, when expressed relative to plasma insulin, HF subjects exhibited a greater change in MSNA for any given change in insulin. Arterial blood pressure responses following meal intake were similar between groups. Collectively, these data suggest that, in addition to improved peripheral insulin sensitivity, endurance training may enhance the central sympathetic effect of insulin to increase MSNA following consumption of a mixed meal.

scholarly journals Arterial Blood Pressure Responses to Cell-free Hemoglobin Solutions and the Reaction with Nitric Oxide

1998 ◽  
Vol 273 (20) ◽  
pp. 12128-12134 ◽  
Author(s):  
Ronald J. Rohlfs ◽  
Eric Bruner ◽  
Albert Chiu ◽  
Armando Gonzales ◽  
Maria L. Gonzales ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Free Hemoglobin ◽  
Arterial Blood ◽  
Blood Pressure Responses

scholarly journals Drinking and arterial blood pressure responses to ANG II in young and old rats

2010 ◽  
Vol 299 (5) ◽  
pp. R1135-R1141 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Ang Ii ◽  
Middle Aged ◽  
Reduced Pressure ◽  
Water Drinking ◽  
Young Rats ◽  
Arterial Blood ◽  
Old Rats ◽  
Blood Pressure Responses

We investigated water drinking and arterial blood pressure responses to intravenous infusions of ANG II in young (4 mo), middle-aged adult (12 mo), and old (29 mo) male Brown Norway rats. Infusions of ANG II began with arterial blood pressure either at control levels or at reduced levels following injection of the vasodilator minoxidil. Under control conditions, mean arterial pressure (MAP) in response to ANG II rose to the same level for all groups, and middle-aged and old rats drank as much or more water in response to ANG II compared with young rats, depending on whether intakes were analyzed using absolute or body weight-adjusted values. When arterial blood pressure first was reduced with minoxidil, MAP in response to ANG II stabilized at significantly lower levels compared with control conditions for all groups. Young rats drank significantly more water under reduced pressure conditions compared with control conditions, while middle-aged and old rats did not. Urine volume in response to ANG II was lower, while water balance was higher, under conditions of reduced pressure compared with control conditions. Baroreflex control of heart rate was substantially reduced in old rats compared with young and middle-aged animals. In summary, young rats appear to be more sensitive to the inhibitory effects of increased arterial blood pressure on water drinking than are older animals.

S  (+)-Ketamine Increases Muscle Sympathetic Activity and Maintains the Neural Response to Hypotensive Challenges in Humans

2001 ◽  
Vol 94 (2) ◽  
pp. 252-258 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Goran Pavlakovic ◽  
Martin C. Michel ◽  
Jürgen Peters
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Concentration ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Outflow ◽  
Arterial Blood ◽  
Ketamine Anesthesia

Background S(+)-Ketamine is reported to exert twofold greater analgesic and hypnotic effects but a shorter recovery time in comparison with racemic ketamine, indicating possible differential effects of stereoisomers. However, cardiovascular regulation during S(+)-ketamine anesthesia has not been studied. Muscle sympathetic activity (MSA) may be an indicator of the underlying alterations of sympathetic outflow. Whether S(+)-ketamine decreases MSA in a similar manner as the racemate is not known. Thus, the authors tested the hypothesis that S(+)-ketamine changes MSA and the muscle sympathetic response to a hypotensive challenge. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy participants before and during anesthesia with S(+)-ketamine (670 microg/kg intravenously followed by 15 microg x kg(-1) x min(-1)). Catecholamine and ketamine plasma concentrations, heart rate, and arterial blood pressure were also determined. MSA responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 microg/kg) before and during S(+)-ketamine anesthesia. In the final step, increased arterial pressure observed during anesthesia with S(+)-ketamine was adjusted to preanesthetic values by sodium nitroprusside infusion (1-6 microg x kg(-1) x min(-1)). Results Anesthesia with S(+)-ketamine (ketamine plasma concentration 713 +/- 295 microg/l) significantly increased MSA burst frequency (mean +/- SD; 18 +/- 6 to 35 +/- 11 bursts/min) and burst incidence (32 +/- 10 to 48 +/- 15 bursts/100 heartbeats) and was associated with a doubling of norepinephrine plasma concentration (from 159 +/- 52 to 373 +/- 136 pg/ml) parallel to the increase in MSA. Heart rate and arterial blood pressure also significantly increased. When increased arterial pressure during S(+)-ketamine was decreased to awake values with sodium nitroprusside, MSA increased further (to 53 +/- 24 bursts/min and 60 +/- 20 bursts/100 heartbeats, respectively). The MSA increase in response to the hypotensive challenge was fully maintained during anesthesia with S(+)-ketamine. Conclusions S(+)-Ketamine increases efferent sympathetic outflow to muscle. Despite increased MSA and arterial pressure during S(+)-ketamine anesthesia, the increase in MSA in response to arterial hypotension is maintained.

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