scholarly journals Effect of spinal microinjections of an antagonist to substance P or somatostatin on the exercise pressor reflex.

1992 ◽  
Vol 70 (2) ◽  
pp. 213-222 ◽  
Author(s):  
L B Wilson ◽  
P T Wall ◽  
K Matsukawa ◽  
J H Mitchell
Keyword(s):  
Substance P ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

scholarly journals Substance P release in the spinal cord during the exercise pressor reflex in anaesthetized cats.

1993 ◽  
Vol 460 (1) ◽  
pp. 79-90 ◽  
Author(s):  
L B Wilson ◽  
I E Fuchs ◽  
K Matsukawa ◽  
J H Mitchell ◽  
P T Wall
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Exercise Pressor Reflex ◽  
P Release ◽  
Pressor Reflex ◽  
Substance P Release

Blockade of non-NMDA receptors attenuates reflex pressor response to static contraction

1994 ◽  
Vol 266 (5) ◽  
pp. H1769-H1776 ◽  
Author(s):  
J. M. Hill ◽  
J. G. Pickar ◽  
M. P. Kaufman
Keyword(s):  
Nmda Receptor ◽  
Substance P ◽  
Receptor Antagonist ◽  
Pressor Response ◽  
Intrathecal Injection ◽  
Ventilatory Responses ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Substance P Receptor ◽  
Pressor Reflex

Considerable evidence suggests that both substance P and glutamate play a role in the spinal transmission of the exercise pressor reflex. We tested two hypotheses. First, after a lumbosacral intrathecal injection of a glutamatergic receptor antagonist, the reflex cardiovascular and ventilatory responses to static contraction are attenuated. Second, after a lumbosacral intrathecal injection of a substance P receptor antagonist and a glutamatergic receptor antagonist, the reflex cardiovascular and ventilatory responses to static contraction are abolished. We found that 1) the reflex cardiovascular responses to static contraction were unaffected (P > 0.05) after the intrathecal injection of the N-methyl-D-aspartate (NMDA) receptor antagonists, dl-2-amino-5-phosphonopentanoate (+/- AP-5) or 3-[(+-)-2-carboxypiperazin-4-yl]propyl-1-phosphonic acid (+/- CPP); 2) the reflex pressor response to static muscular contraction was attenuated by > 50% after the intrathecal injection of the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX); and 3) the reflex pressor response to static contraction was almost abolished after the intrathecal injection of the substance P receptor antagonist, CP-96,345, and CNQX. Our results suggest that substance P and glutamate are two neurotransmitters involved in the spinal transmission of the exercise pressor reflex and that substance P and glutamate exert their effects via neurokinin-1 (NK-1) and non-NMDA receptors, respectively.

Exercise Pressor Reflex is Altered in Korean Obese Children

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 454
Author(s):  
Kwang-IL Kim ◽  
Hyun-Min Choi ◽  
Joon-Hee Lee ◽  
Jong-Mok Chun ◽  
Woo-Ram Han ◽  
...  
Keyword(s):  
Obese Children ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

scholarly journals Mechanoreflex Mediates the Exaggerated Exercise Pressor Reflex in Heart Failure

Circulation ◽  
2005 ◽  
Vol 112 (15) ◽  
pp. 2293-2300 ◽  
Author(s):  
Scott A. Smith ◽  
Jere H. Mitchell ◽  
R. Haris Naseem ◽  
Mary G. Garry
Keyword(s):  
Heart Failure ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

scholarly journals Chronic femoral artery ligation exaggerates the pressor and sympathetic nerve responses during dynamic skeletal muscle stretch in decerebrate rats

2018 ◽  
Vol 314 (2) ◽  
pp. H246-H254 ◽  
Author(s):  
Evan A. Kempf ◽  
Korynne S. Rollins ◽  
Tyler D. Hopkins ◽  
Alec L. Butenas ◽  
Joseph M. Santin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Peripheral Artery Disease ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Artery ◽  
Nerve Activity ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Artery Disease ◽  
Dynamic Stretch

Mechanical and metabolic signals arising during skeletal muscle contraction reflexly increase sympathetic nerve activity and blood pressure (i.e., the exercise pressor reflex). In a rat model of simulated peripheral artery disease in which a femoral artery is chronically (~72 h) ligated, the mechanically sensitive component of the exercise pressor reflex during 1-Hz dynamic contraction is exaggerated compared with that found in normal rats. Whether this is due to an enhanced acute sensitization of mechanoreceptors by metabolites produced during contraction or involves a chronic sensitization of mechanoreceptors is unknown. To investigate this issue, in decerebrate, unanesthetized rats, we tested the hypothesis that the increases in mean arterial blood pressure and renal sympathetic nerve activity during 1-Hz dynamic stretch are larger when evoked from a previously “ligated” hindlimb compared with those evoked from the contralateral “freely perfused” hindlimb. Dynamic stretch provided a mechanical stimulus in the absence of contraction-induced metabolite production that closely replicated the pattern of the mechanical stimulus present during dynamic contraction. We found that the increases in mean arterial blood pressure (freely perfused: 14 ± 1 and ligated: 23 ± 3 mmHg, P = 0.02) and renal sympathetic nerve activity were significantly greater during dynamic stretch of the ligated hindlimb compared with the increases during dynamic stretch of the freely perfused hindlimb. These findings suggest that the exaggerated mechanically sensitive component of the exercise pressor reflex found during dynamic muscle contraction in this rat model of simulated peripheral artery disease involves a chronic sensitizing effect of ligation on muscle mechanoreceptors and cannot be attributed solely to acute contraction-induced metabolite sensitization. NEW & NOTEWORTHY We found that the pressor and sympathetic nerve responses during dynamic stretch were exaggerated in rats with a ligated femoral artery (a model of peripheral artery disease). Our findings provide mechanistic insights into the exaggerated exercise pressor reflex in this model and may have important implications for peripheral artery disease patients.

scholarly journals Thromboxane A 2 Receptors Contribute to the Exaggerated Exercise Pressor Reflex in Rats with Heart Failure

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Alec Butenas ◽  
Korynne Rollins ◽  
Auni Williams ◽  
Stephen Hammond ◽  
Carl Ade ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

The mammalian exercise pressor reflex in health and disease

2005 ◽  
Vol 91 (1) ◽  
pp. 89-102 ◽  
Author(s):  
Scott A. Smith ◽  
Jere H. Mitchell ◽  
Mary G. Garry
Keyword(s):  
Exercise Pressor Reflex ◽  
Health And Disease ◽  
Pressor Reflex

scholarly journals Both central command and exercise pressor reflex activate cardiac sympathetic nerve activity in decerebrate cats

2009 ◽  
Vol 296 (4) ◽  
pp. H1157-H1163 ◽  
Author(s):  
Hirotsugu Tsuchimochi ◽  
Shawn G. Hayes ◽  
Jennifer L. McCord ◽  
Marc P. Kaufman
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventral Root ◽  
Central Command ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Exercise Pressor Reflex ◽  
Cardiac Sympathetic Nerve Activity ◽  
Pressor Reflex ◽  
Decerebrate Cats

Both static and dynamic exercise are known to increase cardiac pump function as well as arterial blood pressure. Feedforward control by central command and feedback control by the exercise pressor reflex are thought to be the neural mechanisms causing these effects during exercise. It remains unknown as to how each mechanism activates cardiac sympathetic nerve activity (CSNA) during exercise, especially at its onset. Thus we examined the response of CSNA to stimulation of the mesencephalic locomotor region (MLR, i.e., central command) and to static muscle contraction of the triceps surae muscles or stretch of the calcaneal tendon in decerebrate cats. We found that MLR stimulation immediately increased CSNA, which was followed by a gradual increase in heart rate, mean arterial pressure, and ventral root activity in a stimulus intensity-dependent manner. The latency of the increase in CSNA from the onset of MLR stimulation ranged from 67 to 387 ms. Both static contraction and tendon stretch also rapidly increased CSNA. Their latency from the development of tension in response to ventral root stimulation ranged from 78 to 670 ms. These findings suggest that both central command and the muscle mechanoreflex play a role in controlling cardiac sympathetic outflow at the onset of exercise.

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