Role played by P2X and P2Y receptors in evoking the muscle chemoreflex

2008 ◽  
Vol 104 (2) ◽  
pp. 538-541 ◽  
Author(s):  
Shawn G. Hayes ◽  
Jennifer L. McCord ◽  
Marc P. Kaufman
Keyword(s):  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
P2y Receptors ◽  
Muscle Afferents ◽  
Thin Fiber ◽  
P2x And P2y Receptors ◽  
Pressor Responses ◽  
Shed Light ◽  
Muscle Chemoreflex

The role played by purinergic 2Y receptors in evoking the muscle chemoreflex is not well defined. To shed light on this issue, we compared the pressor responses with popliteal arterial injection of UTP (1 mg/kg), a selective P2Y agonist, with those to popliteal arterial injection of ATP (1 mg/kg), a P2X and P2Y agonist, and to α,β-methylene ATP (50 μg/kg), a selective P2X1 and P2X3 agonist, in decerebrate unanesthetized cats. We found that injection of ATP and α,β-methylene ATP increased mean arterial pressure by 19 ± 2 and 15 ± 4 mmHg, whereas UTP had no affect on arterial pressure. In addition, the pressor responses to injection of ATP and α,β-methylene ATP were abolished by section of the sciatic nerve, demonstrating that they were reflex in origin. We conclude that P2Y receptors on thin fiber muscle afferents play no role in evoking the muscle chemoreflex.

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

The contribution of muscarinic-receptor-mediated responses to epineurial vascular diameter at the sciatic nerve

2018 ◽  
Vol 96 (8) ◽  
pp. 855-858
Author(s):  
Chelsa Killey ◽  
Shane Cleary ◽  
Julie Orr ◽  
Jefferson C. Frisbee ◽  
Dwayne Jackson ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Muscarinic Receptor ◽  
Topical Application ◽  
Rat Model ◽  
Receptor Agonist ◽  
Vessel Diameter ◽  
Anaesthetized Rat ◽  
Baseline Diameter

This study used an anaesthetized rat model to directly observe changes in diameter of the vessels supplying the sciatic nerve in response to acetylcholine (10−4 M), a muscarinic receptor agonist, and atropine (10−5 M), a muscarinic receptor antagonist. Topical application of acetylcholine resulted in increases in vessel diameter (baseline: 22.0 ± 2.5 μm, acetylcholine: 28.8 ± 3.3 μm), while topical application of atropine resulted in a decrease in diameter (baseline: 26.6 ± 3.2 μm, atropine: 15.5 ± 3.6 μm) of the epineurial vessels. Mean arterial pressure was not affected by either acetylcholine (baseline: 103.8 ± 1.8 mm Hg, acetylcholine: 102.8 ± 3.2 mm Hg) or atropine (baseline: 104.0 ± 1.9 mm Hg, atropine: 105.2 ± 2.2 mm Hg). These data suggest that muscarinic-receptor-mediated responses can affect the diameter of the epineurial vessels at the sciatic nerve. In addition, muscarinic-receptor-mediated responses appear to contribute to baseline diameter of epineurial vessels at the sciatic nerve.

Attenuation of reflex pressor and ventilatory responses to static muscular contraction by intrathecal opioids

1990 ◽  
Vol 68 (6) ◽  
pp. 2466-2472 ◽  
Author(s):  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Opioid Peptides ◽  
Intrathecal Injection ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Reflex Responses ◽  
Ventilatory Responses ◽  
Static Contraction

We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 micrograms in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 +/- 5 (SE) mmHg and 227 +/- 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 +/- 5 mmHg and 37 +/- 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P less than 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid mu- or delta-receptor attenuated the reflex responses to static contraction. Naloxone (1,000 micrograms), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.

Participation of alpha 2-adrenergic receptors in neural vascular tone of canine skeletal muscle

1992 ◽  
Vol 262 (6) ◽  
pp. H1705-H1710 ◽  
Author(s):  
P. Kubes ◽  
M. Melinyshyn ◽  
K. Nesbitt ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Adrenergic Receptors ◽  
Receptor Agonist ◽  
Vascular Tone ◽  
Adrenergic Blockade ◽  
Adrenergic Blockers

Studies were carried out in anesthetized, paralyzed, and ventilated dogs to determine whether postsynaptic alpha 2-adrenergic receptors participated in neurally mediated vascular tone in skeletal muscle. Hindlimb skeletal muscle resistance (RL) and blood flow (QL) were determined before, during, and after reversible cold block of the sciatic nerve. This sequence of observations was repeated 30 min after blockade of alpha 1-adrenergic receptors with prazosin. Then the alpha 2-adrenergic receptors were blocked with yohimbine, and the nerve cold block was repeated. When the sciatic nerve was cold blocked before alpha 1-adrenergic blockade, RL decreased approximately 50% and QL increased 75% (P less than 0.05) and then returned to control when the nerve was rewarmed. After alpha 1-block 76% of neural tone remained as assessed by nerve cooling (P less than 0.05). This phenomenon occurred despite effective alpha 1-adrenergic blockade as assessed by the alpha 1-receptor agonist methoxamine. With alpha 1- plus alpha 2-block no change in RL or QL was seen with nerve cold block. The same protocol was repeated in a second series of animals, but mean arterial pressure, which fell after alpha 1-block in the group above, was maintained by dextran infusion at normotensive levels. In these animals, 40% of neural tone remained after alpha 1-block. Both alpha 1- and alpha 2-adrenergic blockers were again needed to abolish the QL and RL response to nerve cold block. In another series of animals, yohimbine was administered before prazosin. In this series, alpha 2-adrenergic blockade greatly reduced neural tone as assessed by nerve cooling.(ABSTRACT TRUNCATED AT 250 WORDS)

Fluid volumes and pressor responsiveness in two-kidney rabbits with renal artery stenosis

1982 ◽  
Vol 243 (5) ◽  
pp. H779-H787 ◽  
Author(s):  
J. A. Johnson ◽  
K. D. Kurz ◽  
S. Siripaisarnpipat ◽  
D. W. Zeigler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Body Fluid ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Control Group ◽  
Ang Ii ◽  
Pressor Responses

This study examined body fluid volumes, the pressor responses to norepinephrine (NE), and the cardiovascular responses to NE before and during infusion of an angiotensin II (ANG II) antagonist in two-kidney rabbits with unilateral renal artery stenosis (RAS) of 3 and 30 day duration. Three separate experiments were performed. In the first experiment, plasma volume, extracellular fluid volume, and total body water were measured by the distribution volumes of radioiodinated serum albumin, 35SO4, and tritiated water, respectively. No differences were seen for any of these volumes between the 3- or 30-day RAS rabbits and their controls. In the second experiment, pressor responses to infusions of several doses of NE were examined; rabbits with 3- and 30-day RAS had exaggerated pressor responses to all doses of NE when compared with the control rabbits. In the third experiment, infusion of NE at 800 ng.min-1.kg body wt-1 resulted in more pronounced increases in mean arterial pressure and total peripheral resistance (TPR) in the 3- and 30-day RAS rabbits than in the controls; after infusion of [Sar1-Ile8] ANG II the increases in mean arterial pressure and TPR during NE infusion were blunted and were of the same magnitude as in the control group. In all experiments the 30-day RAS rabbits were hypertensive, whereas the 3-day RAS rabbits were normotensive; also, plasma renin activity (PRA) values were normal in both the 3- and 30-day RAS groups. These studies demonstrated that increases in body fluid volumes are not necessary for pressor and vascular hyperresponsiveness probably is mediated by ANG II, despite normal PRA values.

Angiotensin II mediates uterine vasoconstriction through α-stimulation

2004 ◽  
Vol 287 (1) ◽  
pp. H126-H134 ◽  
Author(s):  
Blair E. Cox ◽  
Timothy A. Roy ◽  
Charles R. Rosenfeld
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Pressor Responses ◽  
Adrenergic Activation

Intravenous angiotensin II (ANG II) increases uterine vascular resistance (UVR), whereas uterine intra-arterial infusions do not. Type 2 ANG II (AT2) receptors predominate in uterine vascular smooth muscle; this may reflect involvement of systemic type 1 ANG II (AT1) receptor-mediated α-adrenergic activation. To examine this, we compared systemic pressor and UVR responses to intravenous phenylephrine and ANG II without and with systemic or uterine α-receptor blockade and in the absence or presence of AT1 receptor blockade in pregnant and nonpregnant ewes. Systemic α-receptor blockade inhibited phenylephrine-mediated increases in mean arterial pressure (MAP) and UVR, whereas uterine α-receptor blockade alone did not alter pressor responses and resulted in proportionate increases in UVR and MAP. Although neither systemic nor uterine α-receptor blockade affected ANG II-mediated pressor responses, UVR responses decreased >65% and also were proportionate to increases in MAP. Systemic AT1 receptor blockade inhibited all responses to intravenous ANG II. In contrast, uterine AT1 receptor blockade + systemic α-receptor blockade resulted in persistent proportionate increases in MAP and UVR. Uterine AT2 receptor blockade had no effects. We have shown that ANG II-mediated pressor responses reflect activation of systemic vascular AT1 receptors, whereas increases in UVR reflect AT1 receptor-mediated release of an α-agonist and uterine autoregulatory responses.

Role of cardiac output in the pressor responses to graded muscle ischemia in man

1978 ◽  
Vol 45 (4) ◽  
pp. 574-580 ◽  
Author(s):  
F. Bonde-Petersen ◽  
L. B. Rowell ◽  
R. G. Murray ◽  
G. G. Blomqvist ◽  
R. White ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Total Occlusion ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Leg Exercise

Ten men repeatedly performed leg exercise (100–150 W) for 7 min with 30-min recovery periods interspersed. Both legs were made ischemic by total occlusion (OCCL), first for 3 min immediately after exercise and second for 30 s before exercise ended and 3 min into recovery. In addition legs were occluded for 3 min at rest (seated). OCCL at rest increased mean arterial pressure (MAP) by 9 Torr but did not affect cardiac output (CO) or heart rate (HR). OCCL at the end of exercise significantly raised MAP and HR above control values during 3-min recovery but CO was unaffected. OCCL 30 s before the end of exercise further increased MAP and HR significantly during recovery; MAP, CO, and HR were significantly increased above control values (CO by 2.1 1-min-1) during the 3rd min of recovery. We conclude that a strong reflex from ischemic legs maintains normal or elevated CO during leg OCCL. Thus CO was too high relative to total vascular conductance so that MAP was elevated.

Bradykinin contributes to the exercise pressor reflex: mechanism of action

1993 ◽  
Vol 75 (5) ◽  
pp. 2061-2068 ◽  
Author(s):  
H. L. Pan ◽  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Left Ventricular Pressure ◽  
Muscle Afferents ◽  
Left Ventricular ◽  
Receptor Blockade ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Over Time

This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 microgram of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 micrograms/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abolished by kinin B2-receptor blockade. Similar injection of the kinin B1-receptor agonist des-Arg9-bradykinin caused no cardiovascular responses (n = 6). In eight different animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses to 30 s of electrically stimulated hindlimb contraction were attenuated by 50 +/- 6, 55 +/- 7, and 41 +/- 8%, respectively, after kinin B2-receptor blockade. In eight other animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses were reduced by 58 +/- 8, 66 +/- 6, and 40 +/- 12%, respectively, after inhibition of prostaglandin synthesis with indomethacin (2.5–3 mg/kg iv) and were then abolished by subsequent B2-receptor blockade. These data suggest that bradykinin contributes to the exercise pressor reflex through its action on kinin B2 receptors located on the nerve endings of the muscle afferents.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressor responses to vasopressin in rabbits with 3-day renal artery stenosis

1981 ◽  
Vol 240 (6) ◽  
pp. H862-H867 ◽  
Author(s):  
J. A. Johnson ◽  
S. Ichikawa ◽  
K. D. Kurz ◽  
W. L. Fowler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Vasopressin Infusion ◽  
Pressor Responses

One-kidney rabbits were subjected to renal artery stenosis, and acute experiments were performed 3 days later on conscious animals; one-kidney rabbits without renal artery stenosis served as controls. Rabbits with 3-day renal artery stenosis were normotensive and had normal values for plasma renin activity. Intravenous infusion of arginine vasopressin at 5 mU.min-1.kg body wt-1 for 5 min resulted in a significantly (P less than 0.01) greater increase in mean arterial pressure and total peripheral resistance (TPR) in the renal artery stenosis rabbits than in the controls. Infusion of the angiotensin II (AII) competitive antagonist, [Sar1, Ile8]AII, before the vasopressin infusion abolished the hyperresponsiveness to vasopressin in the renal artery stenosis rabbits and resulted in changes in mean arterial pressure and TPR that were approximately of the same magnitude as the controls. Infusion of [SAr1, Ile8]AII before vasopressin infusion in control rabbits did not alter the cardiovascular responses to vasopressin. Because previous studies have shown that 3-day renal artery stenosis rabbits have exaggerated pressor responses to norepinephrine and that this hyperresponsiveness to norepinephrine is blocked by [Sar1, Ile8]-AII, the present study with vasopressin provided evidence that the increased responsiveness in this model is not specific for a single pressor agent. These studies also demonstrated that AII plays an important role in mediating the exaggerated pressor responses to vasopressin in this prehypertensive model.

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses

1991 ◽  
Vol 70 (1) ◽  
pp. 77-86 ◽  
Author(s):  
S. N. Hussain ◽  
A. Chatillon ◽  
A. Comtois ◽  
C. Roussos ◽  
S. Magder
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Chemical Activation ◽  
Cardiovascular Responses ◽  
Arterial Flow ◽  
Aortic Blood Flow ◽  
Thin Fiber ◽  
The Right

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

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