Abstract 434: Increased Dietary Salt Intake Enhances the Exercise Pressor Reflex

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Katsuya Yamauchi ◽  
Hirotsugu Tsuchimochi ◽  
Sean D Stocker ◽  
Marc P Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Salt Intake ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Sympathetic Responses ◽  
Stimulation Of

Increased dietary salt in rats has been shown to sensitize central sympathetic circuits and enhance sympathetic responses to several stressors, including hyperinsulinemia, intracerebroventricular injection of angiotensin and electrical stimulation of sciatic nerve afferents. These findings prompted us to test the hypothesis that increased dietary salt enhanced the exercise pressor reflex.Male Sprague-Dawley rats were fed 0.1% (n=16) or 4.0% (n=18) NaCl chow for 14-21 days. Then, rats were decerebrated and the exercise pressor reflex was produced by static contraction of the hindlimb muscles through electrical stimulation of the cut peripheral ends of the L4 and L5 ventral roots. We found that contraction produced a significantly greater increase in mean arterial pressure of rats fed 4.0% NaCl (24±2 mmHg) versus 0.1% NaCl (15±2 mmHg). Baseline mean arterial pressure was not different between 0.1% versus 4.0% NaCl diets (79±5 vs 83±4 mmHg). The tension time indices were not different between the 0.1% (17±1 kg per s) versus 4.0% (18.2±2 kg s) NaCl groups (P = 0.422). The enhanced responsiveness to contraction appeared to be attributable to sensitized group III mechanoreceptors because the renal and lumbar sympathetic responses to contraction were augmented within 200 ms of the onset of contraction. Section of the L4 and L5 dorsal roots abolished the pressor responses to contraction in both groups of rats, an effect showing that the responses were reflex in origin. We conclude that increased dietary salt can enhance the reflex sympathetic responses to static exercise.

scholarly journals Increased dietary salt intake enhances the exercise pressor reflex

2014 ◽  
Vol 306 (3) ◽  
pp. H450-H454 ◽  
Author(s):  
Katsuya Yamauchi ◽  
Hirotsugu Tsuchimochi ◽  
Audrey J. Stone ◽  
Sean D. Stocker ◽  
Marc P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Salt Intake ◽  
Arterial Blood Flow ◽  
Dietary Salt ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Pressor Reflex ◽  
Stimulation Of

Increased dietary salt in rats has been shown to sensitize central sympathetic circuits and enhance sympathetic responses to several stressors, including hyperinsulinemia, intracerebroventricular injection of angiotensin, and electrical stimulation of sciatic nerve afferents. These findings prompted us to test the hypothesis that increased dietary salt enhanced the exercise pressor reflex. Male Sprague-Dawley rats were fed 0.1% (low) or 4.0% (high) NaCl chow for 2 to 3 wk. On the day of the experiment, the rats were decerebrated, and the hind limb muscles were statically contracted for 30 s by electrically stimulating the cut peripheral ends of the L4 and L5 ventral roots. We found that contraction produced a significantly greater increase in mean arterial pressure of rats fed 4.0% ( n = 26) vs. 0.1% ( n = 22) NaCl (24 ± 2 vs. 15 ± 2 mmHg, respectively; P < 0.05). Baseline mean arterial pressure was not different between groups (0.1%, 77 ± 4 vs. 4.0% NaCl, 80 ± 3 mmHg). Likewise, the tension time indexes were not different between the two groups ( P = 0.42). Section of the L4 and L5 dorsal roots greatly attenuated both the pressor and cardioaccelerator responses to contraction in both groups of rats, an effect showing that the responses were reflex in origin. Finally, electrical stimulation of the lumbar sympathetic chain produced similar increases in mean arterial pressure and decreases in femoral arterial blood flow and conductance between rats fed 0.1% vs. 4.0% NaCl diets. We conclude that increased dietary salt enhances the exercise pressor reflex.

scholarly journals Exaggerated pressor and sympathetic responses to stimulation of the mesencephalic locomotor region and exercise pressor reflex in type 2 diabetic rats

2019 ◽  
Vol 317 (2) ◽  
pp. R270-R279 ◽  
Author(s):  
Han-Kyul Kim ◽  
Norio Hotta ◽  
Rie Ishizawa ◽  
Gary A. Iwamoto ◽  
Wanpen Vongpatanasin ◽  
...  
Keyword(s):  
Cardiovascular Responses ◽  
Normal Diet ◽  
Central Command ◽  
Sprague Dawley ◽  
Mesencephalic Locomotor Region ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Sympathetic Responses ◽  
Stimulation Of

The cardiovascular responses to exercise are potentiated in patients with type 2 diabetes mellitus (T2DM). However, the underlying mechanisms causing this abnormality remain unknown. Central command (CC) and the exercise pressor reflex (EPR) are known to contribute significantly to cardiovascular control during exercise. Thus these neural signals are viable candidates for the generation of the abnormal circulatory regulation in this disease. We hypothesized that augmentations in CC as well as EPR function contribute to the heightened cardiovascular responses during exercise in T2DM. To test this hypothesis, changes in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in response to electrical stimulation of mesencephalic locomotor region (MLR), a putative component of the central command pathway, and activation of the EPR, evoked by electrically induced hindlimb muscle contraction, were examined in decerebrate animals. Sprague-Dawley rats were given either a normal diet (control) or a high-fat diet (14–16 wk) in combination with two low doses (35 mg/kg week 1, 25 mg/kg week 2) of streptozotocin (T2DM). The changes in MAP and RSNA responses to MLR stimulation were significantly greater in T2DM compared with control (2,739 ± 123 vs. 1,298 ± 371 mmHg/s, 6,326 ± 1,621 vs. 1,390 ± 277%/s, respectively, P < 0.05). Similarly, pressor and sympathetic responses to activation of the EPR in diabetic animals were significantly augmented compared with control animals (436 ± 74 vs. 134 ± 44 mmHg/s, 645 ± 135 vs. 139 ± 65%/s, respectively, P < 0.05). These findings provide the first evidence that CC and the EPR may generate the exaggerated rise in sympathetic activity and blood pressure during exercise in T2DM.

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)

Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip

1998 ◽  
Vol 84 (1) ◽  
pp. 277-283 ◽  
Author(s):  
Sogol Mostoufi-Moab ◽  
Eric J. Widmaier ◽  
Jacob A. Cornett ◽  
Kristen Gray ◽  
Lawrence I. Sinoway
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Venous Blood ◽  
Voluntary Contraction ◽  
Positive Pressure ◽  
Ph Response ◽  
Exercise Pressor Reflex ◽  
Pressure Threshold ◽  
Pressor Reflex

Mostoufi-Moab, Sogol, Eric J. Widmaier, Jacob A. Cornett, Kristen Gray, and Lawrence I. Sinoway. Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip. J. Appl. Physiol. 84(1): 277–283, 1998.—We examined the effects of unilateral, nondominant forearm training (4 wk) on blood pressure and forearm metabolites during ischemic and nonischemic rhythmic handgrip (30 1-s contractions/min at 25% maximal voluntary contraction). Contractions were performed by 10 subjects with the forearm enclosed in a pressurized Plexiglas tank to induce ischemic conditions. Training increased the endurance time in the nondominant arm by 102% ( protocol 1). In protocol 2, tank pressure was increased in increments of 10 mmHg/min to +50 mmHg. Training raised the positive-pressure threshold necessary to engage the pressor response. In protocol 3, handgrip was performed at +50 mmHg and venous blood samples were analyzed. Training attenuated mean arterial pressure (109 ± 5 and 98 ± 4 mmHg pre- and posttraining, respectively, P < 0.01), venous lactate (2.9 ± 0.4 and 1.8 ± 0.3 mmol/l pre- and posttraining, respectively, P < 0.01), and the pH response (7.21 ± 0.02 and 7.25 ± 0.01, pre- and posttraining, respectively, P < 0.01). However, deep venous O2 saturation was unchanged. Training increased the positive-pressure threshold for metaboreceptor engagement, reduced metabolite concentrations, and reduced mean arterial pressure during ischemic exercise.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

scholarly journals Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves

1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Cardiac Responses ◽  
Stimulation Of

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.

Hypothalamic projections of renal afferent nerves in the cat

1980 ◽  
Vol 58 (5) ◽  
pp. 574-576 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Fluid Balance ◽  
Lateral Hypothalamus ◽  
Discharge Rate ◽  
Renal Nerves ◽  
Preoptic Nucleus ◽  
Afferent Nerves ◽  
Stimulation Of

In 10 cats anaesthetized with chloralose the electrical activity of spontaneously active hypothalamic units was recorded for changes in discharge rate during electrical stimulation of renal afferent nerves. The discharge rate of 141 single units was altered by stimulation of either the ipsilateral or contralateral renal nerves. Most of the responsive units were located in the regions of lateral preoptic nucleus, lateral hypothalamus, and paraventricular nucleus. These results demonstrate that renal afferent nerves provide information to hypothalamic structures known to be involved in the regulation of arterial pressure and fluid balance.

Abstract P154: Ultrasound Imaging for Serial Measurements of Venous Diameters in Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Teresa Krieger-Burke ◽  
Bridget M Seitz ◽  
Gregory D Fink ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Real Time ◽  
Ultrasound Imaging ◽  
Imaging System ◽  
Sprague Dawley ◽  
Reliable Technique ◽  
Venous Capacitance ◽  
Anesthetized Rats

The purpose of our study was to investigate serial ultrasound imaging in rats as a means to quantify the diameters of splanchnic veins in real time and the effect of drugs on venous capacitance. A 21 MHz probe ( Vevo 2100 imaging system,Visual Sonics Inc.) was used to collect images containing the portal vein (PV) and the superior mesenteric vein (SMV) in anesthetized male Sprague-Dawley rats maintained at 37°C. Stable landmarks were established and we were able to repeatedly locate specific cross-sections of PV and SMV. When controlled for respiratory and cardiac cycles during measurements, respective diameters of these vessels remained within 0.75±0.15% and 0.2±0.10% of baseline (PV: 2.02±0.15 mm; SMV: 1.67±0.05 mm) when located and measured every 5 minutes over 45 minutes (n=3 rats). PV and SMV remained within 1.0±0.6% and 0.38±0.9% from baseline, respectively, when measured on separate days over 10 weeks in a preliminary study using 2 rats. The consistency of raw vessel measurements allowed these vessels to serve as their own control during subchronic pharmacologic interventions. In a second study, the vasodilator sodium nitroprusside (2 mg/kg, i.v. bolus) was administered to anesthetized rats (n=3) following collection of baseline vessel measurements. PV and SMV diameters increased 37.23±2.4% and 29.77±8.8% from baseline by 30 minutes post drug administration while mean arterial pressure decreased 10.32±1.7 mmHg. Conversely, the administration of the venoconstrictor sarafotoxin (S6C) (5 ng/kg, i.v. bolus) to other anesthetized rats (n=3) decreased PV and SMV diameters 22.10±2.4% and 9.44±1.6% from baseline within 5 minutes, associated with an increase in mean arterial pressure of 12.85±3.2 mmHg. Together these results support serial ultrasound imaging as a reliable technique to accurately measure acute and subchronic changes in the diameter of splanchnic veins concurrent with blood pressure changes in intact rats. The ability to follow rat abdominal vein diameters in real time will assist in determining the role of the venous circulation in blood pressure regulation.

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