Influence of autonomic blockade on cardiovascular responses to exercise in rats

1993 ◽  
Vol 75 (1) ◽  
pp. 155-161 ◽  
Author(s):  
J. M. Overton
Keyword(s):  
Blood Flow ◽  
Cardiovascular Responses ◽  
Beta Blockade ◽  
Sprague Dawley ◽  
Exercise Tests ◽  
Sprague Dawley Rats ◽  
Autonomic Blockade ◽  
Atropine Methyl Nitrate ◽  
Exercise Induced ◽  
Response To Exercise

The purposes of this study were to determine the role of the sympathetic and parasympathetic nervous systems in producing the heart rate (HR) response to dynamic exercise in rats and to determine the effect of attenuation of the HR response to exercise on blood flow redistribution. Sprague-Dawley rats (n = 10) were instrumented with arterial and venous catheters and Doppler flow probes. Mean arterial pressure (MAP), HR, mesenteric blood flow (MBF), and iliac blood flow (IBF) were determined during four exercise tests. On 4 consecutive days, rats were treated with saline (SAL, 1 mg/kg iv), atropine methyl nitrate (ATR, 2 mg/kg), timolol maleate (TIM, 0.5 mg/kg), and combined timolol and atropine. One minute of mild exercise (10 m/min) produced an increase in HR of 90 +/- 6 beats/min after SAL treatment, which was significantly less than the increment after ATR (56 +/- 5 beats/min) or TIM (4 +/- 3 beats/min). For the remainder of graded exercise, ATR treatment produced a modest attenuation in the increment in HR and no effect on MAP, IBF, and MBF. At 30 m/min, TIM markedly blunted the exercise-induced increment in HR (SAL, 138 +/- 8 beats/min; TIM, 53 +/- 4 beats/min) and IBF (SAL, 324 +/- 33%; TIM, 197 +/- 33%) with no effect on MAP or MBF. The results suggest that 1) the sympathetic nervous system is an important mediator of exercise-induced tachycardia in rats and 2) exercised-induced hyperemia, but not MAP, is attenuated by nonselective beta-blockade during exercise in rats.

Lactate is essential for maintenance of euglycemia in iron-deficient rats at rest and during exercise

1993 ◽  
Vol 264 (4) ◽  
pp. E662-E667 ◽  
Author(s):  
J. K. Linderman ◽  
P. R. Dallman ◽  
R. E. Rodriguez ◽  
G. A. Brooks
Keyword(s):  
Iron Deficiency ◽  
Hemoglobin Concentration ◽  
Liver Glycogen ◽  
Beta Blockade ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Iron Deficient ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Exercise Induced

To evaluate the hypothesis that lactate supply is essential to maintain euglycemia during iron deficiency, female Sprague-Dawley rats were assigned to iron-sufficient (50 mg Fe2+/kg diet, +Fe), or iron-deficient (15 mg Fe2+/kg diet, -Fe) dietary groups and were injected with a specific beta 2-adrenergic inhibitor, ICI 118,551 (1.0 mg/kg body wt). Rats were studied at rest or after 30 min of running at 13.4 m/min 0% grade. Dietary iron deficiency decreased hemoglobin concentration 38%, but resting arterial concentrations of glucose ([Glc]), lactate ([La]), or alanine ([Ala]) were unaffected. Administration of ICI 118,551 (beta 2-blockade) decreased [La] and [Glc] 52 and 32% in resting -Fe rats, respectively. beta 2-Blockade attenuated the exercise-induced rise in [La] and decreased [Glc] 31% in exercising -Fe rats. [Ala] were unaffected by iron deficiency or exercise but decreased 24 and 18% because of beta 2-blockade in resting and exercising +Fe rats. Iron deficiency depleted resting liver glycogen concentration 45%, with no additional effect of exercise or beta 2-blockade. beta-Blockade decreased arterial insulin and increased arterial glucagon concentrations in resting -Fe and +Fe rats. During exercise glucagon concentration increased significantly more in -Fe than +Fe rats. Decreased arterial [La] with a corresponding decrease in arterial [Glc] in response to beta 2-blockade support the contention that lactate supply is critical to maintenance of euglycemia in -Fe rats at rest and during exercise.

Effects of propranolol and pindolol on plasma ANP levels in humans at rest and during exercise

1989 ◽  
Vol 257 (2) ◽  
pp. R259-R264
Author(s):  
P. Bouissou ◽  
F. X. Galen ◽  
J. P. Richalet ◽  
M. Lartigue ◽  
F. Devaux ◽  
...  
Keyword(s):  
Heart Rate ◽  
Beta Blockers ◽  
Placebo Treatment ◽  
Beta Blockade ◽  
Intrinsic Sympathomimetic Activity ◽  
Exercise Tests ◽  
Beta Adrenoceptor ◽  
Significant Difference ◽  
Exercise Induced ◽  
Response To Exercise

In attempt to elucidate whether the beta-adrenoceptor is involved in the control of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP level was measured at rest, in recumbent and upright positions, and during graded maximal ergocycle exercise in nine healthy male subjects (23 +/- 0.5 years of age) treated for 3 days with nonselective beta-blockers propranolol (150 mg/day) or pindolol (15 mg/day) or with placebo. The effects of beta-blockers, which differ by their hemodynamic actions at rest because of the intrinsic sympathomimetic activity of pindolol, were compared. Maximal O2 consumption (VO2max) during beta-blockade was not significantly different from the placebo value. Resting heart rate was not affected by pindolol treatment but was decreased with propranolol (-10 beats/min). Both beta-blockers caused a reduction in heart rate at all the exercise intensities. Mean blood pressure was not affected by beta-blockade at rest but was significantly reduced during exercise. During placebo treatment, plasma ANP increased in response to exercise intensities greater than 65% of VO2max. At 100% VO2max plasma ANP was nearly doubled (101.5 +/- 14 pg/ml) compared with the basal value in upright position (56.6 +/- 15 pg/ml). beta-Blockade caused a marked elevation in plasma ANP at all the levels of activity. Despite different hemodynamic responses to pindolol and propranolol, both beta-blockers produced similar increases in the basal level of plasma ANP. These rises were maintained in the course of exercise tests, and no significant difference was found between propranolol and pindolol. We conclude that beta-adrenoceptor mechanisms are not directly responsible for tonic and exercise-induced ANP secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to voluntary and treadmill exercise in rats

1993 ◽  
Vol 75 (3) ◽  
pp. 1334-1340 ◽  
Author(s):  
S. L. Yancey ◽  
J. M. Overton
Keyword(s):  
Blood Flow ◽  
Treadmill Exercise ◽  
Exercise Bout ◽  
Cardiovascular Responses ◽  
Voluntary Exercise ◽  
Treadmill Running ◽  
Sprague Dawley ◽  
Mesenteric Blood Flow ◽  
Doppler Flow ◽  
Sprague Dawley Rats

Male Sprague-Dawley rats (n = 12) were housed in activity wheels and familiarized with treadmill running 2 wk before they were instrumented with Doppler flow probes and a carotid catheter. Mean arterial pressure (MAP), heart rate (HR), mesenteric blood flow (BFmes), and iliac blood flow were determined during bouts of voluntary and treadmill exercise. One voluntary exercise bout (speed = 33 +/- 2 m/min, duration = 26 +/- 5 s) from each rat was selected to compare with 30 s of treadmill exercise at 30 m/min. Voluntary exercise produced increases in MAP (7 +/- 3 mmHg) and HR (63 +/- 7 beats/min) that were significantly less than the increases of 21 +/- 5 mmHg and 95 +/- 9 beats/min, respectively, with treadmill exercise. Voluntary exercise caused an immediate reduction in BFmes of 32 +/- 6%, whereas treadmill exercise produced a significantly greater reduction of 57 +/- 4%. Voluntary and treadmill exercise caused similar increases in iliac blood flow of 112 +/- 15 and 169 +/- 31%, respectively. The patterns of cardiovascular adjustments to the initiation of voluntary exercise are similar to those observed at the initiation of treadmill exercise; however, MAP, HR, and BFmes responses were significantly greater with treadmill exercise.

Lesions of the anteroventral third ventricle region (AV3V) disrupt cardiovascular responses to an elevation in core temperature

2005 ◽  
Vol 288 (6) ◽  
pp. R1783-R1790 ◽  
Author(s):  
Douglas G. Whyte ◽  
Alan Kim Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Core Temperature ◽  
Cardiovascular Response ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Hydration Status ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electrolytic Lesions

Blood flow is redistributed from the viscera to the periphery during periods of heat stress to maximize heat loss. The heat-induced redistribution of blood flow is strongly influenced by nonthermal inputs such as hydration status. At present, little is known about where thermal and nonthermal information is integrated to generate an appropriate effector response. Recently, the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) has been implicated in the integration of thermal and osmotic information. The purpose of the present study was to determine the effects of electrolytic lesions of the AV3V on the cardiovascular response to a passive heat stress in unanesthetized, free-moving male Sprague-Dawley rats. Core temperature was elevated at a constant rate of ∼0.03°C/min in sham- and AV3V-lesion rats using an infrared heat lamp. Changes in mesenteric and hindquarter vascular resistance were determined using Doppler flow probes, and heat-induced salivation was estimated using the spit-print technique. The rise in mean arterial pressure (MAP), heart rate (HR), and mesenteric resistance in response to elevations in core temperature were all attenuated in AV3V-lesion rats; however, hindquarter resistance was unaffected. Heat-induced salivation was also diminished. In addition, AV3V-lesion rats were more affected by the novelty of the experimental environment, resulting in a higher basal core temperature, HR, and MAP. These results indicate that AV3V lesions disrupt the cardiovascular and salivatory response to a passive heat stress in rats and produce an exaggerated stress-induced fever triggered by a novel environment.

mu-Opioid receptors in NTS elicit pressor responses via sympathetic pathways

1987 ◽  
Vol 252 (1) ◽  
pp. H156-H162 ◽  
Author(s):  
A. H. Hassen ◽  
G. Feuerstein
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Baroreflex Function ◽  
Sprague Dawley Rats ◽  
Pressor Responses ◽  
Adrenergic Antagonist ◽  
Atropine Methyl Nitrate ◽  
Mu Receptors

We have evaluated the relative contributions of the sympathetic and parasympathetic nervous systems to the increased mean arterial pressure (MAP) and heart rate (HR) elicited by the selective mu-agonist D-Ala2, MePhe4, Gly-ol5 enkephalin (DAGO) following microinjection (100 nl) into the nucleus of tractus solitarius (NTS) of anesthetized, artificially ventilated Sprague-Dawley rats. The effects of anesthesia and central opioid-receptor activation on baroreflex function were also examined. All cardiovascular responses elicited by DAGO were eliminated by complete C1 spinal transection. Pretreatment with the alpha-adrenergic antagonist phentolamine attenuated the increase in MAP, but not the tachycardia; the beta-blocker propranolol abolished the tachycardia but not the pressor response to DAGO. Adrenalectomy, vagotomy, or pretreatment with atropine methyl nitrate were all without effect. Baroreflexes were attenuated in animals anesthetized with pentobarbital sodium, but were present in urethan-anesthetized rats. DAGO attenuated the increases in MAP and HR elicited following carotid occlusion, but not the bradycardia elicited by a phenylephrine-induced pressor response. These data indicate that mu-receptors in the NTS elicit cardiovascular responses that are mediated by increased sympathetic nerve activity, and accompanied by selective attenuation of baroreflex function.

scholarly journals Eukaryotic initiation factors and protein synthesis after resistance exercise in rats

2000 ◽  
Vol 88 (3) ◽  
pp. 1036-1042 ◽  
Author(s):  
Peter A. Farrell ◽  
Jazmir M. Hernandez ◽  
Mark J. Fedele ◽  
Thomas C. Vary ◽  
Scot R. Kimball ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Resistance Exercise ◽  
Translational Control ◽  
Sprague Dawley ◽  
Initiation Factors ◽  
Eukaryotic Initiation Factors ◽  
Sprague Dawley Rats ◽  
Arterial Plasma ◽  
Response To Exercise

Translational control of protein synthesis depends on numerous eukaryotic initiation factors (eIFs) and we have previously shown ( Am. J. Physiol. Endocrinol. Metab. 276: E721–E727, 1999) that increases in one factor, eIF2B, are associated with increases in rates of protein synthesis after resistance exercise in rats. In the present study we investigated whether the eIF4E family of initiation factors is also involved with an anabolic response to exercise. Male Sprague-Dawley rats either remained sedentary ( n = 6) or performed acute resistance exercise ( n = 6), and rates of protein synthesis were assessed in vivo 16 h after the last session of resistance exercise. eIF4E complexed to eIF4G (eIF4E ⋅ eIF4G), eIF4E binding protein 1 (4E-BP1) complexed to eIF4E, and phosphorylation state of eIF4E and 4E-BP1 (γ-form) were assessed in gastrocnemius. Rates of protein synthesis were higher in exercised rats compared with sedentary rats [205 ± 8 (SE) vs. 164 ± 5.5 nmol phenylalanine incorporated ⋅ g muscle−1 ⋅ h−1, respectively; P < 0.05]. Arterial plasma insulin concentrations were not different between the two groups. A trend ( P = 0.09) for an increase in eIF4E ⋅ eIF4G with exercise was noted; however, no statistically significant differences were observed in any of the components of the eIF4E family in response to resistance exercise. These new data, along with our previous report on eIF2B, suggest that the regulation of peptide chain initiation after exercise is more dependent on eIF2B than on the eIF4E system.

Blood flow in normal and denervated muscle during exercise in conscious rats

1988 ◽  
Vol 255 (6) ◽  
pp. H1509-H1515 ◽  
Author(s):  
M. D. Delp ◽  
R. B. Armstrong
Keyword(s):  
Blood Flow ◽  
Muscular Activity ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Sprague Dawley Rats ◽  
Mechanical Factors ◽  
Denervated Muscles ◽  
Gastrocnemius Muscles ◽  
Low Intensity Exercise ◽  
Hyperemic Response

The purpose of this study was to test the hypothesis that extrinsic mechanical factors, i.e., the dynamic shortening and lengthening imposed on a muscle during limb movements and the rhythmic compressions as surrounding muscles contract and relax, contribute to the initial muscle hyperemia during locomotion in conscious male Sprague-Dawley rats. Soleus and lateral head of gastrocnemius muscles were surgically denervated in one hindlimb several hours before exercise to remove 1) local metabolic vasodilator effects, 2) vasoconstrictor or vasodilatory influences mediated through sympathetic postganglionic fibers, and 3) intrinsic mechanical pumping. Blood flow was measured with radioactive microspheres during preexercise and at 30 s and 5 min of exercise in rats walking at 15 m/min or a motor-driven treadmill. Glycogen concentrations were also measured as an indicator of muscular activity to verify the denervation. Blood flows to control muscles in the normal limb were similar to previously reported values during preexercise and exercise. Denervation, however, decreased preexercise blood flow (69–88%) to muscle composed predominantly of oxidative fibers and increased flow (53%) to muscle composed predominantly of glycolytic fibers. During exercise, blood flow to denervated muscles either remained unchanged or decreased. These data suggest that extrinsic mechanical factors do not significantly contribute to the initial hyperemic response at the onset of low-intensity exercise in normal muscle.

Androgen-mediated sex differences of cardiovascular responses in rats

1978 ◽  
Vol 235 (2) ◽  
pp. H242-H246 ◽  
Author(s):  
P. J. Baker ◽  
E. R. Ramey ◽  
P. W. Ramwell
Keyword(s):  
Sex Differences ◽  
Arachidonic Acid ◽  
Rank Order ◽  
Cardiovascular Responses ◽  
Sprague Dawley ◽  
Similar Treatment ◽  
Depressor Response ◽  
Sprague Dawley Rats ◽  
Significant Change ◽  
Dose Levels

Sex differences in the systemic depressor response to arachidonic acid (50 or 150 microgram/kg iv) were observed in intact and castrated anesthetized Sprague-Dawley rats. The rank order of responsiveness was: castrate males, castrate females, females, males; all four groups were significantly different (P less than 0.05) at the higher dose. Castrated males pretreated with testosterone (1 mg/kg sc) 5 or 7 days previously gave a response at the higher arachidonate dose levels that was of the same order as that obtained with intact males. Similar treatment of castrate males with androgen potentiated (P less than 0.05) the vasopressor action of norepinephrine (0.25 microgram/kg) on day 7 after the testosterone pretreatment. In contrast, treatment with depot estradiol (100 microgram/kg sc) in castrate males produced no significant change in the response to either of the vasoactive compounds on both days 5 and 7 after pretreatment. These data suggest that testosterone may be a significant factor in the development of sex differences in the cardiovascular systems of rats.

Adrenomedullin microinjection into the area postrema increases blood pressure

1997 ◽  
Vol 272 (6) ◽  
pp. R1698-R1703 ◽  
Author(s):  
M. A. Allen ◽  
P. M. Smith ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Area Under The Curve ◽  
Physiological Role ◽  
Cardiovascular Responses ◽  
Hypotensive Effect ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Brain Site

Adrenomedullin (ADM) circulates in the blood at concentrations comparable to other vasoactive peptides with established roles in cardiovascular regulation. Intravenously administered ADM produces a clear hypotensive effect, whereas intracerebroventricular microinjections result in increases in blood pressure (BP). Recently, we demonstrated that ADM influences neurons of the area postrema (AP), a central nervous system site implicated in cardiovascular control. However, to address directly the physiological significance of the actions of ADM at the AP, an in vivo microinjection study was undertaken. ADM, at two concentrations (1 and 10 microM), in volumes of 50, 100, and 200 nl, was microinjected into the AP or NTS of 21 urethan-anesthetized male Sprague-Dawley rats. Microinjection of 10 microM ADM (100 nl) resulted in significant transient (2-5 min) increases in BP [120 s area under the curve (AUC): 684.3 +/- 268.6 mmHg/s (P < 0.05)], and heart rate (HR) [AUC: 12.5 +/- 4.5 beats/min (P < 0.05)]. The lower concentration of ADM (1 microM) had no effect on either BP (179.1 +/- 143.6 mmHg/s) or HR (0.8 +/- 2.6 beats/min). ADM was also microinjected into the immediately adjacent nucleus of the solitary tract, where it was found to be without effect on either BP or HR. This study demonstrates, for the first time, a physiological role for ADM acting at a specific brain site, the AP, to produce significant cardiovascular responses.

scholarly journals Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion

2005 ◽  
Vol 153 (2) ◽  
pp. 345-351 ◽  
Author(s):  
Leif Jansson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Serum Insulin ◽  
Blood Perfusion ◽  
Islet Function ◽  
Sprague Dawley ◽  
Islet Mass ◽  
Islet Blood Flow ◽  
Sprague Dawley Rats ◽  
Duct Ligation

Objectives: The aim of this study was to evaluate islet blood-flow changes during stimulated growth of the islet organ without any associated functional impairment of islet function. Design: A duct ligation encompassing the distal two-thirds of the pancreas was performed in adult, male Sprague–Dawley rats. Methods: Pancreatic islet blood flow was measured in duct-ligated and sham-operated rats 1, 2 or 4 weeks after surgery. In some animals studied 4 weeks after surgery, islet blood flow was also measured also during hyperglycaemic conditions. Results: A marked atrophy of the exocrine pancreas was seen in all duct-ligated rats. Blood glucose and serum insulin concentrations were normal. An increased islet mass was only seen 4 weeks after surgery. No differences in islet blood perfusion were noted at any time point after duct ligation. In both sham-operated and duct-ligated rats islet blood flow was increased during hyperglycaemia; the response was, however, slightly more pronounced in the duct-ligated part of the gland. Conclusions: Normal, physiological islet growth does not cause any major changes in the islet blood perfusion or its regulation. This is in contrast to findings during increased functional demands on the islets or during deteriorated islet function, when increased islet blood flow is consistently seen.

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