Kappa opioids modulate the arterial baroreflex control of heart rate in conscious young sheep

2007 ◽  
Vol 85 (8) ◽  
pp. 811-817 ◽  
Author(s):  
Wei Qi ◽  
Francine G. Smith
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Direct Evidence ◽  
Opiate Receptors ◽  
Random Order ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Physiological Conditions ◽  
Kappa Opioids ◽  
Before And After

The present study tested the hypothesis that κ-opioids modulate the arterial baroreflex control of heart rate in conscious young sheep. Various parameters governing the arterial baroreflex control of heart rate were assessed before and after activation of κ-opiate receptors (KOR) by i.v. administration of the specific KOR agonist U-50488H (experiment 1) or vehicle (experiment 2) to conscious, chronically instrumented lambs aged 42 ± 2 days (n = 6). The 2 experiments were administered in random order at minimum intervals of 48 h. Thirty min after U-50488H treatment, there was an increase in diastolic and mean arterial pressure and in heart rate, returning to control levels by 90 min. A significant increase in the arterial pressure at the midpoint of the baroreflex range and in the minimum heart rate as well as a significant decrease in the heart rate range over which the arterial baroreflex operates were also seen at 30 min after U-50488H, gradually returning to control levels over 120 min. Vehicle had no effect on any of the parameters governing the arterial baroreflex control of heart rate. These data provide the first direct evidence that under physiological conditions in young lambs, the arterial baroreflex control of heart rate is altered after administration of the specific KOR agonist U-50488H, revealing a previously unidentified role for this opioid receptor.

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate

2001 ◽  
Vol 280 (5) ◽  
pp. H2061-H2068 ◽  
Author(s):  
C. Michael Foley ◽  
Richard M. McAllister ◽  
Eileen M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Arterial Baroreflex ◽  
Thyroid Status ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Resting Blood Pressure ◽  
Sympathetic Influence

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.

Arterial baroreflex resetting mediates postexercise reductions in arterial pressure and heart rate

1998 ◽  
Vol 275 (5) ◽  
pp. H1627-H1634 ◽  
Author(s):  
Margaret P. Chandler ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Acute Exercise ◽  
Operating Point ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Bout ◽  
Before And After ◽  
The Relationship

We tested the hypothesis that postexercise reductions in arterial pressure and heart rate (HR) are mediated by a lowering of the operating point and a reduction in the gain of the arterial baroreflex. To test this hypothesis, spontaneous changes in arterial pressure and the reflex responses of HR were examined before and after a single bout of mild to moderate dynamic exercise in 19 spontaneously hypertensive rats (SHR, 10 male and 9 female). Eleven SHR subjected to sinoaortic denervation (SAD) (6 male, 5 female) were also studied. All rats were instrumented with an arterial catheter for the measurement of arterial pressure and HR. After exercise, arterial pressure and HR were reduced below preexercise levels. Furthermore, the operating point and spontaneous gain (G) of the arterial baroreflex were reduced. Specifically, after exercise, the spontaneous range of HR (P1, 50%), the pressure at the midpoint of the pressure range (P3, 13%) and the HR at the midpoint of the HR range (H3, 10%), the spontaneous minimum HR (P4, 8%) and maximum HR (10%), and G (76%) were significantly attenuated. SAD significantly attenuated the relationship between arterial pressure and HR by reducing G (males 94%, females 95%). These results demonstrate that acute exercise resulted in a postexercise resetting of the operating point and a reduction in the gain of the arterial baroreflex. Furthermore, these data suggest that postexercise reductions in arterial pressure and HR are mediated by a lowering of the operating point of the arterial baroreflex.

Angiotensin II modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism in rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1009-R1016 ◽  
Author(s):  
Y. Nishida ◽  
K. L. Ryan ◽  
V. S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Before And After ◽  
Dose Dependent ◽  
Renal Sympathetic

To test the hypothesis that angiotensin II (ANG II) modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism, we examined the effects of intravertebral infusion of ANG II on baroreflex function curves before and after intravertebral administration of the alpha 1-adrenoreceptor antagonist prazosin. Rabbits were chronically instrumented with subclavian and vertebral arterial catheters, venous catheters, and aortic and vena caval occludes. Baroreflex curves were obtained by relating heart rate (HR) to mean arterial pressure during increases and decreases in arterial pressure. Intravertebral infusions of ANG II (5, 10, and 20 ng.kg-1.min-1) produced a dose-dependent shift of the midrange of the curve toward higher pressures (64 +/- 1 to 68 +/- 1, 76 +/- 1, and 85 +/- 2 mmHg, respectively). Pretreatment with prazosin (10 micrograms/kg) via the vertebral artery markedly reduced the shift in the baroreflex curve induced by the highest dose of ANG II (64 +/- 2 to 70 +/- 2 mmHg). These data suggest that ANG II resets the operating point of the HR baroreflex curve to a higher blood pressure and that this effect is mediated via a central alpha 1 mechanism. When the effects of vertebral ANG II on the baroreflex control of renal sympathetic nerve activity (RSNA) were examined, intravertebral administration of ANG II, while reducing the gain and the maximum RSNA, did not reset the RSNA baroreflex curve. These data suggest that ANG II acutely resets the HR baroreflex but not the RSNA baroreflex and that the resetting involves an alpha 1-adrenergic mechanism.

Rapid resetting of baroreflexes in hypertensive dogs

1992 ◽  
Vol 262 (5) ◽  
pp. H1508-H1514
Author(s):  
M. J. Brunner ◽  
M. D. Kligman
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Experimental Hypertension ◽  
Arterial Baroreflex ◽  
Short Term ◽  
Baroreflex Control ◽  
Pentobarbital Sodium ◽  
Reflex Gain ◽  
Pentobarbital Sodium Anesthesia

The hypothesis tested was that the rapid resetting of the arterial baroreflex control of arterial pressure in normotension could be demonstrated in experimental hypertension. After the development of experimental hypertension (using a bilateral renal wrap technique), rapid resetting of arterial pressure and heart rate (HR) was acutely assessed under pentobarbital sodium anesthesia in hypertensive and normotensive vagotomized dogs. The carotid sinus area was isolated and perfused at controlled carotid sinus pressures (CSPs). Baroreflex response [mean arterial pressure (MAP) and HR] curves were measured after three carotid sinus conditioning pressures (50, 125, and 200 mmHg) were applied. For the MAP response, the CSPo (CSP at point of maximum reflex gain) increased significantly to the same extent in both groups with increasing conditioning pressures (with 22.2 and 16.7% resetting in the normotensive group, and 20.3 and 14.2% resetting in the hypertensive group). We conclude that short-term adjustments to changes in prevailing pressure (rapid resetting) occur in the arterial pressure response in experimental hypertension to the same extent seen in normotension.

scholarly journals Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

2006 ◽  
Vol 290 (4) ◽  
pp. R1003-R1011 ◽  
Author(s):  
Andrea G. Bechtold ◽  
Deborah A. Scheuer
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Receptor Expression ◽  
Arterial Baroreflex ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Sprague Dawley Rats ◽  
Corticosteroid Receptor ◽  
Dorsal Hindbrain

Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, we tested the hypothesis that prolonged activation of DHB Cort receptors increases the midpoint and reduces the gain of arterial baroreflex control of heart rate in conscious rats. Small (3–4 mg) pellets of Cort (DHB Cort) or Silastic (DHB Sham) were placed on the surface of the DHB, or Cort was administered systemically by placing a Cort pellet on the surface of the dura (Dura Cort). Baroreflex control of heart rate was determined in conscious male Sprague Dawley rats on each of 4 days after initiation of treatment. Plots of arterial pressure vs. heart rate were analyzed using a four-parameter logistic function. After 3 days of treatment, the arterial pressure midpoint for baroreflex control of heart rate was increased in DHB Cort rats (123 ± 2 mmHg) relative to both DHB Sham (108 ± 3 mmHg) and Dura Cort rats (109 ± 2 mmHg, P < 0.05). On day 4, baseline arterial pressure was greater in DHB Cort (112 ± 2 mmHg) compared with DHB Sham (105 ± 2 mmHg) and Dura Cort animals (106 ± 2 mmHg, P < 0.05), and the arterial pressure midpoint was significantly greater than mean arterial pressure in the DHB Cort group only. Also on day 4, maximum baroreflex gain was reduced in DHB Cort (2.72 ± 0.12 beats·min−1·mmHg−1) relative to DHB Sham and Dura Cort rats (3.51 ± 0.28 and 3.37 ± 0.27 beats·min−1·mmHg−1, P < 0.05). We conclude that Cort acts in the DHB to increase the midpoint and reduce the gain of the heart rate baroreflex function.

Individual differences in the heart rate response to activation of the muscle metaboreflex in humans

2010 ◽  
Vol 299 (5) ◽  
pp. H1708-H1714 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Naoto Fujii ◽  
Mayumi Matsumoto ◽  
Takeshi Nishiyasu
Keyword(s):  
Heart Rate ◽  
Individual Differences ◽  
Arterial Pressure ◽  
Arterial Baroreflex ◽  
Frequency Range ◽  
Autonomic Tone ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Transfer Function Analysis

We tested the hypotheses that the heart rate (HR) response to muscle metaboreflex activation induced by postexercise muscle ischemia (PEMI) varies considerably among subjects and that individual differences in the HR response are associated with differences in cardiac autonomic tone and/or arterial baroreflex function during PEMI. Fifty-one healthy subjects (36 men and 15 women) performed a 1-min isometric handgrip exercise at 50% maximal voluntary contraction, which was followed by a 3.5-min period of imposed PEMI. We estimated cardiac autonomic tone using spectral analysis of beat-to-beat variation in the R-R interval (RRI). In addition, the sensitivity of the arterial baroreflex control of HR (BRS) was evaluated using transfer function analysis of systolic arterial pressure (SAP) and RRI. Although the mean RRI during the PEMI and subsequent recovery period did not differ from the resting value, the variance among the individual differences in RRI between the rest and PEMI periods was significantly greater than between the rest and recovery periods. The changes in RRI elicited by PEMI correlated significantly with changes in the spectral power of the RRI variability in the high-frequency range and the BRS. By contrast, no significant correlation was observed between changes in RRI and changes in mean arterial pressure or the power of the RRI variability in the low-frequency range. This suggests that, in humans, the HR response to PEMI-induced activation of muscle metaboreflex varies considerably from individual to individual and that these differences reflect changes in cardiac parasympathetic tone and spontaneous BRS during PEMI.

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

1984 ◽  
Vol 246 (1) ◽  
pp. H80-H89 ◽  
Author(s):  
G. B. Guo ◽  
F. M. Abboud
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Reflex Inhibition ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Excitatory Effect ◽  
Baroreflex Control ◽  
Reflex Bradycardia ◽  
Background Infusion

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

scholarly journals Nitric oxide and angiotensin II regulate cardiovascular homeostasis and the arterial baroreflex control of heart rate in conscious lambs

2011 ◽  
Vol 13 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Stephanie J Wehlage ◽  
Francine G Smith
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Before And After ◽  
Cardiovascular Homeostasis ◽  
New Evidence

To investigate the potential role of angiotensin II (Ang II) type 1 receptors (AT1Rs) as well as endogenously produced nitric oxide (NO) in regulating cardiovascular homeostasis during ontogeny, experiments were carried out in conscious lambs aged approximately 1 week ( N = 9) and 6 weeks ( N = 11). The arterial baroreflex control of heart rate (HR) was assessed before and after intravenous (IV) infusion of the selective AT1R antagonist, ZD 7155, before and after IV administration of the L-arginine analogue, NG-nitro-L-arginine methyl ester (L-NAME). In both groups, after ZD 7155 alone, mean arterial pressure decreased then increased after L-NAME. At 1 but not 6 weeks, HR decreased after ZD 7155 as well as after L-NAME. At 1 but not 6 weeks, there was a decrease in the HR range after ZD 7155 and after ZD 7155 + L-NAME, as compared to control. There was also a decrease in minimum HR after ZD 7155 + L-NAME at 1 week. These data provide new evidence that, together, Ang II and NO regulate cardiovascular homeostasis as well as the arterial baroreflex of HR early in life which may help to explain the activation of these two systems early in life.

Nitric oxide modulates arterial baroreflex control of heart rate in conscious lambs in an age-dependent manner

2001 ◽  
Vol 280 (5) ◽  
pp. H2255-H2263 ◽  
Author(s):  
Alp Sener ◽  
Francine G. Smith
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Intravenous Administration ◽  
Systolic Arterial Pressure ◽  
Dependent Manner ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Postnatal Maturation ◽  
Age Dependent ◽  
Before And After

Experiments were carried out in conscious chronically instrumented lambs aged 1 ( n = 6) and 6 wk ( n = 5) to evaluate the arterial baroreflex control of heart rate (HR) during postnatal maturation and to investigate any modulatory role of endogenously produced nitric oxide (NO). Before and after intravenous administration of 20 mg/kg of the l-arginine analog N G-nitro-l-arginine methyl ester (l-NAME), the arterial baroreflex was assessed by measuring HR responses to increases and decreases in systolic arterial pressure achieved by intravenous administration of phenylephrine and sodium nitroprusside. The HR range over which the baroreflex operates and minimum HR as well as maximum gain were greater at 1 than at 6 wk of age. These age differences were abolished in the presence ofl-NAME, which decreased the HR range and gain of the arterial baroreflex control of HR at 1 but not at 6 wk of age. These data provide new information that age-dependent effects of the arterial baroreflex appear to result from effects of endogenously produced NO.

Exercise training enhances baroreflex control of heart rate by a vagal mechanism in rabbits with heart failure

2002 ◽  
Vol 92 (6) ◽  
pp. 2403-2408 ◽  
Author(s):  
Jun-Li Liu ◽  
Jay Kulakofsky ◽  
Irving H. Zucker
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Normal Subjects ◽  
Work Capacity ◽  
Logistic Function ◽  
Baroreflex Control ◽  
Before And After

Moderate exercise training (Ex) enhances work capacity and quality of life in patients with chronic heart failure (CHF). We investigated the autonomic components of resting heart rate (HR) and the baroreflex control of HR in conscious, instrumented rabbits with pacing-induced CHF after Ex. Sham and CHF rabbits were exercise trained for 4 wk at 15–18 m/min, 6 days/wk. Arterial pressure and HR were recorded before and after metoprolol (1 mg/kg iv) or after atropine (0.2 mg/kg iv). Mean arterial pressure was altered by infusions of sodium nitroprusside and phenylephrine. The data were fit to a sigmoid (logistic) function. Baseline HRs were 266.5 ± 8.4 and 232.1 ± 1.6 beats/min in CHF and CHF Ex rabbits, respectively ( P < 0.05). In the unblocked state, CHF rabbits had a significantly depressed peak baroreflex slope (1.7 ± 0.3 vs. 5.6 ± 0.7 beats · min−1 · mmHg−1; P < 0.001) and HR range (128.6 ± 34.5 vs. 253.2 ± 20.3 beats/min; P < 0.05) compared with normal subjects. Ex increased baroreflex slope to 4.9 ± 0.3 from 1.7 ± 0.3 beats · min−1 · mmHg−1 in unblocked rabbits ( P < 0.001 compared with CHF non-Ex). Ex did not alter baroreflex function in sham animals. After metoprolol, baroreflex slope was significantly increased in CHF Ex rabbits (1.5 ± 0.2 vs. 3.0 ± 0.2 beats · min−1 · mmHg−1; P < 0.05). After atropine, there was no significant change in baroreflex slope or HR range between CHF Ex and CHF rabbits. These data support the view that enhancement of baroreflex control of HR after Ex is due to an augmentation of vagal tone.

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