Altered heart rate baroreflex during pregnancy: role of sympathetic and parasympathetic nervous systems

1997 ◽  
Vol 273 (3) ◽  
pp. R960-R966 ◽  
Author(s):  
V. L. Brooks ◽  
C. M. Kane ◽  
D. M. Van Winkle
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Late Pregnancy ◽  
Baroreflex Control ◽  
Rate Range ◽  
Before And After ◽  
Reflex Gain ◽  
The Difference ◽  
Perfused Hearts

Two studies were performed to determine whether the attenuation of baroreflex control of heart rate during late pregnancy in conscious rabbits is due to changes in parasympathetic (Para) or sympathetic (Sym) control of the heart. In the first, baroreflex relationships between arterial pressure and heart rate were generated before and after treatment with propranolol (Pro) to block Sym or with methscopolamine (Meth) to block Para. Each rabbit was studied in both the pregnant and nonpregnant state. Pregnancy decreased maximum baroreflex gain from 14.9 +/- 4.0 to 4.8 +/- 0.9 beats.min-1.mmHg-1 (P < 0.01) and decreased heart rate range from 177 +/- 6 to 143 +/- 10 beats/min (P < 0.01), primarily by increasing minimum heart rate (114 +/- 6 to 134 +/- 8 beats/min; P < 0.01). The difference between pregnant and nonpregnant rabbits in baroreflex gain was not altered by Meth but was abolished by Pro, suggesting that it is due to decreased Sym control of the heart. The elevated minimum heart rate of pregnancy persisted after Pro, but was abolished by Meth, suggesting that it is mediated by decreased Para control of the heart. In the second study, isolated buffer-perfused hearts from pregnant and nonpregnant rabbits were treated with increasing doses of isoproterenol (0.3-300 mM) or acetylcholine (0.3-10,000 microM), and the heart rate responses were determined. Hearts from pregnant rabbits were more sensitive to isoproterenol (P < 0.05), but less responsive to acetylcholine (P < 0.05). In conclusion, pregnancy-induced decreases in cardiac reflex gain and range appear to be mediated by alterations in Sym and Para, respectively. The change in Sym occurs proximal to the heart, whereas the decreased contribution of Para may be due, at least in part, to decreased sensitivity of the heart to acetylcholine.

Effect of vasopressin and phenylephrine on arterial pressure and heart rate in conscious dogs

1986 ◽  
Vol 251 (2) ◽  
pp. H253-H260
Author(s):  
J. L. Robinson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Baroreflex Sensitivity ◽  
Conscious Dogs ◽  
Baroreflex Control ◽  
Pressure Stimulus ◽  
Before And After ◽  
Autonomic Receptors ◽  
The Difference

The effect of arginine vasopressin (AVP) and phenylephrine (PE) infusions on mean arterial pressure (MAP) and heart rate (HR) were compared in conscious dogs with all autonomic receptors intact (I), during muscarinic blockade (MB) and during ganglionic blockade (GB). After either MB or GB, the dose-MAP response curve for AVP and PE was shifted to the left of the I response curve; a greater shift was observed with AVP than with PE. The MAP threshold after GB for AVP and PE occurred at 10 and 50% of the threshold dose observed during the I response, respectively. Not only did the MAP threshold occur at a lower dose after MB and GB, but also the slope of the response curve was steeper than that of the I response. Comparing the amount of drug necessary to increase MAP 25 mmHg above control for PE and AVP before and after GB, the intact PE response required 4.3 +/- 1.0 (P less than 0.01) times more drug than during GB versus the intact AVP required 16.8 +/- 2.8 (P less than 0.01) times more drug than during GB. The baroreflex control of HR when all receptors were intact was 3.4 +/- 0.4 (P = 0.001) times more sensitive during AVP compared with PE; no differences were observed after MB. There were no significant changes in HR to AVP or PE after GB, thus indicating a lack of a direct effect of these agents on the HR. Our results show that MB and GB equally potentiate the pressor effects of AVP and PE, and the augmentation was much greater for AVP than for PE. The difference in the potentiation of these two vasoconstrictors is consistent with the finding that the baroreflex sensitivity during AVP was enhanced compared with PE. We have postulated that, in the resting conscious dog, AVP increases the sensitivity of the baroreflex primarily by producing a greater level of parasympathetic tone to the heart in response to a given pressure stimulus.

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

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.

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.

scholarly journals Blockade of neuronal nitric oxide synthase alters the baroreflex control of heart rate in the rabbit

1998 ◽  
Vol 274 (1) ◽  
pp. R181-R186 ◽  
Author(s):  
Hiroshi Murakami ◽  
Jun-Li Liu ◽  
Hirohito Yoneyama ◽  
Yasuhiro Nishida ◽  
Kenji Okada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
No Synthase ◽  
Baroreflex Control ◽  
Neuronal No Synthase ◽  
Significant Difference ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Oxide Synthase

In previous studies we used N G-nitro-l-arginine (l-NNA) to investigate the role of nitric oxide (NO) in baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA).l-NNA increased resting mean arterial pressure (MAP), decreased HR, and did not change or slightly decreased RSNA. These changes complicated the assessment of the central effects of NO on the baroreflex control of HR and RSNA. Therefore, in the present study the effects of the relatively selective neuronal NO synthase inhibitor 7-nitroindazole (7-NI) on the baroreflex control of HR and RSNA were investigated in rabbits. Intraperitoneal injection of 7-NI (50 mg/kg) had no effect on resting HR, MAP, or RSNA. 7-NI significantly reduced the lower plateau of the HR-MAP baroreflex curve from 140 ± 4 to 125 ± 4 and from 177 ± 10 to 120 ± 9 beats/min in conscious and anesthetized preparations, respectively ( P < 0.05). In contrast, there was no significant difference in the RSNA-MAP curves before and after 7-NI administration in conscious or anesthetized preparations. These data suggest that blockade of neuronal NO synthase influences baroreflex control of HR but not of RSNA in rabbits.

Role of V1 receptors in the action of vasopressin on the baroreflex control of heart rate

1993 ◽  
Vol 265 (3) ◽  
pp. R524-R529 ◽  
Author(s):  
J. Luk ◽  
I. Ajaelo ◽  
V. Wong ◽  
J. Wong ◽  
D. Chang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Logistic Model ◽  
Cardiovascular Effects ◽  
Baroreflex Control ◽  
Lower Blood ◽  
V2 Receptor

Arginine vasopressin (AVP) elicits a larger decrease in heart rate for a given increase in arterial pressure than do other vasoconstrictors, but there is disagreement as to whether this results from an increase in baroreflex gain or a resetting of the baroreflex to a lower blood pressure. It is also unclear which type of vasopressin receptor mediates the action of vasopressin on the baroreflex. In the present study, the effects of vasopressin, selective vasopressin V1 and V2 receptor agonists, oxytocin, and a vasopressin V1 receptor antagonist on the baroreflex control of heart rate were investigated in conscious, chronically prepared rabbits. Baroreflex curves were generated with intravenous infusions of phenylephrine and nitroprusside and analyzed using a four-parameter logistic model. Intravenous infusion of vasopressin at 5 ng.kg-1.min-1 increased mean arterial pressure by 9 mmHg and decreased heart rate by 31 beats/min. The arterial pressure at the midrange of the baroreflex curve (BP50) decreased from 75.9 +/- 4.8 to 57.6 +/- 1.7 mmHg (P < 0.01), indicating a shift of the baroreflex curve to a lower pressure, but the gain did not change significantly. The actions of vasopressin on blood pressure, heart rate, and BP50 were completely blocked by pretreatment with d(CH2)5[Tyr(Me)2]AVP, a selective V1 receptor antagonist. Infusion of [Phe2,Ile3,Orn8]AVP, a selective V1 receptor agonist, produced cardiovascular effects similar to those of vasopressin and decreased the BP50 of the baroreflex from 73.0 +/- 2.2 to 63.8 +/- 2.2 mmHg (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice

2003 ◽  
Vol 284 (3) ◽  
pp. H1003-H1007 ◽  
Author(s):  
Baojian Xue ◽  
Hope Gole ◽  
Jaya Pamidimukkala ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Area Postrema ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Intravenous Infusions

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: −3.0 ± 0.9 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: −5.8 ± 0.7 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

Altered heart rate-arterial pressure relation during head-out water immersion in conscious dog

1988 ◽  
Vol 254 (4) ◽  
pp. R595-R601 ◽  
Author(s):  
H. Yoshino ◽  
D. C. Curran-Everett ◽  
S. K. Hong ◽  
J. A. Krasney
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Inferior Vena ◽  
Water Immersion ◽  
Vena Cava ◽  
Systolic Arterial Pressure ◽  
Baroreflex Control ◽  
Rate Range ◽  
Average Gain ◽  
Cholinergic Regulation

The influence of head-out water immersion (WI) (37 degrees C) on baroreflex control of heart rate was studied in five trained, instrumented, conscious dogs. Arterial pressure was raised and lowered using occluder cuffs implanted around the aorta and inferior vena cava. Function curves relating transmural systolic arterial pressure (TSAP = systolic arterial pressure-pleural pressure) to heart rate (HR) were constructed to compare responses in air and during WI. The resting TSAP in air [142 +/- 8 mmHg (mean +/- SE) at 78 +/- 6 beats/min] increased significantly during WI (161 +/- 9 mmHg at 109 +/- 9 beats/min). During WI, the saturation TSAP at the bradycardia plateau of the relation increased significantly, by 19 mmHg, whereas the average gain (slope) of the relation decreased significantly, from -1.426 to -0.752 beats.min-1.mmHg-1. Therefore, WI elicits both a resetting and a decrease of the average gain of the TSAP-HR relation. The heart rate range increased during WI as well. After cholinergic blockade with atropine, WI did not elicit a resetting of the relation and the change in average gain was abolished. However, after beta 1-blockade with metoprolol, the resting TSAP increased significantly during WI and resetting persisted, but the decrease of average gain was abolished. Therefore, the alteration of the TSAP-HR relation in WI is achieved via a modulation of both adrenergic and cholinergic regulation of HR.

Sign in / Sign up

Export Citation Format

Share Document