scholarly journals Role of the area postrema in the modulation of the baroreflex control of heart rate by angiotensin II.

1990 ◽  
Vol 67 (6) ◽  
pp. 1462-1473 ◽  
Author(s):  
S Matsukawa ◽  
I A Reid
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Area Postrema ◽  
Baroreflex Control

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.

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.

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

Endogenous ANG II supports lumbar sympathetic activity in conscious sodium-deprived rats: role of area postrema

1998 ◽  
Vol 275 (1) ◽  
pp. R46-R55 ◽  
Author(s):  
Ling Xu ◽  
John P. Collister ◽  
John W. Osborn ◽  
Virginia L. Brooks
Keyword(s):  
Sympathetic Activity ◽  
Food Restriction ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Ang Ii ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Maximal Gain

This study tests the hypothesis that the area postrema (AP) is necessary for endogenous ANG II to chronically maintain lumbar sympathetic nerve activity (LSNA) and heart rate (HR) in conscious sodium-deprived rats. The effect of the ANG II type 1-receptor antagonist, losartan, on LSNA and HR was determined in rats that were either AP lesioned (APX) or sham lesioned. The sham rats were divided into groups, with (SFR) or without (SAL) food restriction, to control for the decreased food intake of APX rats. Before losartan, basal mean arterial pressure (MAP), HR, and baroreflex control of LSNA and HR were similar between groups, with the exception of lower maximal reflex LSNA and higher maximal gain of the HR-MAP curve in APX rats. In all groups, losartan similarly shifted ( P < 0.01) the LSNA-MAP curve to the left without altering maximal gain. Losartan also decreased ( P < 0.05) minimal LSNA in all groups, and suppressed ( P < 0.01) maximal LSNA (% of control) in SFR (240 ± 13 to 205 ± 15) and SAL (231 ± 21 to 197 ± 26) but not APX (193 ± 10 to 185 ± 8) rats. In general, losartan similarly shifted the HR-MAP curve to a lower MAP in all groups. The results suggest that the AP is not necessary for endogenous ANG II to chronically support LSNA and HR at basal and elevated MAP levels in sodium-deprived rats. However, the AP is required for endogenous ANG II to increase maximal reflex LSNA at low MAP levels.

scholarly journals Acute sympathoexcitatory action of angiotensin II in conscious baroreceptor-denervated rats

2002 ◽  
Vol 283 (2) ◽  
pp. R451-R459 ◽  
Author(s):  
Ling Xu ◽  
Alan F. Sved
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Ang Ii ◽  
Nerve Activity ◽  
Induced Hypotension ◽  
Baroreceptor Reflexes

Angiotensin II (ANG II) has complex actions on the cardiovascular system. ANG II may act to increase sympathetic vasomotor outflow, but acutely the sympathoexcitatory actions of exogenous ANG II may be opposed by ANG II-induced increases in arterial pressure (AP), evoking baroreceptor-mediated decreases in sympathetic nerve activity (SNA). To examine this hypothesis, the effect of ANG II infusion on lumbar SNA was measured in unanesthetized chronic sinoaortic-denervated rats. Chronic sinoaortic-denervated rats had no reflex heart rate (HR) responses to pharmacologically evoked increases or decreases in AP. Similarly, in these denervated rats, nitroprusside-induced hypotension had no effect on lumbar SNA; however, phenylephrine-induced increases in AP were still associated with transient decreases in SNA. In control rats, infusion of ANG II (100 ng · kg−1 · min−1 iv) increased AP and decreased HR and SNA. In contrast, ANG II infusion increased lumbar SNA and HR in sinoaortic-denervated rats. In rats that underwent sinoaortic denervation surgery but still had residual baroreceptor reflex-evoked changes in HR, the effect of ANG II on HR and SNA was variable and correlated to the extent of baroreceptor reflex impairment. The present data suggest that pressor concentrations of ANG II in rats act rapidly to increase lumbar SNA and HR, although baroreceptor reflexes normally mask these effects of ANG II. Furthermore, these studies highlight the importance of fully characterizing sinoaortic-denervated rats used in experiments examining the role of baroreceptor reflexes.

The Role of Endogenous Opiates in the Area Postrema Pressor Pathway

1980 ◽  
Vol 59 (s6) ◽  
pp. 267s-269s ◽  
Author(s):  
Julianna E. Szilagyi ◽  
C. M. Ferrario
Keyword(s):  
Angiotensin Ii ◽  
Vertebral Artery ◽  
Area Postrema ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Endogenous Opiates ◽  
Pressor Responses ◽  
Vasomotor Activity ◽  
The Brain

1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.

Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats

1987 ◽  
Vol 65 (5) ◽  
pp. 834-841 ◽  
Author(s):  
A-R. A. Abdel-Rahman ◽  
Roy Russ ◽  
J. A. Strickland ◽  
W. R. Wooles
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
Pressor Response ◽  
Base Line ◽  
Response Curves ◽  
Baroreflex Control ◽  
Conscious Rats ◽  
Upward Shift ◽  
The Right

In rats anesthetized with α-chloralose, doses of 0.1, 0.5, and 1 g/kg of ethanol produced an upward shift of baroreflex curves constructed by plotting the heart rate response against mean arterial pressure following evoked rises in mean arterial pressures by phenylephrine or angiotensin II. Whereas the upward shift of baroreceptor curves may be related, at least in part, to a higher base-line heart rate after ethanol, the data showed that the 1 g/kg dose of ethanol significantly depressed baroreflex sensitivity, suggesting that higher doses of ethanol impair baroreflex-mediated bradycardia. The phenylephrine, but not the angiotensin II or the nitroprusside, dose–response curves were shifted to the right after ethanol, indicating a decreased pressor responsiveness and suggesting that ethanol may have α-adrenergic blocking activity. This effect was also obtained in conscious rats. That this effect was not influenced by changes in baroreflex sensitivity was supported by the finding that a similar shift of the phenylephrine pressor–response curve was obtained in bilaterally vagotomized and hexamethonium-treated rats. Whether this effect of ethanol on baroreflex control of heart rate was influenced by anesthesia was investigated in conscious rats; the 1 g/kg dose of ethanol that produced the most significant decrease in baroreflex sensitivity was used in these experiments. Ethanol was still able to significantly inhibit baroreflex sensitivity in conscious rats, but the upward shift of the baroreflex curve and the elevated base-line heart rate no longer occurred. On the other hand, none of the three doses of ethanol had any significant effect on baroreflex-mediated tachycardia (in response to nitroprusside-evoked hypotension). The data suggest that high doses of ethanol selectively inhibit baroreflex-mediated bradycardia and that ethanol has an α-blocking-like activity in conscious and anesthetized rats.

scholarly journals Additive effects of heating and exercise on baroreflex control of heart rate in healthy males

2017 ◽  
Vol 123 (6) ◽  
pp. 1555-1562 ◽  
Author(s):  
Tiago Peçanha ◽  
Cláudia L. M. Forjaz ◽  
David. A. Low
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Baroreflex Sensitivity ◽  
Whole Body ◽  
Additive Effects ◽  
Passive Heating ◽  
Baroreflex Control ◽  
Rr Intervals ◽  
Body Heat

This study assessed the additive effects of passive heating and exercise on cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV). Twelve healthy young men (25 ± 1 yr, 23.8 ± 0.5 kg/m2) randomly underwent two experimental sessions: heat stress (HS; whole body heat stress using a tube-lined suit to increase core temperature by ~1°C) and normothermia (NT). Each session was composed of a preintervention rest (REST1); HS or NT interventions; postintervention rest (REST2); and 14 min of cycling exercise [7 min at 40%HRreserve (EX1) and 7 min at 60%HRreserve (EX2)]. Heart rate and finger blood pressure were continuously recorded. cBRS was assessed using the sequence (cBRSSEQ) and transfer function (cBRSTF) methods. HRV was assessed using the indexes standard deviation of RR intervals (SDNN) and root mean square of successive RR intervals (RMSSD). cBRS and HRV were not different between sessions during EX1 and EX2 (i.e., matched heart rate conditions: EX1 = 116 ± 3 vs. 114 ± 3 and EX2 = 143 ± 4 vs. 142 ± 3 beats/min but different workloads: EX1 = 50 ± 9 vs. 114 ± 8 and EX2 = 106 ± 10 vs. 165 ± 8 W; for HS and NT, respectively; P < 0.01). However, when comparing EX1 of NT with EX2 of HS (i.e., matched workload conditions but with different heart rates), cBRS and HRV were significantly reduced in HS (cBRSSEQ = 1.6 ± 0.3 vs. 0.6 ± 0.1 ms/mmHg, P < 0.01; SDNN = 2.3 ± 0.1 vs. 1.3 ± 0.2 ms, P < 0.01). In conclusion, in conditions matched by HR, the addition of heat stress to exercise does not affect cBRS and HRV. Alternatively, in workload-matched conditions, the addition of heat to exercise results in reduced cBRS and HRV compared with exercise in normothermia. NEW & NOTEWORTHY The present study assessed cardiac baroreflex sensitivity during the combination of heat and exercise stresses. This is the first study to show that prior whole body passive heating reduces cardiac baroreflex sensitivity and autonomic modulation of heart rate during exercise. These findings contribute to the better understanding of the role of thermoregulation on cardiovascular regulation during exercise.

Sign in / Sign up

Export Citation Format

Share Document