Ontogeny of the arterial and cardiopulmonary baroreflex during fetal and postnatal life

1997 ◽  
Vol 273 (2) ◽  
pp. R457-R471 ◽  
Author(s):  
J. L. Segar
Keyword(s):  
Nervous System ◽  
Angiotensin Ii ◽  
Cardiovascular System ◽  
Cardiovascular Function ◽  
Postnatal Life ◽  
Fetal Life ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Autonomic Reflexes ◽  
Cardiopulmonary Baroreflex

The autonomic nervous system is intimately involved in regulating cardiovascular function. Sensing mechanisms dispersed throughout the circulation, including arterial baroreceptors, low pressure receptors, and chemosensitive receptors, continually evoke reflexes designed to maintain cardiovascular homeostasis. Although there is a growing body of knowledge regarding neural regulation of the adult cardiovascular system, characterization and understanding of these physiological systems during development is limited. This review highlights developmental changes in the arterial and cardiopulmonary baroreflex during fetal and postnatal life and contrasts the function of these responses with those seen in the adult. Baroreceptors are functional in the immature animal and reset toward higher pressure levels with maturation. In our ovine model, the sensitivity of the efferent limb of the baroreflex is greatest during fetal life and decreases with postnatal development. As in the adult, angiotensin II and arginine vasopressin interact with the sympathetic nervous system early during development to alter baroreflex control of the cardiovascular system. However, the extent to which these hormonal systems influence autonomic reflexes during the fetal and newborn period appears vastly different than in the adult. Endogenous angiotensin II significantly contributes to resetting of the arterial baroreflex early in life, whereas even high circulating levels of vasopressin have little effect on baroreflex function until adulthood. Finally, the ability of cardiopulmonary mechanoreceptors to regulate cardiovascular function is impaired early in development, in sharp contrast to the heightened sensitivity of the arterial baroreflex at this stage of maturation. The potential importance of these autonomic reflexes on cardiovascular function during the perinatal period is highlighted.

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.

scholarly journals Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

2004 ◽  
Vol 55 (6) ◽  
pp. 1042-1049 ◽  
Author(s):  
Patrick Pladys ◽  
Isabelle Lahaie ◽  
Gilles Cambonie ◽  
Gaétan Thibault ◽  
Ngoc Loan Oanh Lê ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Fetal Life ◽  
Arterial Baroreflex

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.

Impaired central mediation of the arterial baroreflex in chronic renal hypertension

1984 ◽  
Vol 246 (5) ◽  
pp. H720-H727 ◽  
Author(s):  
G. B. Guo ◽  
F. M. Abboud
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Sympathetic Nerve Activity ◽  
Renal Hypertension ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Aortic Depressor Nerve ◽  
The Central Nervous System ◽  
Selective Impairment ◽  
Stimulation Of

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

scholarly journals Autonomic nervous system influence on arterial baroreflex control of heart rate during exercise in humans

2005 ◽  
Vol 566 (2) ◽  
pp. 599-611 ◽  
Author(s):  
Shigehiko Ogoh ◽  
James P. Fisher ◽  
Ellen A. Dawson ◽  
Michael J. White ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Autonomic Nervous ◽  
Exercise In Humans

Baroreflex control of sympathetic outflow in pregnant rats: effects of captopril

1990 ◽  
Vol 258 (6) ◽  
pp. R1417-R1423 ◽  
Author(s):  
M. E. Crandall ◽  
C. M. Heesch
Keyword(s):  
Base Line ◽  
Operating Pressure ◽  
Sympathetic Outflow ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Pregnant Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Near Term ◽  
Renal Sympathetic

Arterial baroreflex control of renal sympathetic nerve activity (RSNA) was compared in nonpregnant (NP) and near-term pregnant (P) chloralose-anesthetized rats. Baroreflex curves were obtained by recording reflex changes in RSNA (expressed as a percent of base line) due to increases and decreases in mean arterial pressure (MAP) [intravenous phenylephrine and nitroprusside (NTP)]. The slope, midpoint (EP50), and threshold pressures of the baroreflex curves were compared. Base-line MAP was significantly lower in the pregnant animals (P = 96 +/- 3 vs. NP = 113 +/- 5 mmHg). The baroreflex curves of pregnant animals also had significantly lower threshold (P = 95 +/- 3 vs. NP = 110 +/- 5 mmHg) and midpoint values (P = 105 +/- 4 vs. NP = 119 +/- 5 mmHg). The response to unloading the baroreceptors was attenuated in the pregnant animals as indicated by a decrease in slope of the NTP portion of the baroreflex curve (P = 0.95 +/- 0.17 vs. NP = 1.61 +/- 0.29% nerve activity/mmHg). Responses to blockade of angiotensin-converting enzyme with captopril (2 mg/kg iv) were also examined. There were no differences in EP50 or slope among the control, captopril, and recovery baroreflex curves within either the nonpregnant or pregnant animals. However, after captopril, MAP decreased to a greater extent in the pregnant rats, yet RSNA increased to the same level for the two groups. Thus pregnancy results in a leftward shift of the baroreflex function curve toward a lower operating pressure range. In addition, pregnant rats demonstrated an impaired ability to increase sympathetic outflow above base-line values in response to a hypotensive challenge.

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