Changes in ovine renal sympathetic nerve activity and baroreflex function at birth

Segar, Jeffrey L.; Mazursky, Jon E.; Robillard, J

doi:10.1152/ajpheart.1994.267.5.h1824

Cited by 20 publications

(24 citation statements)

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“…In addition, cortisol replacement results in a resetting or shift of the efferent limb of the HR and RSNA baroreflex toward higher arterial pressure. The immediate postnatal increases in resting HR, MABP, and RSNA and the resetting of the HR and RSNA baroreflex curves are similar to those previously described by this laboratory in intact lambs (31), suggesting that the natural prepartum increase in fetal plasma cortisol concentration is vital for normal autonomic and sympathetic function at birth.…”

Section: Discussionsupporting

confidence: 84%

“…On the other hand, we achieved plasma cortisol levels well within the physiological range present immediately before delivery. Because newborn systemic hemodynamic measurements in ADX ϩ F animals were similar to those reported by others and us in intact animals, we suggest that adequate levels of circulating glucocorticoids are of primary importance in cardiovascular adaptation at birth (23,31,32). Antenatal administration of glucocorticoids augments cardiovascular performance in prematurely delivered lambs, despite these animals' having lower plasma epinephrine levels than controls (22,30).…”

Section: Discussionsupporting

confidence: 82%

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Effects of fetal ovine adrenalectomy on sympathetic and baroreflex responses at birth

Segar¹,

Natta

Fg³

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Studies were performed to test the hypothesis that the absence of adrenal glucocorticoids late in gestation alters sympathetic and baroreflex responses before and immediately after birth. Fetal sheep at 130–131 days gestation (term 145 days) were subjected to bilateral adrenalectomy before the normal prepartum increase in plasma cortisol levels. One group of fetuses ( n = 5) received physiological cortisol replacement with a continuous infusion of hydrocortisone (2 mg · day−1 · kg−1 for 10 days), whereas the other group received 0.9% NaCl vehicle ( n = 5). All animals underwent a second surgery 48 h before the study for placement of a renal nerve recording electrode. Heart rate (HR), mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and baroreflex control of HR and RSNA were studied before and after cesarean section delivery. At the time of study (140–141 days gestation), fetal plasma cortisol concentration was undetectable in adrenalectomized (ADX) fetuses and 58 ± 9 ng/ml in animals receiving cortisol replacement (ADX + F). Fetal and newborn MABP was significantly greater in ADX + F relative to ADX animals. One hour after delivery, MABP increased 13 ± 3 mmHg and RSNA increased 91 ± 12% above fetal values in ADX + F (both P < 0.05) but remained unchanged in ADX lambs. The midpoint pressures of the fetal HR and RSNA baroreflex function curves were significantly greater in ADX + F (54 ± 3 and 56 ± 3 mmHg for HR and RSNA curves, respectively) than ADX fetuses (45 ± 2 and 46 ± 3 mmHg). After delivery, the baroreflex curves reset toward higher pressure in ADX + F but not ADX lambs. These results suggest that adrenal glucocorticoids contribute to cardiovascular regulation in the late-gestation fetus and newborn by modulating arterial baroreflex function and sympathetic activity.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionsupporting

confidence: 82%

Effects of fetal ovine adrenalectomy on sympathetic and baroreflex responses at birth

Segar¹,

Natta

Fg³

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This increased activity has previously been shown to be important in regulating several of the cardiovascular and autonomic adaptations which occur during the transition from fetal to newborn life (1,25). More evidence that the RAS may be involved in the regulation of cardiac growth comes from pharmacological studies using inhibitors of the system by blocking the effects of ACE and the ANG-II AT1 receptor.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin Converting Enzyme Inhibition Decreases Cell Turnover in the Neonatal Rat Heart

Choi

2002

Pediatric Research

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The renin angiotensin system plays an important role in growth and development. Exposure of the neonate to an ACE inhibitor increases mortality and results in growth retardation and abnormal development. We have demonstrated that ACE inhibition in the developing kidney increases apoptosis and decreases cell proliferation, which may account for renal growth impairment. To evaluate the role of endogenous angiotensin in cardiac development, the relationship between ACE inhibition, cell proliferation, apoptosis, several modulators of apoptosis (bcl-2, bcl-xl, and clusterin) was examined in the developing rat heart. Thirty-five newborn rat pups were treated with enalapril (30 mg/kg/d) or a vehicle (control group) for 7 d, and hearts were removed for rt-PCR and Western blotting of bcl-2, bcl-xl, and clusterin. An additional 10 rat pups were treated with hydralazine (10 mg/kg/d) or a vehicle, to serve as a hypotensive control. Cell proliferation was determined by PCNA immunostaining, and apoptosis was detected using the total TUNEL technique. Enalapril treatment resulted in a 24% mortality, reduced body weight, and decreased heart weight (p Ͻ 0.05). Enalapril decreased proliferating myocytes by 23%, and reduced proliferating cardiac interstitial cells by 8.1% (p Ͻ 0.05). Enalapril also decreased myocytes apoptosis by 60%, but the proportion of myocytes undergoing apoptosis was 10-fold less than that of proliferating cells. Cardiac bcl-2 mRNA, clusterin mRNA, bcl-2 protein, and bcl-xl protein content were not changed, but clusterin protein expression was decreased by enalapril treatment. Hydralazine did not alter cardiac cell proliferation or apoptosis. We conclude that ACE inhibition decreases cell turnover in the developing rat heart, which may contribute to cardiac growth impairment. The loss of myocytes may lead to greater myocyte hypertrophy and myocardial damage during later life. The renin angiotensin system (RAS) plays a role in the maintenance of systemic arterial pressure in the newborn, and provides a homeostatic response to hypovolemia (1). Davidson (1) demonstrated parallel increases in plasma renin activity in arterial ANG-II concentration occurred in the immediate minutes after delivery. Furthermore, the release of catecholamines may be stimulated by the production of ANG II, and the activation of the sympathoadrenal system at birth has been implicated in several adaptive processes and structural integrity (2).In newborn animals and human infants, the activity of the RAS increases at birth, which is important in regulating cellular growth and organ differentiation (1, 3). ANG-II, which is a final product of the RAS, has been reported to exert atrophic effect on cardiac myocytes in cultures (4) and in vivo (5). ANG-II may stimulate a growth response in cardiac tissue indirectly, by increased blood pressure and total peripheral vascular resistance, which develops in response to ANG-II receptor coupling in the vasculature (5). Alternatively, ANG-II may have a direct effect by coupling to its cardiac membrane...

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“…To determine some of the mechanisms regulating the expression of renal AT, receptors during development in sheep, we first investigated the role of renal nerves. Because RSNA increases rapidly at birth (42) and renal nerves contribute to the increase in PRA and renal renin mRNA expression at birth (19,23), we postulated that renal nerves could also modulate renal AT, gene expression. More specifically, we speculated that the increase in RSNA and RAS activity at birth could activate a negative-feedback loop that may restrain the increase in renal AT, gene expression.…”

Section: Discussionmentioning

confidence: 99%

Ontogenic Changes and Regulation of Renal Angiotensin II Type 1 Receptor Gene Expression during Fetal and Newborn Life

et al. 1994

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Factors regulating the expression of the angiotensin I1 subtype 1 (AT,) receptor during fetal life have not been investigated previously. The present study was designed 1) to characterize the ontogeny of AT, receptor gene expression in the kidney of fetal and newborn sheep and 2) to determine the influence of both glucocorticoids and renal nerves in modulating AT, gene expression during fetal life and during the transition from fetal to newborn life. We first isolated and cloned a PCR product that has 98 and 94% homology with the cDNA encoding the bovine and pig AT, receptors, respectively, and 99 and 98% homology with the corresponding deduced protein sequences. Probing with this cDNA, we demonstrated that renal AT, mRNA expression did not change significantly during the last trimester of gestation in fetal sheep or immediately after birth but decreased significantly 10 d after birth. We also demonstrated that renal denervation in the fetus had no effect on renal AT, gene expression in 24-h-old newborn lambs. On the other hand, we observed in 130-d twin fetuses that a continuous intraperitoneal infusion (1 mL/h) of cortisol (3 mg/h or 6.2 p,mol/h) for 48 h in one of the twins increased the fetal plasma cortisol concentration from 32.0 + 7.1 to 1126 r 231 nmol/L and produced a significant decrease ( p < 0.005) in renal AT, gene expression compared with the control twin receiving an intraperitoneal infusion of 0.9% NaCl. In summary, this study demonstrates that renal AT, gene expression is elevated during fetal life and decreases after birth. It is also shown that glucocorticoids, but not renal nerves, contribute to the regulation of renal AT, gene expression during development. (Pediatr Res 36: 755-762, 1994)Abbreviations RAS, renin-angiotensin system AII, angiotensin I1 AT,, angiotensin I1 subtype 1 receptor AT,, angiotensin I1 subtype 2 receptor PCR, polymerase chain reaction RSNA, renal sympathetic nerve activity PRA, plasma renin activity rRNA, ribosomal RNA It has become apparent that the physiologic role of the RAS changes during embryonic and fetal maturation (1-4). Early during development, the RAS exerts a major influence o n cellular growth and organ differentiation (3-6). It is only later during fetal life that the RAS becomes an important modulator of blood pressure and distinct A11 receptor subtypes (AT, and AT,) (3, 9, 10). The AT, receptor subtype is expressed early during embryonic life in the rat (11,12), predominates in the fetal mesenchyme (3), and shows a marked decrease in expression during fetal and postnatal maturation (3). On the other hand, the AT, receptor subtype appears later during fetal development in the rat (3, 9, 10) and seems t o b e localized mainly in areas related t o blood pressure regulation and fluid homeostasis (3). Recent studies in rats have also shown that the AT, receptor gene is expressed in the fetal kidney, liver, adrenal, and heart and that the expression of this gene is developmentally regulated (9, lo), in agreement with previous A11 radioligand and in situ rece...

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Changes in ovine renal sympathetic nerve activity and baroreflex function at birth

Cited by 20 publications

References 0 publications

Effects of fetal ovine adrenalectomy on sympathetic and baroreflex responses at birth

Effects of fetal ovine adrenalectomy on sympathetic and baroreflex responses at birth

Angiotensin Converting Enzyme Inhibition Decreases Cell Turnover in the Neonatal Rat Heart

Ontogenic Changes and Regulation of Renal Angiotensin II Type 1 Receptor Gene Expression during Fetal and Newborn Life

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