Role of β‐adrenoceptor‐adenylate cyclase system in the developmental decrease in sensitivity to isoprenaline in foetal and neonatal rat heart

Tanaka, Hikaru; Shigenobu, Koki

doi:10.1111/j.1476-5381.1990.tb12065.x

Cited by 30 publications

(12 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The calculated half-maximal effective concentration for isoprenaline in these experiments was shown to be in the lower nanomolar range, which is ϳ10-fold less than those reported from studies in neonatal rat hearts and adult rat papillary muscle [ϳ50 nM; (52,91)]. The relative isoprenaline-induced increase in force appears smaller in engineered constructs than in adult heart preparations (ϳ2-fold vs. 4 -5-fold, Table 1), which may again indicate immaturity.…”

Section: Tissue Engineering To Model (Human) Heart Tissue Functioncontrasting

confidence: 38%

Physiological aspects of cardiac tissue engineering

Eschenhagen

Eder

Vollert

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Cardiac tissue engineering aims at repairing the diseased heart and developing cardiac tissues for basic research and predictive toxicology applications. Since the first description of engineered heart tissue 15 years ago, major development steps were directed toward these three goals. Technical innovations led to improved three-dimensional cardiac tissue structure and near physiological contractile force development. Automation and standardization allow medium throughput screening. Larger constructs composed of many small engineered heart tissues or stacked cell sheet tissues were tested for cardiac repair and were associated with functional improvements in rats. Whether these approaches can be simply transferred to larger animals or the human patients remains to be tested. The availability of an unrestricted human cardiac myocyte cell source from human embryonic stem cells or human-induced pluripotent stem cells is a major breakthrough. This review summarizes current tissue engineering techniques with their strengths and limitations and possible future applications.

show abstract

Section: Tissue Engineering To Model (Human) Heart Tissue Functioncontrasting

confidence: 38%

Physiological aspects of cardiac tissue engineering

Eschenhagen

Eder

Vollert

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…In the case of the ventricular myocardium of rats (reviewed by Shigenobu, 1990), a tenfold decrease in the sensitivity to NA and isoprenaline occurs in the early postnatal period concurrently with the increase in sympathetic innervation density (Shigenobu et al, 1988;Tanaka & Shigenobu, 1990a). Sympathetic denervation studies (Ishii et al, 1982;Goto et al, 1985) and organ culture experiments (Tanaka et al, 1988a;Tanaka & Shigenobu, 1990b) revealed that sympathetic innervation is not only responsible for the pre-junctional component of the decreased sensitivity, but also exerts a long-term influence on myocardial properties to maintain the sensitivity to agonists at normal level. Whether the developmental decrease in sensitivity of the P-adrenoceptor-mediated effects (Tanaka et al, 1994) and conversion of o-adrenoceptor-mediated effects from positive to negative (Figure 1) Osnes et al, 1985), in hypoxia (Heathers et al, 1988), hypertension (Limas & Limas, 1987) and experimentally induced diabetes mellitus (Heijnis & van Zwieten, 1992).…”

Section: Discussionmentioning

confidence: 99%

Sustained negative inotropism mediated by α‐adrenoceptors in adult mouse myocardial developmental conversion from positive response in the neonate

Tanaka

Manita

Matsuda

et al. 1995

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

1 Inotropic responses to x-adrenoceptor stimulation and the effects of antagonists were examined in isolated ventricular preparations from neonatal and adult mice. 2 Phenylephrine, in the presence of propranolol, produced positive inotropic responses in neonates up to 1 week after birth, while it produced negative inotropic responses in mice older than 3 weeks. 3 Both positive and negative responses to phenylephrine in neonates and adults, respectively, were antagonized by prazosin, WB4101 (2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane) and 5-methylurapidil, but not by atropine, yohimbine or chlorethylclonidine. 4 Noradrenaline (NA) produced positive inotropic responses both in the neonate and adult; the responses were observed in a lower concentration-range in the neonate than in the adult. WB4101 produced a significant leftward shift of the concentration-response curve for noradrenaline in adult preparations while only a slight rightward shift was observed in the neonate. 5 Our results demonstrate the presence of x-adrenoceptor-mediated inotropic responses in the mouse ventricular myocardia. The response to phenylephrine changes from a positive to a negative effect during postnatal development. The responses are mediated by a,-adrenoceptors, and modulate the overall inotropic response to NA in the adult.

show abstract

“…Sympathetic innervation of the newborn heart modulates P-adrenoceptor number and function [7,28] presumably by downregulat ing receptor number through norepinephrine release. Alterations in the development of in nervation in the heart of the newborn rat by blocking nerve growth with antibody to nerve growth factor [14, 32] or 6-hydroxydopa [33] alter the normal postnatal changes in P-adrenoceptors.…”

Section: Receptor Density and Affinitymentioning

confidence: 99%

Ontogeny of Rat Myocardial A<sub>1</sub> Adenosine Receptors

Cothran

Lloyd²,

Taylor

et al. 1995

Neonatology

View full text Add to dashboard Cite

Adenosine functions as a counterregulatory hormone in the myocardium by decreasing work and thereby protecting the myocardium against ischemia. Functional adenosine A₁ receptors could serve as an important regulatory system in the developing preinnervated heart by balancing the humoral sympathetic input to the heart. The aims of this study were to determine if A₁ adenosine receptors were functionally coupled to their G_i protein in the immature preinnervated heart and to determine if A₁ adenosine receptors were present in greater numbers in the immature heart. One- to 3-day-old rat ventricular cardiomyocyte cultures were exposed to (1) control conditions; (2) isoproterenol, a β-receptor agonist; (3) R-PIA, an A₁ agonist, or (4) isoproterenol and R-PIA. cAMP levels were determined by RIA in each group. Adenosine A₁ receptor density and the equilibrium dissociation constant were determined by binding of an adenosine At receptor antagonist in newborn, 1-week-old, 2-week-old, and adult rat hearts. A₁ stimulation decreased the isoproterenol-induced increase in cAMP by 30%, demonstrating functional A₁ receptors in immature preinnervated myocytes. The A₁ receptor density in the newborn age group was twice the adult and 2-week-old level. We conclude that A₁ receptors in the immature heart are functionally coupled to their effector and that A₁ receptors are present in greater numbers in the immature heart.

show abstract

Role of β‐adrenoceptor‐adenylate cyclase system in the developmental decrease in sensitivity to isoprenaline in foetal and neonatal rat heart

Cited by 30 publications

References 20 publications

Physiological aspects of cardiac tissue engineering

Physiological aspects of cardiac tissue engineering

Sustained negative inotropism mediated by α‐adrenoceptors in adult mouse myocardial developmental conversion from positive response in the neonate

Ontogeny of Rat Myocardial A<sub>1</sub> Adenosine Receptors

Contact Info

Product

Resources

About