Age-related differences in beta-adrenergic regulation of repolarization in canine epicardial myocytes

1996 ◽  
Vol 271 (3) ◽  
pp. H1174-H1181 ◽  
Author(s):  
F. Charpentier ◽  
Q. Y. Liu ◽  
M. R. Rosen ◽  
R. B. Robinson
Keyword(s):  
Ventricular Myocardium ◽  
Control Site ◽  
Developmental Changes ◽  
Delayed Rectifier ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Control Value ◽  
Age Related ◽  
Patch Technique ◽  
Epicardial Myocytes

Developmental changes occur in beta-adrenergic modulation of repolarization in canine. Purkinje fibers that may have important implications for rhythm and arrhythmias. No comparable data exist for ventricular myocardium. Therefore, we studied developmental changes in beta-adrenergic regulation of repolarization and delayed rectifier potassium current (IK) in canine ventricular epicardium. We first investigated the effects of isoproterenol (Iso) on action potentials (AP) recorded from epicardial slices with standard microelectrodes, and then we further determined the mechanisms of Iso action using the nystatin-perforated patch technique on isolated epicardial myocytes. In microelectrode studies Iso (10(-7) M) induced a shortening of the AP in preparations from adult dogs but not in those from dogs < 30 days old. These results were confirmed on AP recorded from single myocytes. Although the plateau was increased by Iso at all ages, the AP at 90% of repolarization was shortened (P < 0.05, n = 6) in adult but unchanged in < 30-day-old myocytes (NS, n = 6). Voltage-clamp studies showed that IK of adult cells was increased from a control value of 10.23 +/- 1.87 to 13.43 +/- 1.92 pA/pF with Iso (step to +50 mV, P < 0.05, n = 6), but IK was not modified in cells from young animals (6.49 +/- 2.72 pA/pF in control and 6.56 +/- 2.62 pA/pF with Iso, n = 4). Increasing the Iso concentration to 10(-5) M failed to increase IK significantly (n = 4). However, 10(-7) M Iso did increase L-type Ca2+ current from 172 +/- 31 to 262 +/- 42 pA (P < 0.05, n = 4), consistent with the effect to increase the AP plateau. These results show that there are developmental changes in beta-adrenergic regulation of repolarization in canine epicardium and that the control site of developmental changes is in the IK channel rather than the beta-adrenergic receptor cascade.

Pertussis toxin enhances the beta-adrenergic and blocks the alpha-adrenergic regulation of renin secretion in renal cortical slices

Life Sciences ◽  
1986 ◽  
Vol 38 (11) ◽  
pp. 1005-1011 ◽  
Author(s):  
José Pedraza-Chaverrí ◽  
M.Carmen Alatorre-González ◽  
JoséCarlos Peña ◽  
J.Adolfo García-Sáinz
Keyword(s):  
Pertussis Toxin ◽  
Renin Secretion ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Cortical Slices

Abstract 17185: Sympathetic Reinnervation is Required for Mammalian Cardiac Regeneration

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Ian A White ◽  
Julie Gordon ◽  
Wayne Balkan ◽  
Joshua M Hare
Keyword(s):  
Sympathetic Innervation ◽  
Cardiac Regeneration ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Neonatal Mouse ◽  
Left Ventricular Myocardium ◽  
Autonomic Nerves ◽  
Mouse Heart ◽  
Minimal Scarring ◽  
Age Related

Rationale: Established animal models of tissue and limb regeneration demonstrate a critical dependence on concurrent reinnervation by the peripheral nervous system. The abundance of autonomic nerves in the mammalian heart suggests they play a similar role in the response to cardiac injury. Objective: To test the hypothesis that reinnervation is required for innate neonatal cardiac regeneration. Methods and Results: Crossing Wnt1:cre transgenic mice with a double-tandem (td) tomato reporter strain identified all neural crest-derived cell lineages including the peripheral autonomic nerves in the heart. Whole mount epi-fluorescence microscopy facilitated the clear resolution of subepicardial autonomic nerves in the mouse ventricles providing unprecedented detail of the subepicardial neuroanatomy of the mouse heart. We confirmed that sympathetic nerve structures envelop the entire heart, and importantly, exhibit robust re-growth into the regenerating myocardium following resection of the left ventricular apex in neonatal mice. While innervated hearts regenerate with minimal scarring to the left ventricular myocardium, we report that innate cardiac regeneration was inhibited following sympathectomy, as determined by cross-sectional percentage of viable LV myocardium (n=9, 0.87±1.4% vs. n=6, 14.05±4.4% ; p<0.01). Conclusions: Ablation of post-ganglionic sympathetic nerves blocks the innate regenerative capacity of neonatal mouse hearts. Therefore, the innate ability of the neonatal mouse heart to undergo regeneration in response to injury is dependent on sympathetic innervation of the ventricular myocardium. This finding has significant implications for adult regeneration following myocardial infarction where nerve growth is hindered by age related influences and scar tissue.

scholarly journals Age-related differences in the cutaneous vascular response to exogenous angiotensin II

2019 ◽  
Vol 316 (3) ◽  
pp. H516-H521
Author(s):  
James A. Lang ◽  
Alex C. Krajek
Keyword(s):  
Older Adults ◽  
Angiotensin Ii ◽  
Ringer Solution ◽  
Control Site ◽  
Laser Doppler ◽  
Type Ii ◽  
Ang Ii ◽  
Age Related ◽  
Forearm Skin ◽  
Doppler Flux

Angiotensin II (ANG II) is locally produced in human skin and contributes to the reflex vasoconstriction (VC) response in aged but not young skin. We hypothesized that the exogenous ANG II-mediated VC response would be greater in older adults and would be affected by inhibition of adrenoreceptor or ANG II type II receptor (AT2R) pathways. Three microdialysis (MD) fibers were placed in the forearm skin of 11 young (26 ± 3 yr) and 11 older (68 ± 4 yr) individuals for perfusion of 1) Ringer solution (control), 2) adrenoreceptor blockade with yohimbine + propranolol, and 3) AT2R inhibition with PD-123319. ANG II was then added to the perfusates at eight graded dose concentrations ranging from 10−10 to 10−3 M. Laser Doppler flux was measured at each MD site, and cutaneous vascular conductance (CVC) was calculated as CVC =  laser Doppler flux/mean arterial pressure and normalized to baseline CVC values collected before ANG II perfusion (%ΔCVCbaseline). At the control site, older adults (−34 ± 4%ΔCVCbaseline) exhibited a greater peak VC compared with young adults (−22 ± 2%ΔCVCbaseline, P < 0.05), which was attenuated with adrenoreceptor blockade. Young skin exhibited a vasodilation in response to lower ANG II doses that was inhibited with AT2R inhibition. AT2R inhibition also increased the VC response to higher ANG II doses such that young skin responded similarly to older skin. These results indicate that ANG II has a greater VC influence in older than young individuals. Furthermore, ANG II may be affecting multiple targets, including adrenergic and AT2R pathways. NEW & NOTEWORTHY Intradermal perfusion of successive doses of angiotensin II (ANG II) revealed a role for ANG II type II receptors and dose-dependent, ANG II-mediated vasodilation in young but not older adults. In contrast, older adults exhibited greater vasoconstriction for a given dose of ANG II. The increased vasoconstriction in older adults was subsequently blunted with adrenoreceptor blockade, which indicates an interaction between ANG II and adrenergic signaling pathways in the cutaneous microcirculation.

Emotion regulation from early adolescence to emerging adulthood and middle adulthood

2014 ◽  
Vol 38 (2) ◽  
pp. 182-194 ◽  
Author(s):  
Peter Zimmermann ◽  
Alexandra Iwanski
Keyword(s):  
Emotion Regulation ◽  
Early Adolescence ◽  
Methodological Approach ◽  
Developmental Changes ◽  
Middle Adulthood ◽  
Emotion Regulation Strategies ◽  
Age Related ◽  
Emotion Regulation Strategy ◽  
Regulation Strategies ◽  
Age Range

Despite the growing research on emotion regulation, the empirical evidence for normative age-related emotion regulation patterns is rather divergent. From a life-span perspective, normative age changes in emotion regulation may be more salient applying the same methodological approach on a broad age range examining both growth and decline during development. In addition, emotion-specific developmental patterns might show differential developmental trends. The present study examined age differences in seven emotion regulation strategies from early adolescence (age 11) to middle adulthood (age 50) for the three emotions of sadness, fear, and anger. The results showed specific developmental changes in the use of emotion regulation strategies for each of the three emotions. In addition, results suggest age-specific increases and decreases in many emotion regulation strategies, with a general trend to increasing adaptive emotion regulation. Specifically, middle adolescence shows the smallest emotion regulation strategy repertoire. Gender differences appeared for most emotion regulation strategies. The findings suggest that the development of emotion regulation should be studied in an emotion-specific manner, as a perspective solely on general emotion regulation either under- or overestimates existing emotion-specific developmental changes.

scholarly journals Developmental changes in story-evoked responses in the neocortex and hippocampus

2021 ◽  
Author(s):  
Samantha Syd Cohen ◽  
Christopher Baldassano
Keyword(s):  
Division Of Labor ◽  
Life Events ◽  
Developmental Changes ◽  
Fmri Data ◽  
Evoked Responses ◽  
Age Related ◽  
Brain Responses ◽  
Episodic Encoding ◽  
Upcoming Event ◽  
Event Representations

How does the representation of naturalistic life events change with age? Here we analyzed fMRI data from 415 children and adolescents (5 - 19 years) as they watched a narrative movie. In addition to changes in the degree of inter-subject correlation (ISC) with age in sensory and medial parietal regions, we used a novel measure (between-groups ISC) to reveal age-related shifts in the responses across the majority of the neocortex. Over the course of development, brain responses became more discretized into stable and coherent events, and shifted earlier in time to anticipate upcoming event transitions. However, hippocampal responses to event boundaries actually decreased with age, suggesting a shifting division of labor between episodic encoding processes and schematic event representations between the ages of 5 and 19.

beta-Adrenergic regulation of adenosine 3',5'-monophosphate concentration in brain microvessels

Science ◽  
1979 ◽  
Vol 204 (4390) ◽  
pp. 330-332 ◽  
Author(s):  
T. Herbst ◽  
M. Raichle ◽  
J. Ferrendelli
Keyword(s):  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Brain Microvessels

Abstract 170: Arginase Contributes to Delayed Constriction of Large Cerebral Arteries in a Model of Subarachnoid Hemorrhage

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Weiyun Sun ◽  
Kathleen K Kibler ◽  
Herman Kwansa ◽  
Ewa Kulikowicz ◽  
Weizhu Tang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ex Vivo ◽  
Cerebral Arteries ◽  
Arginase Activity ◽  
Male Rats ◽  
Control Value ◽  
Age Related ◽  
Arterial Constriction ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

Introduction: Increased arginase activity can limit nitric oxide synthase activity and contribute to age-related increase in aortic stiffness. Hypothesis: Subarachnoid hemorrhage (SAH) produces a delayed increase in arginase activity that contributes to delayed decreases in diameter of major cerebral arteries. Methods: Male rats underwent injection of blood into the cisterna magna on day 0 and again on day 2. Shams had double injection of artificial CSF. Measurements of arginase activity on vessels in the Circle of Willis and pia matter were made with an assay based on the conversion of radiolabeled arginine to urea. Measurements of diameter of basilar, posterior (PCA), middle (MCA), and anterior (ACA) cerebral arteries were made ex vivo after perfusion with paraformaldehyde and black latex casting. Results: Arginase activity (nmol of urea/min/mg of protein) increased from the control value of 13±3 (±SE; n=17) to 24±6 (n=6) at 3 days, 36±14 (n=4) at 5 days, and 48±16 (n=9) at 7 days after SAH and then recovered at 10 days (14±5; n=4) and 14 days (18±6; n=5) after SAH. Infusion of the arginase inhibitor 2(S)-amino-6-boronohexanoic acid (ABH) for 7 days after SAH with an ip osmotic pump blocked the increase in arginase activity (10±2; n=4). Assessment of arterial diameter at 3, 5, 7, 10, and 14 days after SAH revealed the smallest diameters occurring at 7 days (except for MCA which occurred at 5 days). Continuous ip infusion of 10 mg/kg/day ABH significantly attenuated the decrease in diameter (μm) 7 days after SAH in PCA (sham = 249±9, n=8; SAH = 209±12, n=10; SAH+ABH = 255±9, n=6) and ACA (sham = 178±11; SAH = 141±11; SAH+ABH = 198±10). Effects on basilar artery were of marginal significance (P=0.065). Conclusion: SAH produces an increase in vascular arginase activity that is temporally related to delayed decreases in diameter of cerebral arteries. Inhibition of arginase activity prevents the decrease in diameter at 7 days after SAH, thereby indicating a contribution of arginase to delayed arterial constriction/remodeling in post-fixed arteries.

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