Enhanced cardiac response to catecholamines in physically trained cats

Wyatt, H.L.; Chuck, Leonard; Rabinowitz, Betty; Tyberg, J. V.; Parmley, William W.

doi:10.1152/ajpheart.1978.234.5.h608

Cited by 28 publications

(23 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PLBt abundance was elevated with training in hypertension (SHR-TRD) versus WKY (PϽ0.05), with similar SERCA2A among groups ( Figure 6). Phospholamban phosphorylated at Ser 16 was significantly lower in SHR-SED than both WKY (PϽ0.05) and SHR-TRD (PϽ0.01). Additionally, greater phospholamban phosphorylated at Thr 17 was observed in SHR-TRD versus SHR-SED (PϽ0.01), whereas no difference was observed between WKY and SHR-SED.…”

Section: Western Blotsmentioning

confidence: 94%

“…26 Target antigens were probed with the following nonphosphorylation-specific monoclonal antibodies: SERCA (Sigma), phospholamban total (PLBt; Upstate Biotechnology), ryanodine receptor C3-33 (RyRt; Research Diagnostics), L-type calcium channel ␣1c subunit (LTCC; Chemicon), sodium-calcium exchanger (NCX; Swant), and GAPDH (Biogenesis). Phosphorylation-specific polyclonal antibodies Ser 2809-RyR (RyRp), Ser16-PLB (Ser 16 ), and Thr17-PLB (Thr 17 ) (gift from Dr J. Colyer, University of Leeds, Leeds, UK) also were probed. In addition, we used antibodies for GRK2 (Upstate) and actin (Sigma).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…1,6 -10 For example, ␤-adrenergic receptor kinase (␤ARK1 or GRK2) has been shown to be centrally involved in blunting ␤-adrenergic receptor signaling in pressure-overload hypertrophy. 11 Given that exercise training has been shown to enhance ␤-adrenergic responsiveness [12][13][14][15][16][17][18] without increasing ␤-receptor density, 18 -20 we hypothesized that exercise training could rectify defective myocardial ␤-adrenergic receptor responsiveness in hypertrophy. Thus, the purposes of the present study were to use an SHR model to (1) to establish whether exercise training could mitigate hypertrophy associated with hypertension, (2) to examine whether exercise training could increase both inotropic and lusitropic responses to ␤-adrenergic stimulation and pacing, (3) to examine how exercise training affects GRK2, and (4) to examine whether exercise training alters the abundance and phosphorylation of Ca 2ϩ cycling proteins.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Improved Myocardial β-Adrenergic Responsiveness and Signaling With Exercise Training in Hypertension

et al. 2005

View full text Add to dashboard Cite

Background-Cardiac responses to ␤-adrenergic receptor stimulation are depressed with pressure overload-induced cardiac hypertrophy. We investigated whether exercise training could modify ␤-adrenergic receptor responsiveness in a model of spontaneous hypertension by modifying the ␤-adrenergic receptor desensitizing kinase GRK2 and the abundance and phosphorylation of some key Ca 2ϩ cycling proteins. Ϫ7 mol/L) and pacing stress (8.5 Hz). The peak LV developed pressure/ISO dose response was shifted rightward 100-fold in SHR relative to WKY. The peak ISO LV developed pressure response was similar between WKY and SHR-SED and increased in SHR-TRD (PϽ0.05). SHR-TRD showed the greatest lusitropic response to ISO (PϽ0.05) and offset the pacing-induced increase in LV end-diastolic pressure and the time constant of isovolumic relaxation () observed in WKY and SHR-SED. Improved cardiac responses to ISO in SHR-TRD were associated with normalized myocardial levels of GRK2 (PϽ0.05). SHR displayed increased L-type Ca 2ϩ channel and sodium calcium exchanger abundance compared with WKY (PϽ0.001). Training increased ryanodine receptor phosphorylation and phospholamban phosphorylation at both the Ser 16 and Thr 17 residues (PϽ0.05). Conclusions-Exercise training in hypertension improves the inotropic and lusitropic responsiveness to ␤-adrenergic receptor stimulation despite augmenting LV wall thickness. A lower GRK2 abundance and an increased phosphorylation of key Ca 2ϩ cycling proteins may be responsible for the above putative effects. (Circulation. 2005;111:3420-3428.)

show abstract

Section: Western Blotsmentioning

confidence: 94%

Section: Western Blot Analysismentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Improved Myocardial β-Adrenergic Responsiveness and Signaling With Exercise Training in Hypertension

et al. 2005

View full text Add to dashboard Cite

show abstract

“…However, data in chronic exercise training models are less clear. Exercise training studies in nonpathological models have elicited variable results with respect to myocardial ␤-AR responsiveness, with some studies showing increased (29,49,52), decreased (11,17), or no change (34, 37) with training. The unpredictable adaptive pattern of the ␤-AR with training in normotensive myocardium is likewise reflected in variable observations reported in the plasticity of the adenylyl cyclase step in the cascade.…”

Section: Increased [Ca 2ϩmentioning

confidence: 99%

“…In the basal state, adenylyl cyclase has been shown to be increased (6), decreased (16,33), or unaltered (12,30,42) with training. Likewise, agonist stimulated adenylyl cyclase has also been reported to be increased (30,39,52), decreased (12,30), or unaltered with training (6,12,42). Thus, in normotensive rodent myocardium, it is difficult to generate any categorical conclusions with respect to how exercise training impacts ␤-AR responsiveness and adenylyl cyclase activity.…”

Section: Increased [Ca 2ϩmentioning

confidence: 99%

Effects of forskolin on inotropic performance and phospholamban phosphorylation in exercise-trained hypertensive myocardium

Kolwicz

Kubo

MacDonnell

et al. 2007

Journal of Applied Physiology

View full text Add to dashboard Cite

responsiveness is downregulated in left ventricular (LV) hypertrophy induced by chronic hypertension. While exercise training in hypertension enhances ␤-AR responsiveness, the role of adenylyl cyclase remains unclear. The purpose of the present study was to test whether treadmill running in the spontaneously hypertensive rat (SHR) model improves LV responsiveness to forskolin (FOR) or the combination of FOR ϩ isoproterenol (FORϩISO). Female SHR (16-wk) were randomly placed into sedentary (SHR-SED; n ϭ 7) or treadmill-trained (SHR-TRD; n ϭ 8) groups. Wistar-Kyoto (WKY; n ϭ 7) animals acted as normotensive controls. Langendorff, isovolumic LV performance was established at baseline and during incremental FOR infusion (1 and 5 mol/l) and FORϩISO (5 mol/l ϩ 1ϫ10 Ϫ8 mol/l). Heart rate, systolic blood pressure, and heart-to-body weight ratio were lower in WKY relative to both SHR groups (P Ͻ 0.05). LV performance and heart rate significantly increased in all groups to a similar extent with incremental FOR infusion. However, in the presence of 5 mol/l FOR, ISO increased LV developed pressure, positive change in LV pressure, and negative change in LV pressure to a greater extent in SHR-TRD relative to SHR-SED (P Ͻ 0.05). Phospholamban phosphorylation at the Thr 17 was greater in SHR-TRD relative to SHR-SED and WKY (P Ͻ 0.05). Absolute LV developed pressure was moderately correlated with phospholamban phosphorylation at both the Ser 16 (r ϭ 0.64; P Ͻ 0.05) and Thr 17 (r ϭ 0.52; P Ͻ 0.05). Our data suggest that the adenylyl cyclase step in the ␤-AR cascade is not downregulated in the early course of hypertension and that the enhanced ␤-AR responsiveness with training is likely mediated at levels other than adenylyl cyclase. Our data also suggest that ␤-AR inotropic responsiveness in the presence of direct adenylyl cyclase agonism is improved in trained compared with sedentary SHR hearts.heart; hypertrophy; diastole; proteins; spontaneously hypertensive rat THE ␤-ADRENERGIC RECEPTOR (␤-AR) system is an integral pathway in regulating myocardial inotropy and lusitropy, particularly during the stress of exercise (43,46,51). With hypertension, however, the ␤-AR system is downregulated via receptor uncoupling (10, 27) and is clearly one hallmark of the maladaptive phenotype associated with compensatory hypertrophy (50). Recent data from our laboratory have shown that exercise training improves ␤-AR responsiveness in the spontaneously hypertensive rat (SHR) model by mitigating the left ventricular (LV) abundance of the ␤-AR receptor desensitizing kinase, G protein receptor kinase 2 (GRK2) (27). As a result of "restored" ␤-AR signaling, PKA-mediated phosphorylation of key sarcoplasmic reticulum (SR) Ca 2ϩ handling proteins, such as the ryanodine receptor and phospholamban (PLB), were improved with training (27). However, given that direct adenylyl cyclase/cAMP signaling may also be altered with hypertension (9, 28, 31), it remains unclear from our previous work whether "downstream-associated" ␤-AR mechanisms are likewise improved...

show abstract

Motor training and physical fitness: Possible short‐ and long‐term influences on the development of individual differences in behavior

Bekoff

1988

Developmental Psychobiology

View full text Add to dashboard Cite

Individual differences in the behavior of young and adult animals have been documented in diverse species. Possible sources of such variation are of interest to scientists representing many disciplines, including behavior, genetics, and population and evolutionary biology. Two variables that may be important in the ontogeny and maintenance of behavioral differences are (1) individual physical (aerobic and anaerobic) fitness and (2) possible genetic variations underlying individual abilities to engage in, and to benefit from, motor training early in life. The differential development of aerobic and anaerobic capacities may play a significant role in the ontogeny of individual differences in the performance of various motor skills. There also may be short- and long-term consequences of variations in physical fitness that influence individual abilities to perform energy demanding acts during aggressive encounters, interactions with prey or predators, and courtship and breeding. Genetic studies of a limited number of species indicate that specific genotypes are correlated with individual variations in motor performance, even among conspecifics. Multidisciplinary research concerning possible relationships among the ontogeny of physical fitness, genetics, and variations in behavior is needed. Recent work on the relationship between individual differences in physical fitness and variations in the behavior of adult cold-blooded vertebrates provides a good model for comparative research on warm-blooded species.

show abstract

Enhanced cardiac response to catecholamines in physically trained cats

Cited by 28 publications

References 0 publications

Improved Myocardial β-Adrenergic Responsiveness and Signaling With Exercise Training in Hypertension

Improved Myocardial β-Adrenergic Responsiveness and Signaling With Exercise Training in Hypertension

Effects of forskolin on inotropic performance and phospholamban phosphorylation in exercise-trained hypertensive myocardium

Motor training and physical fitness: Possible short‐ and long‐term influences on the development of individual differences in behavior

Contact Info

Product

Resources

About