scholarly journals Enhanced beta-1 adrenergic receptor responsiveness in coronary arterioles following intravenous stromal vascular fraction therapy in aged rats

Aging ◽  
2019 ◽  
Vol 11 (13) ◽  
pp. 4561-4578
Author(s):  
Gabrielle Rowe ◽  
Natia Q. Kelm ◽  
Jason E. Beare ◽  
Evan Tracy ◽  
Fangping Yuan ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Stromal Vascular Fraction ◽  
Aged Rats ◽  
Coronary Arterioles

Long‐term β‐adrenergic receptor blockade increases levels of the most mature thymocyte subsets in aged rats

2007 ◽  
Vol 7 (5) ◽  
pp. 674-686 ◽  
Author(s):  
V. Pešić ◽  
B. Plećaš‐Solarović ◽  
K. Radojević ◽  
D. Kosec ◽  
I. Pilipović ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Blockade ◽  
Aged Rats ◽  
Adrenergic Receptor Blockade

scholarly journals Effects of β-adrenergic receptor agonists on drinking and arterial blood pressure in young and old rats

2011 ◽  
Vol 300 (4) ◽  
pp. R1001-R1008 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Connie L. Grobe ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Aged Rats ◽  
Middle Aged ◽  
Young Rats ◽  
Arterial Blood ◽  
Age Related ◽  
Old Rats

These experiments examined water-drinking and arterial blood pressure responses to β-adrenergic receptor activation in young (4 mo), “middle-aged” adult (12 mo), and old (29 mo) male rats of the Brown-Norway strain. We used isoproterenol to simultaneously activate β1- and β2-adrenergic receptors, salbutamol to selectively activate β2-adrenergic receptors, and the combination of isoproterenol and the β2-adrenergic receptor antagonist ICI 118,551 to stimulate only β1-adrenergic receptors. Animals received one of the drug treatments, and water drinking was measured for 90 min. About 1 wk later, animals received the same drug treatment for measurement of arterial blood pressure responses for 90 min. In some rats, levels of renin and aldosterone secretion in response to isoproterenol or salbutamol were measured in additional tests. Old and middle-aged rats drank significantly less after isoproterenol than did young rats and also had greater reductions in arterial blood pressure. Old and middle-aged rats drank significantly less after salbutamol than did young rats, although reductions in arterial blood pressure were equivalent across the ages. The β2-adrenergic antagonist ICI 118,551 abolished drinking after isoproterenol and prevented most of the observed hypotension. Renin secretion after isoproterenol and salbutamol was greater in young rats than in middle-aged rats, and wholly absent in old rats. Aldosterone secretion was reduced in old rats compared with young and middle-aged rats after treatment with isoproterenol, but not after treatment with salbutamol. In conclusion, there are age-related differences in β-adrenergic receptor-mediated drinking that can be explained only in part by age-related differences in renin secretion after β-adrenergic receptor stimulation.

?-Adrenergic receptor activity of cerebral microvessels is reduced in aged rats

1991 ◽  
Vol 16 (4) ◽  
pp. 447-451 ◽  
Author(s):  
Arshag D. Mooradian ◽  
Philip J. Scarpace
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Activity ◽  
Aged Rats ◽  
Cerebral Microvessels

scholarly journals Physiological levels of thrombospondin-1 decrease NO-dependent vasodilation in coronary microvessels from aged rats

2016 ◽  
Vol 310 (11) ◽  
pp. H1842-H1850 ◽  
Author(s):  
Chris Nevitt ◽  
Grant McKenzie ◽  
Katelyn Christian ◽  
Jeff Austin ◽  
Sarah Hencke ◽  
...  
Keyword(s):  
Coronary Microvascular Dysfunction ◽  
Coronary Perfusion ◽  
Aged Rats ◽  
Peripheral Vasculature ◽  
No Donor ◽  
Flow Reserve ◽  
Thrombospondin 1 ◽  
Old Rats ◽  
Coronary Arterioles

Aging and cardiovascular disease are associated with the loss of nitric oxide (NO) signaling and a decline in the ability to increase coronary blood flow reserve (CFR). Thrombospondin-1 (Thbs-1), through binding of CD47, has been shown to limit NO-dependent vasodilation in peripheral vascular beds via formation of superoxide (O2−). The present study tests the hypothesis that, similar to the peripheral vasculature, blocking CD47 will improve NO-mediated vasoreactivity in coronary arterioles from aged individuals, resulting in improved CFR. Isolated coronary arterioles from young (4 mo) or old (24 mo) female Fischer 344 rats were challenged with the NO donor, DEA-NONO-ate (1 × 10−7 to 1 × 10−4 M), and vessel relaxation and O2− production was measured before and after Thbs-1, αCD47, and/or Tempol and catalase exposure. In vivo CFR was determined in anesthetized rats (1–3% isoflurane-balance O2) via injected microspheres following control IgG or αCD47 treatment (45 min). Isolated coronary arterioles from young and old rats relax similarly to exogenous NO, but addition of 2.2 nM Thbs-1 inhibited NO-mediated vasodilation by 24% in old rats, whereas young vessels were unaffected. Thbs-1 increased O2− production in coronary arterioles from rats of both ages, but this was exaggerated in old rats. The addition of CD47 blocking antibody completely restored NO-dependent vasodilation in isolated arterioles from aged rats and attenuated O2− production. Furthermore, αCD47 treatment increased CFR from 9.6 ± 9.3 (IgG) to 84.0 ± 23% in the left ventricle in intact, aged animals. These findings suggest that the influence of Thbs-1 and CD47 on coronary perfusion increases with aging and may be therapeutically targeted to reverse coronary microvascular dysfunction.

scholarly journals Effects of age and exercise training on coronary microvascular smooth muscle phenotype and function

2018 ◽  
Vol 124 (1) ◽  
pp. 140-149 ◽  
Author(s):  
Judy M. Muller-Delp ◽  
Kazuki Hotta ◽  
Bei Chen ◽  
Bradley J. Behnke ◽  
Joshua J. Maraj ◽  
...  
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Exercise Training ◽  
Vascular Smooth Muscle ◽  
Contractile Function ◽  
Late Life ◽  
Contractile Dysfunction ◽  
Aged Rats ◽  
Smooth Muscle Proliferation ◽  
Coronary Arterioles

Coronary microvascular function and blood flow responses during acute exercise are impaired in the aged heart but can be restored by exercise training. Coronary microvascular resistance is directly dependent on vascular smooth muscle function in coronary resistance arterioles; therefore, we hypothesized that age impairs contractile function and alters the phenotype of vascular smooth muscle in coronary arterioles. We further hypothesized that exercise training restores contractile function and reverses age-induced phenotypic alterations of arteriolar smooth muscle. Young and old Fischer 344 rats underwent 10 wk of treadmill exercise training or remained sedentary. At the end of training or cage confinement, contractile responses, vascular smooth muscle proliferation, and expression of contractile proteins were assessed in isolated coronary arterioles. Both receptor- and non-receptor-mediated contractile function were impaired in coronary arterioles from aged rats. Vascular smooth muscle shifted from a differentiated, contractile phenotype to a secretory phenotype with associated proliferation of smooth muscle in the arteriolar wall. Expression of smooth muscle myosin heavy chain 1 (SM1) was decreased in arterioles from aged rats, whereas expression of phospho-histone H3 and of the synthetic protein ribosomal protein S6 (rpS6) were increased. Exercise training improved contractile responses, reduced smooth muscle proliferation and expression of rpS6, and increased expression of SM1 in arterioles from old rats. Thus age-induced contractile dysfunction of coronary arterioles and emergence of a secretory smooth muscle phenotype may contribute to impaired coronary blood flow responses, but arteriolar contractile responsiveness and a younger smooth muscle phenotype can be restored with late-life exercise training. NEW & NOTEWORTHY Aging impairs contractile function of coronary arterioles and induces a shift of the vascular smooth muscle toward a proliferative, noncontractile phenotype. Late-life exercise training reverses contractile dysfunction of coronary arterioles and restores a young phenotype to the vascular smooth muscle.

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