The effect of age on the responses of human isolated arteries to noradrenaline.

Scott, Pamela Sharkey; Reid, JL

doi:10.1111/j.1365-2125.1982.tb01365.x

Cited by 63 publications

(19 citation statements)

References 9 publications

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“…In contrast to these findings, our results suggest that one index of adrenergic nerve density, In support of our findings that the adrenergic responsiveness of vascular smooth muscle does not change with advancing age, it has recently been demonstrated that sensitivity to NE of isolated arteries from humans ranging from 30 to 83 years in age is similar (Scott and Reid, 1982). Furthermore, maximal contractile responses to NE expressed as a percentage of maximal responses to KG did not change with age in these human vessels.…”

supporting

confidence: 83%

Vascular adrenergic neuroeffector function does not decline in aged rats.

Duckles¹,

Carter²,

Williams³

1985

Circulation Research

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SUMMARY. To investigate adrenergic control of blood vessels during aging, rats aged 6, 12, 20, and 27 months were studied using in vitro techniques. Accumulation of [ 3 H]norepinephrine, one index of adrenergic nerve density, did not alter with age in the femoral or renal arteries or renal vein. In the femoral vein [ 3 H]norepinephrine accumulation was greater at 6 and 27 months of age. Norepinephrine sensitivity was determined in both an innervated vessel, the femoral artery, and a non-innervated vessel, the carotid artery. In both cases, sensitivity to norepinephrine did not alter with age. In the renal and femoral arteries and veins, no significant changes in maximum responses to norepinephrine (10~5 M), potassium chloride, or transmural nerve stimulation were seen with advancing age. Furthermore, frequency response curves (2-16 Hz, 200 pulses) did not differ with age for any of the four vessels studied, with one exception. The response to stimulation at 4 Hz of the femoral vein from 6-month-old rats was significantly larger than responses at other ages. During nerve stimulation, the renal vein exhibited rapid contractions superimposed upon the maintained contractile response. This type of rapid contraction occurred only rarely (1 out of 5) in the renal vein from 27-month-old rats. In summary, neither adrenergic nerve density as reflected by [ 3 H]norepinephrine accumulation nor norepinephrine sensitivity decline with age. As the net effect of various components, the ability of vascular smooth muscle to respond to adrenergic nerve stimulation is also maintained during advancing age. (Circ Res 56: 109-116, 1985)

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supporting

confidence: 83%

Vascular adrenergic neuroeffector function does not decline in aged rats.

Duckles¹,

Carter²,

Williams³

1985

Circulation Research

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“…If this were to be the case the vascular responsiveness to noradrenaline would be apparently unaltered. This is suggested by reports from several groups (Frolkis et al, 1975;Scott & Reid, 1982;Hyland & Docherty, 1985;Hynes & Duckles, 1987). Furthermore, several reviews have stressed that the results on the evolution of o-adrenoceptor vasoconstrictor mechanisms with age are inconsistent (Fleisch, 1980;Kelly & O'Malley, 1984;Bennett & Gardiner, 1988;Vanhoutte, 1988).…”

Section: Introductionmentioning

confidence: 66%

Reduction of endothelial function with age in the mesenteric arterial bed of the normotensive rat

Atkinson¹,

Tatchum-Talom²,

Capdeville-Atkinson³

1994

British J Pharmacology

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1Age-related changes in endothelial vasodilator function were studied in an in vitro preparation of the mesenteric arterial bed removed from male, normotensive, Wistar rats. 2 Animals were killed at 2, 12 or 22 months of age, the superior mesenteric artery was cannulated and the gut removed. The mesenteric arterial bed was perfused at a constant flow rate of 4 ml min-' and perfusion pressure was taken as an index of arteriolar tone. 3 The muscarinic agonist, carbachol, antagonized noradrenaline-induced vasoconstriction in the presence, but not in the absence, of endothelium. This cholinoceptor agonist-induced release of endothelial-derived relaxing factor (EDRF) was impaired in 22 month old rats. 4 Noradrenaline-induced vasoconstriction increased following removal of endothelium suggesting that agonist-induced release of EDRF attenuates vasoconstrictor responses to noradrenaline measured in the presence of endothelium. 5 Removal of endothelium had less effect on noradrenaline-induced vasoconstriction in old rats suggesting once again that agonist-induced release of EDRF is impaired in old rats. 6 The noradrenaline dose-response curve established in the presence of endothelium was shifted to the left in 22 month old rats. 7 In conclusion, aging in the rat appears to lead to a reduction in endothelial vasodilator function in a resistance vessel.

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“…However, although the ageing rat heart has reduced isoprenaline sensitivity in vitro, this does not appear to be attributable to changes in ,8-adrenoceptor number or affinity, adenyl cyclase stimulation or protein kinase activation (Guarnieri et al, 1980;Lakatta et al, 1975). Since the inotropic response of the myocardium to calcium in vitro was the same in young and old rat hearts (Guarnieri et al, 1980) (Scott & Reid, 1982).…”

Section: Discussionmentioning

confidence: 99%

Responsiveness to beta‐adrenergic receptor stimulation: the effects of age are cardioselective.

Kendall¹,

Woods²,

Wilkins³

et al. 1982

Brit J Clinical Pharma

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1 To examine the influence of age on beta‐adrenergic receptor mechanisms, we have observed the cardiovascular, bronchial and metabolic effects of an intravenous infusion of the beta‐adrenoceptor agonist terbutaline in healthy young and elderly female subjects (mean ages 20.9 and 72.1 years respectively). 2 There was a highly significant fall in systolic blood pressure in the elderly, in contrast to the rise in systolic pressure seen in the young subjects. A similar fall in diastolic pressure occurred in both groups, indicating comparable beta‐adrenoceptor‐mediated vasodilatation. The fall in mean arterial pressure was significantly greater in the old than in the young subjects. The increase in heart rate was significantly less in the elderly. 3 Changes in plasma glucose and potassium during the infusion were similar in the two groups. 4 The observed abnormality of myocardial sensitivity to beta‐adrenergic receptor stimulation, which is not associated with a generalized blunting of beta‐adrenoceptor mediated effects, may significantly impair autonomic cardiovascular regulation in the elderly.

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The effect of age on the responses of human isolated arteries to noradrenaline.

Cited by 63 publications

References 9 publications

Vascular adrenergic neuroeffector function does not decline in aged rats.

Vascular adrenergic neuroeffector function does not decline in aged rats.

Reduction of endothelial function with age in the mesenteric arterial bed of the normotensive rat

Responsiveness to beta‐adrenergic receptor stimulation: the effects of age are cardioselective.

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