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

Stevens, MJ; Lipe, S.; Rf, Moulds

doi:10.1111/j.1365-2125.1982.tb04971.x

Cited by 36 publications

(13 citation statements)

References 7 publications

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“…The pitfalls of expressing the response to norepinephrine as a percentage of the maxi mum response to potassium [11,19] have been previously addressed [19]. Since aging does not necessarily influence the response to both stimulants similarly [ 19; fig.…”

Section: Discussionmentioning

confidence: 99%

“…Several au thors [4,5,8,19,36] have wrestled with this issue, and it has yet to be resolved. In recog nition of this, some authors [4,8] have pre sented their data in more than one way.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the contractile response to norepinephrine and/or potassium (and sometimes to other agonists) has been reported to increase [4,5,13], decrease [8,9,13,15,16,20], or remain unchanged [10][11][12]17] with advancing age. Furthermore, the vascular response to nor epinephrine in some instances first increased and then decreased with advancing age [14], while in other cases aging influenced the responses to norepinephrine and potassium differently [19]. In still other cases, senes cence resulted in a decrease [20] or no change [18] in sensitivity of presynaptic a 2-receptor-mediated responses, a decrease [20] or no change [17,18] in postsynaptic a r mediated responses, and a decrease [18] in postsynaptic a 2-mediated responses.…”

Section: Introductionmentioning

confidence: 99%

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Age-Related Changes in Responsiveness of the Rat Aorta to Depolarizing and Receptor-Mediated Contractile Stimuli and to Calcium Antagonism1

Olah

Rahwan²

1987

Pharmacology

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This study was undertaken to determine the relative age-dependent responsiveness of the rat aorta to depolarizing (potassium) and receptor-activating (norepinephrine) contractile stimulants, and to the calcium antagonists propyl-methylenedioxyindene (pr-MDI) and nifedipine. Pr-MDI exhibits intracellular calcium antagonistic and calcium channel blocking properties in this tissue, while nifedipine acts principally as a calcium channel blocker. Thoracic strips from young (4–6 months old) and senescent (22–23 months old) Fischer F344 rats were contracted with KCl (10–60 mmol/l) or norepinephrine (10^–9–5 × 10^–6 mol/l). Aortae from old rats were significantly more sensitive to norepinephrine than aortae from young rats, while the reverse was observed for KCl. Pr-MDI (10^–5–10^–4 mol/l) significantly relaxed the aortic contractions induced by norepinephrine (10–7 mol/l, a nondepolarizing concentration producing 88% of maximum response in young and old aortae) and by KCl (50 mmol/l, a depolarizing concentration producing 96 % of maximum response in young and old aortae). However, there were no age-related differences in sensitivity to the relaxant effects of pr-MDI against either stimulant. Pr-MDI was more effective in relaxing KCl-induced contractions than those induced by norepinephrine. Similar results were obtained with nifedipine (10^–10–10^–6 mol/l). These results indicate that senescence of the rat aorta is accompanied by an enhanced responsiveness of adrenergic α-receptor-mediated contraction, a reduced responsiveness to depolarizing stimuli, and no change in sensitivity to calcium antagonism.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Several au thors [4,5,8,19,36] have wrestled with this issue, and it has yet to be resolved. In recog nition of this, some authors [4,8] have pre sented their data in more than one way.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Age-Related Changes in Responsiveness of the Rat Aorta to Depolarizing and Receptor-Mediated Contractile Stimuli and to Calcium Antagonism1

Olah

Rahwan²

1987

Pharmacology

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“…Furthermore, depres sion of cardiac adrenergic responsiveness is a feature of aging apparently shared by both man and rat [Kreider et al, 1984], In terms of the vasculature, substantial similarities between man and rat in the effect of age have also been documented. Sensitivity to norepinephrine of arteries isolated from hu mans ranging from 30 to 83 years of age does not change with age [Stevens et al, 1982]; this has also been shown to be true in the rat [Duckies et al, 1985], Analysis of concentration-response curves to norepi nephrine in the carotid and femoral arteries shows that sensitivity to alpha-adrenergic stimulation does not change with age from 6 to 27 months. The concentration of nor epinephrine to produce 50% of a maximal response (EC50) was constant with age.…”

mentioning

confidence: 94%

Influence of Age on Vascular Adrenergic Responsiveness

Duckles¹

1987

J Vasc Res

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The adrenergic neuroeffector mechanism of blood vessels in Fischer 344 rats was studied from young adulthood to senescence. Norepinephrine (NE) content is maintained through senescence in all veins studied as well as in the superior mesenteric artery. In contrast, NE content declined at 27 months of age in all other arteries studied. Nevertheless, vascular reactivity in vitro to adrenergic nerve stimulation and to NE was well maintained. As to beta-adrenergic responsiveness, this showed a marked decline in arteries from 1 to 6 months of age, but was unchanged in the jugular vein from 3 to 27 months. Overall, then, adrenergic responsiveness of vascular smooth muscle is well maintained in aged rats. However, this study focuses on a discrete aspect of blood pressure control in a species where atherosclerosis is not prominent. Alterations at other sites could be responsible for changes in the overall function of adrenergic cardiovascular control.

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“…Owing to the lack of plasma catecholamine data, the mechanism of the exaggerated pressure response and vasoconstriction in middle-aged subjects could not be solved. However, the maximum response to norepineph rine in blood vessels was found to be increased with age in rats [ 19], whereas aging had no effect on responsiveness to norepinephrine in larger arteries in men [20],Therefore, the exaggerated pressure response immediately after smoking in middle-aged subjects seemed to be due to aadrenergic receptor stimulation induced by nicotine.…”

Section: Discussionmentioning

confidence: 92%

Effect of Age on Blood Pressure Response to Cigarette Smoking

Kurihara

1995

Cardiology

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The plasma nicotine level and hemodynamic parameters were evaluated after cigarette smoking in young (group I, 17 men) and middle-aged habitual smokers (group II, 17 men). The amount of increase in plasma nicotine concentration after smoking was related to the percent change of mean blood pressure in both groups. The total peripheral vascular resistance index (TPRI) increased significantly at 10 min after smoking and reduced thereafter in group I, whereas the TPRI increased till 30 min after in group II. Thus, smoking raised the TPRI for a longer time in the middle-aged subjects due to a decrease in aortic elasticity with aging.

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

Abstract: Chloramphenicol in the newborn infant. A physiological explanation of its toxicity when given in excessive dose. New Engl. J. Med., 262, 787-794. system do not change with increasing age.

Cited by 36 publications

References 7 publications

Age-Related Changes in Responsiveness of the Rat Aorta to Depolarizing and Receptor-Mediated Contractile Stimuli and to Calcium Antagonism1

Age-Related Changes in Responsiveness of the Rat Aorta to Depolarizing and Receptor-Mediated Contractile Stimuli and to Calcium Antagonism1

Influence of Age on Vascular Adrenergic Responsiveness

Effect of Age on Blood Pressure Response to Cigarette Smoking

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