Vascular Contraction: Effect of Age and Extracellular Calcium

Cohen, Marlene L.; Berkowitz, Barry A.

doi:10.1159/000158085

Cited by 32 publications

(36 citation statements)

References 15 publications

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“…Results from previous studies have been conflicting on the importance of extracellular calcium in the altered vascular responsiveness seen with aging. Both Carrier et al 8 10 In the present study, no indication of an altered vascular contractile responsiveness to calcium was observed. These data are supported by a recent study 20 demonstrating no change in 45 Ca uptake in rat aorta with increasing age.…”

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confidence: 50%

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Effect of age on blood pressure and membrane-dependent vascular responses in the rat.

Soltis

1987

Circulation Research

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Alterations in endothelium-dependent, sodium pump-mediated, and calcium-dependent responses of vascular smooth muscle were investigated in 5-7-, 24-26-, and 50-52-week-old male Sprague-Dawley rats. Age-dependent changes in systolic blood pressure were also determined. Although systolic blood pressure increased significantly with age, rats in all 3 age groups were considered normotensive. Initial studies on the passive force-response characteristics of strips of aortic and femoral arterial smooth muscle revealed that the level of passive force required for maximum active tension generation increased with increasing age. Subsequent studies were carried out using optimum passive force requirements. Endothelium-dependent relaxations of aortic smooth muscle induced by acetylcholine and the calcium ionophore A23187 decreased significantly with increasing age. An age-dependent decrease in the contractile response of aortic smooth muscle to ouabain and potassium-free physiological salt solution (PSS) was observed. Potassium relaxation of femoral smooth muscle following contraction to norepinephrine (NE) in a potassium-free PSS was also significantly attenuated with increasing age. No age-related alterations in calcium sensitivity (in the presence of 10~7 M NE) or calcium relaxation (membrane stabilization) of femoral arterial smooth muscle was seen. These results show that endothelium-dependent and sodium pump-mediated responses are reduced in vascular smooth muscle of the rat with increasing age. However, no changes in calcium-dependent responses are apparent. These observations are discussed in relation to the vascular changes observed in hypertension. (Circulation Research 1988;62:889-897)

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confidence: 50%

“…A similar response was seen at 0.1 mM KC1 in 24-26-week-old rats. ED 10 and ED 50 values are presented in Table 5.…”

Section: Sodium Pump-mediated Responsesmentioning

confidence: 99%

Effect of age on blood pressure and membrane-dependent vascular responses in the rat.

Soltis

1987

Circulation Research

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“…Thus, aortae from immature (1-2 months) to mature (12-14 months) rats ex hibited an increased [8] or unchanged [9] dependence of norepinephrine-induced con tractions on extracellular calcium with age, while in rabbit aorta (neonatal to 6-monthold) there was a decreased dependence of norepinephrine on extracellular calcium with age [5], Finally, while evidence from human stud ies points to a greater sensitivity of the vas culature to the calcium channel blocker vera pamil with advancing age from 20 to 80 years [21], the opposite seems to be the case with the rabbit aorta isolated between birth and 6 months of age [5].…”

Section: Introductionmentioning

confidence: 91%

“…The inconsistencies hold true regardless of whether the comparisons are made between immature and young [4][5][6][7], young and adult [8,9], or young and old (senescent) [10][11][12][13][14][15][16][17][18][19][20] experimental subjects, and is not explainable on the basis of species differences or differ ences in vascular beds examined. 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].…”

Section: Introductionmentioning

confidence: 99%

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.

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“…t is generally thought that vascular responses to vasoconstrictors are depressed in older animals [1][2][3][4][5][6] and humans. 7,8 The effects of aging on the vascular responses to endothelin-1 (ET-1), however, are more controversial.…”

mentioning

confidence: 99%

Paradoxically Enhanced Endothelin-B Receptor–Mediated Vasoconstriction in Conscious Old Monkeys

Asai¹,

Kudej

Takagi

et al. 2001

Circulation

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Background-We investigated the effects of aging on the responses to endothelin (ET) in conscious old (19.8Ϯ0.6 years) and young adult (6.8Ϯ0.3 years) monkeys and compared these results with those of other vasoconstrictors, eg, phenylephrine (PE) and angiotensin II (Ang II). Methods and Results-The monkeys (Macaca fascicularis) were chronically instrumented. Baseline total peripheral resistance (TPR) was not different between the 2 groups. As expected, TPR rose less (PϽ0.05) with PE (5 g/kg) in old monkeys (34Ϯ3%) than in young monkeys (57Ϯ6%); TPR also rose less with Ang II. Surprisingly, TPR rose more (PϽ0.05) with endothelin-1 (ET-1, 25 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ) in old monkeys (36Ϯ6%) than in young monkeys (10Ϯ2%). An ET B receptor agonist, sarafotoxin (S6c, 30 ng ⅐ kg Ϫ1 ⅐ min

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Vascular Contraction: Effect of Age and Extracellular Calcium

Cited by 32 publications

References 15 publications

Effect of age on blood pressure and membrane-dependent vascular responses in the rat.

Effect of age on blood pressure and membrane-dependent vascular responses in the rat.

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

Paradoxically Enhanced Endothelin-B Receptor–Mediated Vasoconstriction in Conscious Old Monkeys

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