Involvement of uptake1 and uptake2 in terminating the cardiovascular activity of noradrenaline in normotensive and genetically hypertensive rats.

Bell, Christopher; Kushinsky, Roslyn

doi:10.1113/jphysiol.1978.sp012487

Cited by 13 publications

(6 citation statements)

References 30 publications

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“…Acute adrenalectomy has also been shown to suppress, markedly, the secondary component of biphasic pressor response to spinal cord stimulation in pithed rats (Flavahan et al 1985;Tsujimoto et al 1987). By contrast, however, it has been reported that pressor responses to spinal cord stimulation (Bell & Kushinsky 1978) and to locus coeruleus stimulation (Drolet & Gauthier 1987) after acute surgical adrenalectomy remained comparable with those observed before adrenalectomy. It has also been shown that adrenal demedullation had little effect on the overall pressor response to reflex stimulation or to direct spinal cord stimulation (Yamaguchi & Kopin 1979;Sakaguchi et al 1983).…”

Section: Discussionmentioning

confidence: 85%

Evidence That Increases in Circulating Catecholamines of Adrenal Origin Are Not Involved in Pressor Response to Bilateral Carotid Occlusion in Anaesthetized Dogs

Brassard

Yamaguchi

1989

Clin Exp Pharma Physio

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1. We studied whether or not circulating catecholamines of adrenal origin play a major role in cardiovascular responses evoked by bilateral carotid artery occlusion (3 min) in anaesthetized dogs. 2. In the control group, the following parameters increased significantly (P less than 0.05) during bilateral carotid occlusion: aortic systolic pressure, heart rate, net adrenal catecholamine output, net renal noradrenaline output, and plasma catecholamine concentrations in aortic blood. Similar responses were obtained during the second occlusion performed approximately 25 min after the first occlusion. 3. After functional adrenalectomy (ADRX: diversion of adrenal venous blood flow), the increase in aortic adrenaline concentration observed during bilateral carotid occlusion was abolished. The increase in aortic noradrenaline concentration during the occlusion was significantly attenuated by approximately 60% (P less than 0.01) after ADRX. 4. The increase in net renal noradrenaline output during bilateral carotid occlusion after ADRX was not different from that observed before ADRX. Similarly, the response of aortic systolic pressure and heart rate during the occlusion was unaffected by ADRX. Furthermore, the increase in net adrenal catecholamine output during the occlusion was not affected by ADRX itself. 5. From these results, we conclude that the increase in circulating catecholamines of adrenal origin during bilateral carotid occlusion is not a major determinant for the increases in aortic pressure and heart rate. The results suggest that these cardiovascular responses during the occlusion are mediated principally by neuronal noradrenaline released from peripheral sympathetic nerve terminals.

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Section: Discussionmentioning

confidence: 85%

Evidence That Increases in Circulating Catecholamines of Adrenal Origin Are Not Involved in Pressor Response to Bilateral Carotid Occlusion in Anaesthetized Dogs

Brassard

Yamaguchi

1989

Clin Exp Pharma Physio

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“…Hermsmeyer (1976) has proposed that it is the increased K-and Na-permeability which is indirectly the cause of the increased noradrenaline sensitivity. The resting membrane potential of the SHR and WKY cells is the same (Hermsmeyer, 1976;Bell & Kushinsky, 1978). Therefore an increased K-and Na-permeability might be expected to cause or require an increased Na-K electrogenic pump activity in the SHR cells, and there is now experimental evidence for such an increased activity (Hermsmeyer, 1976;Webb & Bohr, 1979).…”

Section: Calcium Activationmentioning

confidence: 94%

An Increased Calcium Sensitivity of Mesenteric Resistance Vessels in Young and Adult Spontaneously Hypertensive Rats

Mulvany

Nyborg

1980

British J Pharmacology

195

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1 We have measured the calcium sensitivity in response to noradrenaline stimulation and potassium depolarization of isolated segments of 100 to 200 gm mesenteric resistance vessels from spontaneously hypertensive (SHR) and control Wistar-Kyoto (WKY) rats. The rats were either young (4 wk) or adult (4 months), that is of ages before or after the SHRs had developed elevated blood pressure. Experiments were performed under conditions in which the effect of noradrenaline uptake by, and the potassium-induced noradrenaline release from, the nerve terminals in the vessel walls was eliminated. 2 The response of the SHR and WKY vessels to noradrenaline under conditions where only the extracellular calcium appeared to have been removed was similar. When subsequently stimulated maximally by noradrenaline, the calcium-sensitivity of the SHR vessels (Ca-ED50 -0.1 mM) was greater than that of the WKY vessels (Ca-EDs5 -0.2 mM). When depolarized by potassium, all vessels were less sensitive to calcium and there was little difference in the calcium sensitivity of SHR and WKY vessels in either age group (Ca-ED50 o 0.8 mM). 3 The results suggest that whereas the potassium (potential)-dependent calcium permeability of the SHR smooth muscle cell membrane is normal, the noradrenaline-induced calcium permeability is abnormally high. The presence of this abnormality in the vessels from the young SHRs suggests that it may be a factor involved in the aetiology of hypertension in the SHR.

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“…Previous studies have failed to demonstrate significant vascular effects following stimulation of the adrenal medulla (Celander, 1954;Bell & Kushinsky, 1978;Yamaguchi & Kopin, 1979;Docherty, 1979), suggesting that extra-synaptic or 'hormonal' (Ariens & Simonis, 1976) receptor sites may have a limited role in cardiovascular regulation (see also , Neil, 1975;Lewis, 1975). The aim of the present study was to investigate the vascular effects evoked by sympathoadrenal stimulation in the pithed rat in order to determine which populations of postjunctional adrenoceptors might be activated, under physiological conditions, by the sympathetic nervous system and whether these could account for all of the response.…”

Section: Introductionmentioning

confidence: 99%

Analysis of the α‐adrenoceptor‐mediated, and other, components in the sympathetic vasopressor responses of the pithed rat

Flavahan

Grant

Greig

et al. 1985

British J Pharmacology

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The vascular receptors activated following sympatho-adrenal stimulation were determined by analysing the effects of 'selective' antagonists on the vasopressor response to spinal sympathetic nerve activation in the pithed rat. The net vascular response to adrenal stimulation was a balance between alpha-adrenoceptor-mediated vasoconstriction and beta-adrenoceptor-mediated vasodepression. Part of the alpha-adrenoceptor-mediated response was 'prazosin-sensitive' (alpha 1) and the remainder was abolished by rauwolscine (alpha 2). As with adrenal stimulation, direct sympathetic nerve stimulation of the vasculature evoked pressor responses which were partly resistant to prazosin. Rauwolscine only partly blocked the prazosin-sensitive component. Reserpine pretreatment led to smaller responses than prazosin plus rauwolscine. Thus, the response resistant to alpha-adrenoceptor antagonists could be mediated, in part, by adrenoceptors distinct from alpha-adrenoceptors, as currently defined. alpha, beta-Methylene ATP reduced the nerve-mediated pressor response after alpha-adrenoceptor blockade or reserpine pretreatment but not in drug-free controls. The results suggest that stimulation of the adrenal medulla can produce a vasopressor response which consists of summating alpha 1- and alpha 2-adrenoceptor-mediated components, and is identical to the effect of injected adrenaline. In contrast, the response to vasopressor nerve stimulation appears to be essentially mediated by alpha 1-adrenoceptors, with a facilitatory influence from alpha 2-adrenoceptors. A further response obtained after alpha-adrenoceptor blockade may contain a purinergic component and another which is adrenergic but not mediated by stimulation of alpha-adrenoceptors.

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Involvement of uptake1 and uptake2 in terminating the cardiovascular activity of noradrenaline in normotensive and genetically hypertensive rats.

Cited by 13 publications

References 30 publications

Evidence That Increases in Circulating Catecholamines of Adrenal Origin Are Not Involved in Pressor Response to Bilateral Carotid Occlusion in Anaesthetized Dogs

Evidence That Increases in Circulating Catecholamines of Adrenal Origin Are Not Involved in Pressor Response to Bilateral Carotid Occlusion in Anaesthetized Dogs

An Increased Calcium Sensitivity of Mesenteric Resistance Vessels in Young and Adult Spontaneously Hypertensive Rats

Analysis of the α‐adrenoceptor‐mediated, and other, components in the sympathetic vasopressor responses of the pithed rat

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