Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension

Vanhoutte, Paul M.; Webb, R. Clinton; Collis, Michael G.

doi:10.1042/cs059211s

Cited by 37 publications

(13 citation statements)

References 121 publications

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“…15 Previous reports on neuronal uptake, obtained in in vitro or ex vivo preparations, have found a diversified pattern of activity in the different tissues and phases of hypertension development in the SHR model. Neuronal uptake has been found to be normal in the cardiac and vascular tissues 24 and increased in the skeletal muscle and the kidney 5 of young SHR, but it is reduced in the heart 10 and increased in the resistance arteries 25 in hypertensive SHR. Furthermore, it has been reported that aging progressively reduces neuronal uptake of NE, 24,26 suggesting that in older SHR the contribution of the reduced reuptake in the maintenance of greater interstitial NE levels may become more important.…”

Section: Discussionmentioning

confidence: 99%

“…Neuronal uptake has been found to be normal in the cardiac and vascular tissues 24 and increased in the skeletal muscle and the kidney 5 of young SHR, but it is reduced in the heart 10 and increased in the resistance arteries 25 in hypertensive SHR. Furthermore, it has been reported that aging progressively reduces neuronal uptake of NE, 24,26 suggesting that in older SHR the contribution of the reduced reuptake in the maintenance of greater interstitial NE levels may become more important. In human hypertension, a recent report showed an impairment of total and cardiac NE neuronal reuptake, 27 suggesting a functional reduction in NE presynaptic transporter activity linked to a possible gene mutation.…”

Section: Discussionmentioning

confidence: 99%

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Sympathetic Activation in Adipose Tissue and Skeletal Muscle of Hypertensive Rats

et al. 2002

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Abstract-The activation of the sympathetic nervous system is a common feature of arterial hypertension and other cardiovascular diseases. This activation might be dependent on an altered baroreflex control of vascular resistance of which the inhibitory response on sympathetic activity appears impaired. The aim of the study was to monitor during the natural course of arterial hypertension in spontaneously hypertensive (SHR) and age-matched Wistar Kyoto (WKY) rats (5, 16, 30, and 54 weeks of age) the peripheral sympathetic activity expressed as interstitial norepinephrine (NE) release and as tyrosine hydroxylase (TH) activity, the rate-limiting enzyme of NE synthesis, in the differently baroreflexcontrolled subcutaneous adipose tissues and skeletal muscles. Blood pressure and plasma NE in SHR were similar to WKY at 5 weeks of age but increased at all other ages. Body weight was similar in both 5-week-old rats but reduced in SHR at all other ages. The interstitial NE levels were greater in both SHR tissues at all ages as compared with WKY. In adipose tissue of SHR, TH activity was higher at all ages as compared with WKY, whereas TH activity in skeletal muscle was higher only after the development of hypertension. These data show that in both SHR tissues, an increase of interstitial NE release is always present during its lifespan. This suggests that increased sympathetic activation in the SHR model is not specific to baroreflex-controlled tissues such as skeletal muscle but involves also subcutaneous adipose tissue, the sympathetic efferents of which are independent from baroreflexes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sympathetic Activation in Adipose Tissue and Skeletal Muscle of Hypertensive Rats

et al. 2002

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“…Such changes also increase metabolic activity and provide an early signal for vascular smooth muscle hypertrophy that, when combined with Abnormal neurogenic influences from altered tone of the putative pressor center could cause changes in vascular smooth muscle sensitivity. These neurogenic influences could stem from alterations in norepinephrine release and uptake 19 or changes in membrane potential of vascular smooth muscle. 20 The vascular smooth muscle of the spontaneously hypertensive rat has been shown to have a less negative resting membrane potential, a reduced K + equilibrium potential, and an enhanced electrogenic component to the resting membrane potential.…”

Section: Discussionmentioning

confidence: 99%

Hypertensive mechanisms associated with centrally administered aldosterone in dogs.

Kageyama

Bravo

1988

Hypertension

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SUMMARY The mechanism by which intracerebroventricularty administered aldosterone increases arterial pressure was investigated in trained, conscious dogs with cannulas chronically implanted in a lateral cerebral ventricle. In salt-replete and salt-depleted dogs, artificial cerebrospinal fluid with or without aldosterone (0.05 /ig/kg/hr) was infused intracerebroventricularly for 12 days by an osmotic minipump. A similar dose of aldosterone was infused subcutaneously for 12 days. Aldosterone infused intracerebroventricularly increased blood pressure significantly in both salt-replete and salt-depleted dogs. In salt-replete animals the hypertension was associated with increased total peripheral resistance without concomitant changes in blood volume, cardiac output, or in any of the neurohumoral parameters measured. We conclude that this type of hypertension is resistance-mediated from its outset and appears to be relatively independent of salt and water retention. The mechanism by which intracerebroventricularly administered aldosterone increases vascular resistance remains to be determined. (Hypertension 11: 750-753, 1988) KEY WORDS hemodynamics mineralocorticoid hypertension « centrally administered aldosterone H IGH affinity specific binding sites for mineralocorticoids have been described in various areas of the brain. 1 " 4 Quantitative autoradiography with intravenously injected [ 3 H]aldosterone has shown a wide distribution of specific binding sites in the brain, including the anterior hypothalamus, hippocampus, anterior pituitary, nucleus ventromedialis hypothalami, nucleus ambiguus, nucleus tractus solitarii, locus ceruleus, and area postrema.3 The functional importance of these binding sites was recently examined by Gomez-Sanchez in the rat.3 She found that a dose of aldosterone that was too small to produce changes in blood pressure when infused systemically produced elevations of blood pressure when infused into the lateral cerebral ventricle. The fact that the pressor effect could be blocked by the concomitant infusion of a specific aldosterone antagonist, prorenone, lent support to the concept that these mineralocorticoid binding sites in the brain are functional and that they could subserve a role in cardiovascular regulation.We have extended these observations by confirming

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“…It has been suggested that, since the release of norepinephrine by peripheral nerve endings of the vascular wall is greater than normal in the young SHR, this enhancement of the exocytotic process may be one of the factors causing hypertension; 1 "* 1 •• " this would be of particular importance in view of the increased sympathetic traffic to the cardiovascular periphery which has been described also at the early stage of the disease. 6 ' 18 ' ' a ' v If it is assumed that the experiments on the Tyrode perfused kidneys of adult SHR reflect the behavior of the adrenergic neurotransmission in the intact animal, the present study implies that, if the release of norepinephrine in the blood vessel wall plays a role in maintaining the increased peripheral resistance in the chronic stage of the hypertensive process, this can only be attributed either to such central increases in sympathetic traffic, or to the presence of locally produced or circulating facilitators of the exocytotic release of norepinephrine.'' "…”

Section: Discussionmentioning

confidence: 99%

Decreased release of norepinephrine in the isolated kidney of the adult spontaneously hypertensive rat.

Vanhoutte¹,

Browning²,

Coen³

et al. 1982

Hypertension

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SUMMARY Renal resistance vessels of the mature spontaneously hypertensive rat (SHR) exhibit an increased reactivity to exogenous norepinephrine, but a normal response to renal nerve stimulation. This difference could be due either to depression of the exocytotic process or to accelerated disposition of the released transmitter. We compared the overflow of norepinephrine in isolated perfused kidneys from adult SHR and normotensive rats. After previous incubation with *H-norepinephrine, renal nerve stimulation caused smaller increases in the overflow of intact tritlated transmitter and its metabolites in kidneys from SHR than in those from normotensive controls. A similar difference was found when the amounts of endogenous norepinephrine were measured radioenzyraatlcally. The tissue content of norepinephrine was comparable in kidneys from both hypertensive and normotensive animals. The uptake of * H-norepinephrine was similar in the kidneys from SHR and normotensive controls; cocaine caused a comparable depression of the 'H-uptake in both groups. These data indicate that in the adult SHR the exocytotic release of norepinephrine is depressed, which then explains the normal vasoconstrictor response to renal nerve stimulation despite the increased responsiveness of the vascular smooth muscle cells to norepinephrine. IN the isolated Tyrode-perfused kidney of the young spontaneously hypertensive rat (SHR), the vasoconstrictor response to periarterial nerve stimulation is larger than that observed in kidneys from normotensive control animals, at a time when the responsiveness to exogenous norepinephrine is comparable in both groups; the greater response to nerve stimulation is paralleled by a greater than normal overflow of endogenous norepinephrine. "' These observations demonstrate that at the early stages of hypertension, the adrenergic nerve endings release more transmitter in the SHR than in normotensive rats. Isolated Perfused Kidney PreparationRats were anesthetized with pentobarbitone-sodium (50 mg/kg, i.p.) and the abdomen opened by midline incision. The right renal artery, the left spermatic artery, and the left suprarenal artery were ligated. A cannula was inserted into the aorta rostral to the renal arteries and positioned with its tip adjacent to the left renal artery. The cannula was secured by a ligature, and the aorta caudal to the left renal artery was tied off and cut. The left kidney and cannulated segment of the aorta were removed from the animal and placed in a chamber containing Tyrode's solution at 37°C. This procedure interrupted the blood supply to the kidney for 15 to 30 seconds while the cannula was inserted, and before perfusion with Tyrode's solution was commenced.The isolated kidney was perfused with Tyrode's solution (37°C), using a constant flow roller pump (Gilson, Minipuls II, Middleton, Wisconsin). The perfusion rate was set at 6.2 ml/min; earlier work has shown that this rate ensures optimal perfusion conditions for the kidney of both normotensive and hypertensive rats.*-7 ' 10 Ren...

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Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension

Cited by 37 publications

References 121 publications

Sympathetic Activation in Adipose Tissue and Skeletal Muscle of Hypertensive Rats

Sympathetic Activation in Adipose Tissue and Skeletal Muscle of Hypertensive Rats

Hypertensive mechanisms associated with centrally administered aldosterone in dogs.

Decreased release of norepinephrine in the isolated kidney of the adult spontaneously hypertensive rat.

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