Uptake and Metabolism of Noradrenaline by Blood Vessels of Perinephritic Hypertensive Dogs

Garrett, J; Castro-Tavares, J.; Branco, D.

doi:10.1159/000158342

Cited by 5 publications

(6 citation statements)

References 10 publications

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“…The latter possi bility is supported by the finding that in iso lated blood vessels, the neuronal uptake and accumulation of NE is considerably greater in blood vessels from SHR rats than in ves sels from WKY rats [Webb et al, 1981;Whall et al, 1980], It is now well established that in a variety of stress states (including sympathetic neuronal stimulation), there is an enhanced concentration of NE in plasma from WKY rats [Roizen et al, 1975;McCarty and Kopin, 1978;Kvetnansky et al, 1979;Picotti et al, 1982], The latter findings are consistent with an enhanced releasable pool of NE in vascular sympathetic nerves. It should be noted, however, that in two other nongenetic experimental models of hyperten sion NE contents of blood vessels are gener ally decreased [Garrett et al, 1981;Crabb et al, 1980] The most significant observation from the present findings is the existence of a differ ence in tissue concentrations of a readily mea surable neurotransmitter substance in sympa thetically innervated tissues from SHR and WKY rats. Moreover, these differences are not restricted to isolated vascular beds, but are detectable in other organs and glands.…”

Section: Discussioncontrasting

confidence: 46%

Altered Catecholamine Contents in Vascular and Nonvascular Tissues in Genetically Hypertensive Rats

Head¹,

Cassis²,

Robinson³

et al. 1985

J Vasc Res

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We have measured the catecholamine (CA) contents in hearts, mesenteric vasculature, abdominal aorta, inferior vena cava, vasa deferentia and salivary glands from genetically hypertensive rats (SHR) and normotensive Kyoto-Wistar rats (WKY). We noted differences between the norepinephrine (NE) contents of individual tissues from SHR and WKY rats and have used two different analytical procedures for the measurement of NE to confirm these differences. Comparisons between tissue contents of NE in SHR and WKY rats indicated a greater content of NE in the following tissues from the SHR: heart, mesenteric artery, abdominal aorta, inferior vena cava and vasa deferentia. A modest elevation of NE [but not epinephrine (E)] was observed in adrenal glands from SHR rats. The NE contents of salivary glands from SHR and WKY rats were indistinguishable from each other. The results suggest that there may exist a generalized increase in NE contents in the peripheral vasculature of SHR rats. Furthermore, this increase is also present in the vasa deferentia, but not the salivary gland. The results draw attention to altered concentrations of NE in vascular and selected nonvascular tissues in the SHR.

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Section: Discussioncontrasting

confidence: 46%

Altered Catecholamine Contents in Vascular and Nonvascular Tissues in Genetically Hypertensive Rats

Head¹,

Cassis²,

Robinson³

et al. 1985

J Vasc Res

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“…Arterial hyper trophy could be the consequence of a trans mural chronic hypertension, since similar reactions of smooth muscle to an enhanced load have been described for arterial smooth muscle in chronic experimental hyperten sion [11,17,22,[25][26][27][42][43][44] and small intestine smooth muscle [19][20][21]. Further, Azevedo et al [5] and Garret et al [22] recently showed that hypertrophied mesen teric arteries taken from perinephritic hyper tensive dogs also showed degenerative adrenergic nerves accompanied by a de crease in their noradrenaline content.…”

Section: Origin O F the Artery Wall Structural Modificationsmentioning

confidence: 98%

Ultrastructural Changes in the Cerebral Artery Wall Induced by Long-Term Sympathetic Denervation

Dimitriadou

Aubineau²,

Taxi³

et al. 1988

J Vasc Res

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This study was performed to determine to what extent the morphology of the rabbit middle cerebral artery is affected by the absence of the sympathetic nervous system. Six weeks after unilateral ablation of the superior cervical ganglion, which induced ipsilateral degeneration and disappearance of the perivascular noradrenergic nerve fibers, comparison between the ipsi- and the contralateral middle cerebral arteries revealed that the denervated arterial wall underwent significant thickening. This thickening was principally due to hypertrophy of the smooth muscle cells (SMC), together with an increase in the amount of medial and adventitial collagen. The hypertrophied SMC showed important morphological and ultrastructural modifications – irregular shape, increase in the number of organdies (particularly of Golgi apparatus, free ribosomes, rough endoplasmic reticulum and microtubules), large indented nuclei rich in euchromatin – indicating profound changes in their metabolic and contractile activity which could result in an alteration of their mechanical properties. As these alterations were strictly ipsilateral to the sympathectomy it is likely that they are the direct consequence of the suppression of a regulatory ‘trophic’ factor linked to the presence of sympathetic nerve fibers. This concept is reinforced by the fact that the first SMC affected are those situated at the media/adventitial border, in the vicinity of adventitial nerve bundles. Thus, the sympathetic nervous system appears to play a key role in the long-term regulation of the cerebral vascular tree structure.

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“…8 -9 Tissue concentrations of norepinephrine are reported to be decreased in mesenteric artery and heart in renal hypertensive animals. 10 " On the other hand, the density of sympathetic innervation has been shown to increase in brain arteries of the spontaneously hypertensive rats (SHR). 5 l2 Furthermore, autoregulation of lower and higher limits of cerebral blood flow has been reported to change in hypertensive animals.…”

mentioning

confidence: 99%

Autonomic innervation of cerebral blood vessels decreases in renal hypertensive rats.

Saito¹,

Lee²

1985

Hypertension

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SUMMARY The ultrastructural distribution of the autonomic nerves of brain arteries was investigated in renal (one-kidney, one clip) hypertensive and normotensive Wistar-Kyoto rats. Sympathetic and nonsympathetic nerve terminals were found only in the adventitial layer of brain arteries of renal hypertensive and normotensive rats. In both normotensive and renal hypertensive rats the total nerve endings were dense in anterior cerebral artery, moderately dense in middle cerebral artery, and sparse in basilar artery. In normotensive rats, nonsympathetic nerves outnumbered sympathetic nerves in anterior cerebral, middle cerebral, and basilar arteries. In renal hypertensive rats these two types of nerve terminals in close apposition to smooth muscle decreased in anterior cerebral and basilar arteries, while those in middle cerebral arteries remained unchanged. These results suggest that the potential neurogenic control of cerebral blood vessels as well as the trophic effect of sympathetic nerves on brain blood vessels may decrease in renal hypertensive rats. As this finding contrasts with that in spontaneously hypertensive rats, the pattern of innervation in brain arteries may differ in different types of hypertension. (Hypertension 7: 514-518, 1985) KEY Tissue concentrations of norepinephrine are reported to be decreased in mesenteric artery and heart in renal hypertensive animals.10 " On the other hand, the density of sympathetic innervation has been shown to increase in brain arteries of the spontaneously hypertensive rats (SHR).5 -l2 Furthermore, autoregulation of lower and higher limits of cerebral blood flow has been reported to change in hypertensive animals. 13 "" These results suggest that autonomic nerves undergo some changes when the animal becomes hypertensive. Alterations in the pattern of autonomic nerves may be different depending on the type of hypertensive model. In this study, we therefore examined and compared the ultrastructural distribution of sympathetic and nonsympathetic nerve terminals and their relationship to smooth muscle cells in the cerebral arterial walls of renal (one-kidney, one clip) hypertensive rats (RHR) and normotensive rats (NR). MethodsThe experiments were performed on normotensive male Wistar-Kyoto rats. Chronic renal hypertension was induced in 7-week-old rats by placing a silver clip (internal diameter, 0.25 mm) over the left renal artery through a left lumbar incision and followed 1 week later by contralateral nephrectomy. The control animals were sham-operated. The left kidney was exposed after a lumbar incision and was manipulated without compressing the artery. The operating time was approximately the same as that of the procedure for artery clipping. One week later the contralateral kidney was also exposed but not removed. All of the procedures were accomplished with the rats under sodium pentobarbital (Nembutal, 50 mg/ml). The systol-

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Uptake and Metabolism of Noradrenaline by Blood Vessels of Perinephritic Hypertensive Dogs

Cited by 5 publications

References 10 publications

Altered Catecholamine Contents in Vascular and Nonvascular Tissues in Genetically Hypertensive Rats

Altered Catecholamine Contents in Vascular and Nonvascular Tissues in Genetically Hypertensive Rats

Ultrastructural Changes in the Cerebral Artery Wall Induced by Long-Term Sympathetic Denervation

Autonomic innervation of cerebral blood vessels decreases in renal hypertensive rats.

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