Effect of Various Lesions in the Nucleus Tractus Solitarii of the Rat on Blood Pressure, Heart Rate and Cardiovascular Reflex Responses

Zandberg, P.; Palkovits, Miklós; W, de Jong

doi:10.3109/10641967809068613

Cited by 28 publications

(11 citation statements)

References 46 publications

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“…Indeed, NTS lesions are known to increase sympathoadrenal activity. 2 These results appear, at first, to contradict previous reports 4 -5 that NTS hypertension is caused solely by increased sympathetic outflow. Such a conclusion was based on the demonstration that destruction of sympathetic nerve terminals by systemic injection of 6-hydroxydopamine plus adrenalectomy or treatment with ganglionic or a-adrenergic blocking agents reversed the hypertension.…”

Section: Discussioncontrasting

confidence: 60%

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Sved¹,

Imaizumi²,

Talman³

et al. 1985

Hypertension

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SUMMARY Lesions of the nucleus tractus solitarius (NTS) were studied to determine whether they elevate plasma vasopressin levels and, if so, whether these elevated levels of vasopressin contribute to the hypertension caused by NTS lesions. Bilateral electrolytic lesions of the NTS caused acute, severe hypertension in rats anesthetized with chloralose and in conscious, freely moving rats. After placement of the NTS lesions there was a greater than tenfold elevation in plasma vasopressin levels. Administration of an antagonist of the vasoconstrictor action of vasopressin markedly diminished the hypertension in both conscious and anesthetized rats. Following ganglionic blockade with chlorisondamine, NTS lesions still elicited hypertension, and the magnitude of the hypertension was not different from that observed in rats not treated with chlorisondamine. The hypertension produced by lesions of the NTS in ganglionic-blocked rats was completely abolished by administration of a vasopressin antagonist. These results indicate that (1) NTS lesions elevate plasma vasopressin levels and (2) elevated plasma vasopressin contributes to the hypertension produced by such lesions. (Hypertension 7: 262-267, 1985) KEY WORDS • sympathetic nervous system brain stem * central nervous system blood pressure • posterior pituitary B ILATERAL electrolytic lesions of the nucleus tractus solitarius (NTS) have been shown to elicit arterial hypertension in the rat, cat, and dog. "4 In the rat, in which the hypertension is fulminant, the increase in arterial pressure (AP) has been attributed solely to an increase in sympathetic discharge. Thus a-adrenergic blockade with phentolamine, chemosympathectomy with 6-hydroxydopamine, or ganglionic blockade will block the development of hypertension after lesion of the NTS. 45 As the NTS is the site of termination of all arterial and cardiopulmonary baroreceptor afferents, 6 the increase of sympathetic activity has been attributed to removal of tonic sympathoinhibitory influences exerted by baroreceptors. In addition to governing the activity of the autonomic nervous system, information provided by baroreceptors also has been shown to tonically inhibit the release of arginine vasopressin (AVP) from the posterior pituitary. 7 -9 Therefore, NTS lesions might lead to increased release of this hormone. As baroreceptor denervation markedly potentiates the pressor activity of AVP, 10 " elevated plasma AVP levels may contribute to the hypertension evoked by bilateral NTS lesions. This article describes experiments that support this hypothesis. MethodsExperiments were performed on male SpragueDawley rats weighing approximately 300 g (Taconic Farms, Germantown, NY). Animals were housed in pairs under controlled lighting and temperature conditions, with ad libitum access to food and tap water for at least 1 week before the experiments began.Rats were anesthetized with halothane (2% in 100% O, administered by a cone placed over the nose). One cannula (PE-50 tubing filled with heparinized saline) was placed in...

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Section: Discussioncontrasting

confidence: 60%

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Sved¹,

Imaizumi²,

Talman³

et al. 1985

Hypertension

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“…The sympathoadrenal system appears to be the other pressor system involved in producing NTS hypertension. As in an earlier study, 3 NTS lesions markedly increased plasma catecholamine levels, indicating increased sympathoadrenal activity (see Table 1). In the same animals, plasma renin activity was not increased, suggesting that the renin-angiotensin system is not involved in this model of hypertension.…”

Section: Treatmentsupporting

confidence: 82%

Peripheral pressor systems in hypertension caused by nucleus tractus solitarius lesions.

Sved¹

1986

Hypertension

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SUMMARY The roles of vasopressin, the sympathoadrenal system, and the renin-angiotensin system in the production of hypertension after bilateral destruction of the nucleus tractus solitarius (NTS) were examined in chloralose-anesthetized rats. Since the activity of the renin-angiotensin system is high in anesthetized rats, additional studies were performed in unanesthetized, freely moving rats to evaluate the role of the renin-angiotensin system in hypertension caused by NTS lesions. Hypertension produced by bilateral electrolytic NTS lesions in rats was accompanied by elevated plasma levels of vasopressin (approximately 7-fold), norepinephrine (> 10-fold), and epinephrine (> 10-fold), but not of plasma renin activity. These results suggest that this form of hypertension is due to increased sympathoadrenal activity and increased vasopressin release into plasma and that the renin-angiotensin system is not involved. In rats with NTS lesions, blockade of vasopressin or the sympathoadrenal system, but not the renin-angiotensin system, elicited an acute decrease in arterial pressure. However, blockade of either vasopressin or the autonomic nervous system before production of the lesions had no effect on the resulting hypertension, indicating that in the absence of either one of these systems bilateral NTS lesions still result in severe hypertension. Although the renin-angiotensin system does not normally contribute to this hypertension, it does appear to contribute to the elevation in blood pressure once the actions of vasopressin have been blocked. In rats pretreated with a vasopressin antagonist, plasma renin activity increased following NTS lesions and the angiotensin converting enzyme inhibitor captopril decreased blood pressure. These results indicate that hypertension induced by bilateral NTS destruction is produced by complex interactions among the sympathoadrenal system, vasopressin, and the renin-angiotensin system. 5 Recently, we 6 demonstrated that the release of arginine vasopressin (AVP) into the circulation contributes to the fulminating hypertension caused by NTS lesions in the rat. We found that NTS lesions markedly elevated plasma AVP levels and that an AVP antagonist partially reversed the hypertension caused by these lesions. Furthermore, in rats in which the autonomic nervous system had been blocked, NTS lesions still caused hypertension, which was totally reversed by the AVP antagonist. However, the previous studies addressed only whether AVP was involved in NTS hypertension; they did not examine the interactions of AVP with other pressor systems (i.e., sympathoadrenal system and renin-angiotensin system) in producing the hypertension. These interactions are examined in the present study. Materials and MethodsExperiments were performed on male SpragueDawley rats aged approximately 10 weeks and weighing approximately 300 g (Taconic Farms, Germantown, NY, USA). Animals were housed in groups under controlled lighting and temperature conditions, with ad libitum access to food and tap water for at lea...

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“…The present microinjection studies did not allow a more precise localization since there was an elongated rostro-caudal distribution of the injection volume (0.4 pl) along the NTS over a distance of approximately 1200 pm, as shown with radioactive noradrenaline and, previously, with methylene blue and ~4C-clonidine (Zandberg and De Jong, 1977a,b). Interestingly these results indicate a differentiation between the area from which hypertension can be evoked by lesions and the area which, when injected with catecholamines, evokes a decrease of blood pressure, because only lesions of the NTS located rostral of the A2-region elicited hypertension (Zandberg et al, 1978).…”

Section: Discussionmentioning

confidence: 85%

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

Zandberg

Jong

Wied

1979

European Journal of Pharmacology

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160

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Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata, European J. Pharmacol. 55 (1979) 43--56.The effect of various catecholamines and a-mimetics, given by microinjection in the A2-region of the nucleus tractus solitarii (NTS), on blood pressure was investigated in anesthetized male rats. A dose-dependent decrease of blood pressure and heart rate was induced by adrenaline as the most effective drug, followed by noradrenaline, dopamine, a-methylnoradrenaline and octopamine. Ablation of the rostral or caudal part of the NTS, or removal of the area postrema did not diminish the effect of a-methylnoradrenaline. Higher doses of noradrenaline and a-methylnoradrenaline caused an initial rise of blood pressure, while the blood pressure lowering effect of noradrenaline was diminished, and that of a-methylnoradrenaline and dopamine delayed. Isoprenaline and the (+)-stereoisomers of noradrenaline and a-methylnoradrenaline were ineffective. The hypotensive effect of dopamine was not prevented by systemic injection of the dopamine ~-hydroxylase inhibitor FLA 63. Prior application of haloperidol, yohimbine and phentolamine antagonized the hypotensive response to dopamine and a-methylnoradrenaline. Application of peripherally effective a-mimetics into the A2-region had no or little effect, while high doses increased blood pressure. Tyramine and clonidine caused some decrease of blood pressure. Clonidine also decreased blood pressure when it was applied in the area of the locus coeruleus. Application of isoprenaline in the locus coeruleus also decreased blood pressure while in contrast adrenaline, noradrenaline, dopamine and 0l-methylnoradrenaline increased blood pressure. The present data suggest that the catecholaminergic receptors in the A2-region of the NTS differ from the classic vascular a-receptor and that the NTS also may contain structures which can antagonize the decrease in blood pressure. Catecholamines a-Mimetics Locus coeruleusDecrease of blood pressure Nucleus tractus solitarii

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Effect of Various Lesions in the Nucleus Tractus Solitarii of the Rat on Blood Pressure, Heart Rate and Cardiovascular Reflex Responses

Cited by 28 publications

References 46 publications

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Peripheral pressor systems in hypertension caused by nucleus tractus solitarius lesions.

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

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