Postjunctional regulation by angiotensin II of α1-adrenoceptor-mediated pressor responses in the rat

Marano, Giuseppe; Argiolas, Livio

doi:10.1016/0014-2999(94)90309-3

Cited by 16 publications

(10 citation statements)

References 18 publications

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“…This effect was antagonized by the AT 1 R antagonist valsartan but not by the AT 2 R antagonist PD123319 [17] . A crosstalk between ␣ 1 -AR and AT 1 R could be taking place in VSM contraction [20] .…”

Section: Discussionmentioning

confidence: 86%

“…Ang II infusion potentiates PHE pressor response in vivo [17,19,20] . This effect was antagonized by the AT 1 R antagonist valsartan but not by the AT 2 R antagonist PD123319 [17] .…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, Ang II enhances norepinephrine release from the adrenergic nervous terminal [17] , modulates its action at a postsynaptic level [18] , and potentiates the pressor effect of phenylephrine (PHE) [17,19,20] . Also, there is evidence supporting that ␣ 1 -AR contributes to AT 1 R-mediated Ang II hypertrophic effects [21] .…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin-II-Dependent Changes in Alpha-1 Adrenoceptor Vascular Expression in Pregnant Rats

López-Sánchez¹,

Valdés²,

Godínez-Hernández³

et al. 2009

Pharmacology

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Vessels from pregnant animals show a blunted response to adrenergic agonists. In this work, we explored if pregnancy reduces α₁-adrenergic receptor (α₁-AR)-mediated vascular smooth muscle protein expression as well as agonist-induced contraction in rat aorta, and if angiotensin II (Ang II) levels during pregnancy are related to these changes. Female Wistar rats were divided randomly into nonpregnant (NP) and pregnant groups (first week: P1, second week: P2, third week: P3). Subsets of animals were treated with captopril (5 mg kg^–1 day^–1 for 7 days; n = 6). Phenylephrine (PHE) concentration-response curves were constructed (1 × 10^–9 to 3.1 × 10^–5 mol/l) and α_1A-, α_1B- and α_1D-AR were measured in the aorta by immunoblot. Captopril decreased α-AR expression in the NP group. In contrast, pregnancy decreased α_1A-, α_1B- and α_1D-AR levels and captopril prevented this reduction. PHE sensitivity was decreased in the thoracic and abdominal aorta in the P2 group, with no changes in E_max, and E_max was decreased in the abdominal aorta in all experimental groups. Our results suggest that Ang II levels during pregnancy are related to a decrease in aortic α₁-AR expression. The physiological meaning of this finding remains to be established.

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Section: Discussionmentioning

confidence: 86%

“…Ang II infusion potentiates PHE pressor response in vivo [17,19,20] . This effect was antagonized by the AT 1 R antagonist valsartan but not by the AT 2 R antagonist PD123319 [17] .…”

Section: Discussionmentioning

confidence: 99%

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Angiotensin-II-Dependent Changes in Alpha-1 Adrenoceptor Vascular Expression in Pregnant Rats

López-Sánchez¹,

Valdés²,

Godínez-Hernández³

et al. 2009

Pharmacology

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“…Angiotensin II (Ang II) stimulates the sympathetic system by activating central nervous tone and catecholamine release 2 and by facilitating the release of catecholamines from peripheral sympathetic neurons via ganglionic 3,4 and axonal presynaptic receptors. 5,6 Ang II has been shown to increase vascular sensitivity to noradrenaline in rats and isolated vessels, [7][8][9] so that Ang II and noradrenaline exert synergistic actions on vascular tone. As such, it could be proposed that blockade of endogenous Ang II by AT 1 blockers might alter vascular reactivity to exogenous noradrenaline.…”

mentioning

confidence: 99%

Reduction of Vascular Noradrenaline Sensitivity by AT ₁ Antagonists Depends on Functional Sympathetic Innervation

et al. 2004

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Abstract-Blockade of angiotensin II type-1 (AT 1 ) receptors has been shown to reduce the magnitude of the blood pressure response to noradrenaline in pithed rats via an unidentified mechanism. Dose-response curves were established for the noradrenaline-induced (10 Ϫ12 to 10 Ϫ7 mol/kg) increase of diastolic blood pressure in pithed rats treated with tubocurarine, propranolol, and atropine. Candesartan (1 mg/kg) increased the ED 50 of the noradrenaline response (1.3Ϯ0.1 nmol/kg) up to 20-fold. Vasopressor responsiveness to noradrenaline was attenuated specifically, whereas the vasopressin-induced increase in diastolic blood pressure was maintained. Specific involvement of AT 1 receptors was confirmed by equivalent actions of losartan. Blockade of norepinephrine transporter or ␣ 2 -adrenoceptors using desipramine or rauwolscine reduced the losartan-induced shifts in the ED 50 values of noradrenaline by 63% and 21%, respectively. Combined blockade of norepinephrine transporter and ␣ 2 -adrenoceptors eliminated the influence of losartan on noradrenaline sensitivity (ED 50 5.5Ϯ1.3 versus 5.6Ϯ1.2 nmol/kg), a result also observed after sympathetic denervation by reserpine (ED 50 7.1Ϯ0.8 versus 7.8Ϯ0.8 nmol/kg). Our experiments show that the reduction of vascular noradrenaline sensitivity by AT 1 blockade is dependent on the intact functioning of both neuronal noradrenaline uptake via norepinephrine transporter and presynaptic ␣ 2 -mediated autoinhibition, exclusively provided by the sympathetic innervation. These newly identified mechanisms may contribute to the antihypertensive and protective actions of AT 1 blockers. 1 The mechanisms of the various interactions between the renin-angiotensin-aldosterone system and the sympathetic system have been established at different levels and have been shown to bear prominent pathophysiological implications. Angiotensin II (Ang II) stimulates the sympathetic system by activating central nervous tone and catecholamine release 2 and by facilitating the release of catecholamines from peripheral sympathetic neurons via ganglionic 3,4 and axonal presynaptic receptors. 5,6 Ang II has been shown to increase vascular sensitivity to noradrenaline in rats and isolated vessels, 7-9 so that Ang II and noradrenaline exert synergistic actions on vascular tone. As such, it could be proposed that blockade of endogenous Ang II by AT 1 blockers might alter vascular reactivity to exogenous noradrenaline. Indeed AT 1 blockers provoked a reduction in vascular sensitivity to noradrenaline in pithed rats, 6 although discrepant findings were obtained even where similar experimental approaches were pursued. 10 This controversy still requires clarification, particularly as regards the mechanisms by which AT 1 blockers might reduce vascular catecholamine sensitivity.In arterial smooth muscle, Ang II has been shown to potentiate noradrenaline sensitivity by activating protein kinase C and thereby increasing calcium sensitivity. 8 Moreover, short-duration in vivo pretreatment with Ang II also primes the is...

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“…In vivo animal studies have shown that angiotensin (Ang) II enhances adrenergic receptor function, which results in increased vasoconstriction and myocardial damage. [3][4][5] In healthy volunteers, Seidelin and colleagues 6 showed that low physiological doses of Ang II and norepinephrine interacted synergistically to produce an enhanced vasopressor response. Also in healthy volunteers, Lang and colleagues 7 showed that the ␣ 1 -adrenoceptor blocker prazosin blunted the antinatriuretic effect of Ang II.…”

mentioning

confidence: 99%

Vasopressor Response to Angiotensin II Infusion in Patients With Chronic Heart Failure Receiving β-Blockers

et al. 2003

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Background-A synergistic interaction between the angiotensin II (Ang II) type 1 receptor and ␣ 1 -adrenergic receptors has been described. We hypothesized that the nonselective ␤-antagonist carvedilol, through its ␣ 1 -adrenergic blocking properties, may modulate vascular reactivity to Ang II in patients with chronic heart failure (CHF). Accordingly, we compared the vasopressor response to infused Ang II in patients treated with carvedilol and metoprolol, a selective ␤-antagonist. Methods and Results-All subjects were treated with carvedilol or metoprolol for at least 3 months. ACE inhibitor therapy was standardized to enalapril 40 mg/d or the maximally tolerated dose. Exogenous Ang II was administered as sequential intravenous bolus injections (2.5 to 30 ng/kg) titrated to a rise in radial artery systolic pressure of Ն20 mm Hg.

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Postjunctional regulation by angiotensin II of α1-adrenoceptor-mediated pressor responses in the rat

Cited by 16 publications

References 18 publications

Angiotensin-II-Dependent Changes in Alpha-1 Adrenoceptor Vascular Expression in Pregnant Rats

Angiotensin-II-Dependent Changes in Alpha-1 Adrenoceptor Vascular Expression in Pregnant Rats

Reduction of Vascular Noradrenaline Sensitivity by AT ₁ Antagonists Depends on Functional Sympathetic Innervation

Vasopressor Response to Angiotensin II Infusion in Patients With Chronic Heart Failure Receiving β-Blockers

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Postjunctional regulation by angiotensin II of α1-adrenoceptor-mediated pressor responses in the rat

Cited by 16 publications

References 18 publications

Angiotensin-II-Dependent Changes in Alpha-1 Adrenoceptor Vascular Expression in Pregnant Rats

Angiotensin-II-Dependent Changes in Alpha-1 Adrenoceptor Vascular Expression in Pregnant Rats

Reduction of Vascular Noradrenaline Sensitivity by AT 1 Antagonists Depends on Functional Sympathetic Innervation

Vasopressor Response to Angiotensin II Infusion in Patients With Chronic Heart Failure Receiving β-Blockers

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Reduction of Vascular Noradrenaline Sensitivity by AT ₁ Antagonists Depends on Functional Sympathetic Innervation