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

Vittorio, Timothy J.; Lang, Chim C.; Katz, Stuart D.; Packer, Milton; Mancini, Donna; Jorde, Ulrich P.

doi:10.1161/01.cir.0000045666.04794.14

Cited by 9 publications

(3 citation statements)

References 38 publications

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“…This effect could be related to the results obtained by Vittorio et al, where the treatment with metoprolol and carvedilol produced an increase in BP in response to Ang-II infusion. 24 In relation to the combination therapy, the antihypertensive mechanisms are not sufficiently studied. In this way, through synergist mechanism, the use of interactions decreased the BP by using lower doses of captopril and propranolol, 25 these results were corroborated by us with this combination.…”

Section: Discussionmentioning

confidence: 99%

Combination of β Adrenergic Receptor Block and Renin–Angiotensin System Inhibition Diminished the Angiotensin II-Induced Vasoconstriction and Increased Bradykinin-Induced Vasodilation in Hypertension

et al. 2017

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In hypertension, the combination therapy is frequently used to obtain a better therapeutic effect and reduce adverse effects. One effective combination is with inhibitors and β-blockers of renin–angiotensin system. Although the mechanisms of action of each drug are already known, the antihypertensive mechanism is more complex and therefore the combined treatment mechanism is unclear. Specifically, the effect of the treatments of angiotensin-converting enzyme inhibitor or AT1 receptor antagonist with β-blocker on the angiotensin II and bradykinin reactivity has not been studied. For this reason, we evaluated the interaction between propranolol and captopril or losartan on vascular reactivity to bradykinin and angiotensin II in spontaneously hypertensive rat. We constructed concentration–response curves to angiotensin II and bradykinin after treatment of SHR with propranolol–captopril or propranolol–losartan by using rat aortic rings. While losartan or captopril with propranolol potentiated bradykinin-induced vasodilation effect, the propranolol–losartan interaction decreased the angiotensin II-induced vasoconstriction. In addition, the combinations did not reduce the heart rate significantly. These results suggest that the combined therapy decreased blood pressure to normotensive values and showed less effect for angiotensin II and greater effect for bradykinin than monotherapy which could contribute in the antihypertensive effect.

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Section: Discussionmentioning

confidence: 99%

Combination of β Adrenergic Receptor Block and Renin–Angiotensin System Inhibition Diminished the Angiotensin II-Induced Vasoconstriction and Increased Bradykinin-Induced Vasodilation in Hypertension

et al. 2017

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“…Our findings showed that irbesartan treatment attenuated vasopressor response to NA, PE, and ME, whereas interactions between RAAS and SNS have already been established [ 18 ], and this can be confirmed from the study done by Raasch et al, wherein the systemic vascular responses to NA were diminished after pretreatment with losartan [ 67 ]. However, Ang-II suggests facilitating sympathetic neurotransmission at various sites such as CNS and presynaptic sympathetic nerve terminals [ 68 ]. Additionally, there are findings that in hyperinsulinemia scenarios, pioglitazone enhances adrenergic neurons' control over the blood vessels [ 69 , 70 ].…”

Section: Discussionmentioning

confidence: 99%

Interaction between Nuclear Receptor and Alpha‐Adrenergic Agonist Subtypes in Metabolism and Systemic Hemodynamics of Spontaneously Hypertensive Rats

Afzal,

Sattar,

Albokhadaim

et al. 2024

PPAR Research

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Partial and full PPAR‐γ agonists have shown promising effects and antihypertensive and antidiabetic agents through increased plasma adiponectin concentration. This study is aimed at examining the role of PPAR‐γ, alpha‐adrenoceptors, and adiponectin receptors in the modulation of vasopressor responses to angiotensin II (Ang II) and adrenergic agonists, after a subset treatment of partial and full PPAR‐γ agonists, each individually, and also when coupled with adiponectin in SHRs. The antioxidant potential and metabolic indices for these animals were also determined. Group I (WKY) and group II (SHR) were designated as normotensive control and hypertensive control, respectively. Groups III (SHR) and IV (SHR) received irbesartan (30 mg/kg) and pioglitazone (10 mg/kg) orally for 28 days, and groups V (SHR), VI (SHR), and VII (SHR) were treated with adiponectin (2.5 μg/kg) intraperitoneally alone, in combination with irbesartan, and in combination with pioglitazone, respectively, from days 21 to 28 only. On day 29, sodium pentobarbitone (60 mg/kg) was used to anesthetize all test animals, and systemic hemodynamic and plasma adiponectin concentrations and in vitro and in vivo antioxidant potential were measured. As compared to the WKY control, the SHR control group’s noninvasive blood pressure and basal mean arterial pressure were significantly greater, along with increased arterial stiffness, lower plasma nitric oxide, adiponectin concentration, and antioxidant enzyme levels (all P < 0.05). However, they were gradually normalized by single drug treatments in all groups, and to a greater extent in the SHR + Irb + Adp group (P < 0.05). In the acute study, the dose dependant mean arterial pressure responses to intravenously administered adrenergic agonists and angiotensin‐II were significantly larger in SHRs as compared to WKY by 20‐25%. Adiponectin alone and in combination significantly blunted vasopressor responses to these alpha‐adrenergic agonists in the SHR + Pio + Adp group by 63%, whereas attenuated responses to ANG‐II administration to 70% in SHR + Irb + Adp. In conclusion, the combined treatment of adiponectin with PPAR‐agonists reduced the systemic vascular responses to adrenergic agonists and improved arterial stiffness. This an evidence of the interaction of adiponectin receptors, PPAR‐γ, alpha‐adrenoceptors, and ANG‐II in the systemic vasculature of SHRs. A significant level of synergism has also been proved among full PPAR‐γ agonists and adiponectin receptors.

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“…Pharmacodynamics is such that blood pressure increases within minutes, is sustained at a fixed infusion rate, and returns to preinfusion values within minutes after cessation of the infusion (50). As such, direct links between dosages and changes in organ system responses could not be obtained across all studies.…”

Section: Discussionmentioning

confidence: 99%

Clinical Experience With IV Angiotensin II Administration: A Systematic Review of Safety

Busse

Wang

Chalikonda

et al. 2017

Critical Care Medicine

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

Cited by 9 publications

References 38 publications

Combination of β Adrenergic Receptor Block and Renin–Angiotensin System Inhibition Diminished the Angiotensin II-Induced Vasoconstriction and Increased Bradykinin-Induced Vasodilation in Hypertension

Combination of β Adrenergic Receptor Block and Renin–Angiotensin System Inhibition Diminished the Angiotensin II-Induced Vasoconstriction and Increased Bradykinin-Induced Vasodilation in Hypertension

Interaction between Nuclear Receptor and Alpha‐Adrenergic Agonist Subtypes in Metabolism and Systemic Hemodynamics of Spontaneously Hypertensive Rats

Clinical Experience With IV Angiotensin II Administration: A Systematic Review of Safety

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