Reversibility of structural changes in the resistance vessels in hypertension: a review of studies with pindolol.

Dunér, H

doi:10.1111/j.1365-2125.1987.tb03269.x

Cited by 2 publications

(1 citation statement)

References 2 publications

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“…The present results corroborate that the intrinsic sympathomimetic activity of certain ␤-adrenoceptor drugs observed in human clinics might be related to the interplay of multiple ␤-adrenoceptors (1,11,21). It is known that some ␤ 1 -and ␤ 2 -adrenergic antagonists such as pindolol act as ␤ 3 -adrenoceptor agonists (4,39).…”

Section: Discussionsupporting

confidence: 92%

NO production and eNOS phosphorylation induced by epinephrine through the activation of β-adrenoceptors

Figueroa

Poblete

Fernández

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Epinephrine plays a key role in the control of vasomotor tone; however, the participation of the NO/cGMP pathway in response to beta-adrenoceptor activation remains controversial. To evaluate the involvement of the endothelium in the vascular response to epinephrine, we assessed NO production, endothelial NO synthase phosphorylation, and tissue accumulation of cGMP in the perfused arterial mesenteric bed of rat. Epinephrine elicited a concentration-dependent increase in NO (EC(50) of 45.7 pM), which was coupled to cGMP tissue accumulation. Both NO and cGMP production were blocked by either endothelium removal (saponin) or NO synthase inhibition (N(omega)-nitro-L-arginine). Blockade of beta(1)- and beta(2)-adrenoceptors with 1 microM propranolol or beta(3)-adrenoceptor with 10 nM SR 59230A displaced rightward the concentration-NO production curve evoked by epinephrine. Selective stimulation of beta(1)-, beta(2)-, or beta(3)-adrenoceptors also resulted in NO and cGMP production. Propranolol (1 microM) inhibited the rise in NO induced by isoproterenol or the beta(2)-adrenoceptor agonists salbutamol, terbutaline, or fenoterol. Likewise, 10 nM SR 59230A reduced the effects of the beta(3)-adrenoceptor agonists BRL 37344, CGP 12177, SR 595611A, or pindolol. The NO production induced by epinephrine and BRL 37344 was associated with the activation of the phosphatidylinositol 3-kinase/Akt pathway and phosphorylation of eNOS in serine 1177. In addition, in anaesthetized rats, bolus administration of isoproterenol, salbutamol, or BRL 37344 produced NO-dependent reductions in systolic blood pressure. These findings indicate that beta(1)-, beta(2)-, and beta(3)-adrenoceptors are coupled to the NO/cGMP pathway, highlighting the role of the endothelium in the vasomotor action elicited by epinephrine and related beta-adrenoceptor agonists.

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Section: Discussionsupporting

confidence: 92%

NO production and eNOS phosphorylation induced by epinephrine through the activation of β-adrenoceptors

Figueroa

Poblete

Fernández

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Comparison of the side‐effects of pindolol and atenolol in the treatment of hypertension

Abrahamsen

Digranes²,

Gisholt³

1990

Journal of Internal Medicine

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A double-blind multicentre study of 349 hypertensive patients was performed to compare the side-effects of the two beta-blockers atenolol (selective beta 1-blocker) and pindolol (beta 1- and beta 2-blocker with Intrinsic sympathomimetic activity (ISA] in equipotential doses (100 mg atenolol vs. 15 mg pindolol). Male and female patients aged 20-65 years with essential hypertension WHO stages I and II were included. Patients were examined 1 and 6 months after the start of treatment, and side-effects were recorded. The antihypertensive effect was similar for the two drugs. After 1 month there was significantly less bradycardia (P less than 0.01), cold hands and feet (P less than 0.05) and tiredness (P less than 0.02) in the pindolol group, and less sleep disturbance (P less than 0.02) in the atenolol group. After 6 months there was no significant difference in sleep disturbance, but the differences in the other side-effects remained significant.

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Reversibility of structural changes in the resistance vessels in hypertension: a review of studies with pindolol.

Cited by 2 publications

References 2 publications

NO production and eNOS phosphorylation induced by epinephrine through the activation of β-adrenoceptors

NO production and eNOS phosphorylation induced by epinephrine through the activation of β-adrenoceptors

Comparison of the side‐effects of pindolol and atenolol in the treatment of hypertension

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