Local modulation of adrenergic neuroeffector interaction in the blood vessel well.

Vanhoutte, P. M.; Verbeuren, Tony J.; Webb, R. C.

doi:10.1152/physrev.1981.61.1.151

Cited by 415 publications

(201 citation statements)

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“…Indeed, circulatory angiotensin II will have profound pressor effects not only because it directly activates vascular smooth muscle, but also because it amplifies the vasoconstrictor control exerted by the sympathetic nervous system at different levels (central nervous system, ganglionic transmission, adrenergic neuroeffector interaction) (Shepherd & Vanhoutte, 1979;Vanhoutte et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

Why are converting enzyme inhibitors vasodilators?

Vanhoutte

Auch-Schwelk

Biondi

et al. 1989

Brit J Clinical Pharma

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1. The primary action of the converting enzyme inhibitors to prevent the formation of angiotensin II can explain a decrease in peripheral vascular resistance in patients with elevated, but not in those with normal or reduced plasma renin levels. 2. The inhibition of the breakdown of bradykinin will potentiate the vasodilator properties of the endogenously produced peptide. These include direct relaxation of certain vascular smooth muscle, production of vasodilator prostanoids and release of endothelium‐derived relaxing factor(s). The greater release of the latter in the kidney could exert a negative feedback on the release of renin. 3. In addition, converting enzyme inhibitors may directly (by a prejunctional effect) and indirectly (by curtailing the production of angiotensin II) reduce the release of noradrenaline in the blood vessel wall. 4. Converting enzyme inhibitors may also directly reduce the responsiveness of vascular smooth muscle to vasoconstrictor stimuli (e.g. alpha‐adrenoceptor activation). 5. The different effects of these therapeutic agents may concur to induce peripheral vasodilatation.

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Section: Introductionmentioning

confidence: 99%

Why are converting enzyme inhibitors vasodilators?

Vanhoutte

Auch-Schwelk

Biondi

et al. 1989

Brit J Clinical Pharma

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“…We and others [26] have observed that microinjections of α,β-methylene ATP into the NTS produce transitory hypotension, bradycardia, and hindlimb vasodilation, presumably due to sympathoinhibition. The hindlimb vasodilation seen in response to stimulation of the HDA [6] apparently involve withdrawal of sympathetic activity to blood vessels, via norepinephrine acting in α adrenoceptors [52,53] and epinephrine release by the adrenal glands acting on β2 receptors in blood vessels [5,6]. The activation of P2 receptors in the NTS following stimulation of the HDA in this study seems to intermediate both the withdrawal in sympathetic tone and the release of epinephrine.…”

Section: Hindlimb Vasodilation In Alerting-defense Responses Is Mediamentioning

confidence: 49%

Interaction of medullary P2 and glutamate receptors mediates the vasodilation in the hindlimb of rat

Korim

Ferreira-Neto

Pedrino

et al. 2012

Purinergic Signalling

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In the nucleus tractus solitarii (NTS) of rats, blockade of extracellular ATP breakdown to adenosine reduces arterial blood pressure (AP) increases that follow stimulation of the hypothalamic defense area (HDA). The effects of ATP on NTS P2 receptors, during stimulation of the HDA, are still unclear. The aim of this study was to determine whether activation of P2 receptors in the NTS mediates cardiovascular responses to HDA stimulation. Further investigation was taken to establish if changes in hindlimb vascular conductance (HVC) elicited by electrical stimulation of the HDA, or activation of P2 receptors in the NTS, are relayed in the rostral ventrolateral medulla (RVLM); and if those responses depend on glutamate release by ATP acting on presynaptic terminals. In anesthetized and paralyzed rats, electrical stimulation of the HDA increased AP and HVC. Blockade of P2 or glutamate receptors in the NTS, with bilateral microinjections of suramin (10 mM) or kynurenate (50 mM) reduced only the evoked increase in HVC by 75 % or more. Similar results were obtained with the blockade combining both antagonists. Blockade of P2 and glutamate receptors in the RVLM also reduced the increases in HVC to stimulation of the HDA by up to 75 %. Bilateral microinjections of kynurenate in the RVLM abolished changes in AP and HVC to injections of the P2 receptor agonist α,β-methylene ATP (20 mM) into the NTS. The findings suggest that HDA-NTS-RVLM pathways in control of HVC are mediated by activation of P2 and glutamate receptors in the brainstem in alerting-defense reactions.

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“…23 Ach also is a potent stimulator of eNOS, resulting in increased NO. Thus, it is plausible that Ach, released during the neural stimulation of erection, functions to RhoAaRho-kinase K Chitaley et al inhibit the vasoconstrictor effects of sympathetic stimulation in addition to increasing local NO.…”

Section: Initial Results Establishing the Importance Of Rho-kinase Inmentioning

confidence: 99%

“…Parasympathetic innervation of the penis releases acetylcholine (Ach), and this neurotransmitter may enhance erection by inhibiting the release of norepinephrine and by stimulating endothelial NO production. 3,4,23 Additionally, neurons containing vasoactive intestinal polypeptide (VIP) have been found in cavernosal tissue, and the administration of VIP leads to an increase in CCP, leading to erection. 7 ± 9 Components of the arachidonic acid metabolic pathway have also been localized in the penis, and it has long been suggested that prostaglandins may also contribute to the erectile response as PGE 1 has been used successfully in the treatment of erectile dysfunction.…”

Section: Mechanisms Of Cavernosal Vasorelaxationmentioning

confidence: 99%

RhoA/Rho-kinase: a novel player in the regulation of penile erection

2001

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Current research has centered around the role of nitric oxide in the stimulation of cavernosal vasodilation and erection. However, recent evidence from our lab details the importance of endogenous vasoconstrictor mechanisms in maintaining a¯accid penile state, and further demonstrates that the inhibition of endogenous vasoconstriction is suf®cient to stimulate erection in a rat model. In this article, we suggest inhibition of endogenous vasoconstriction as a potential therapeutic avenue in the treatment of erectile dysfunction. We also speculate on potential physiologic mechanisms by which endogenous vasoconstriction is inhibited in order for arousalinitiated vasorelaxation, and erection, to occur.

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Local modulation of adrenergic neuroeffector interaction in the blood vessel well.

Cited by 415 publications

References 0 publications

Why are converting enzyme inhibitors vasodilators?

Why are converting enzyme inhibitors vasodilators?

Interaction of medullary P2 and glutamate receptors mediates the vasodilation in the hindlimb of rat

RhoA/Rho-kinase: a novel player in the regulation of penile erection

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