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. 2016 Sep 22;390(1):25–35. doi: 10.1007/s00210-016-1302-y

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© The Author(s) 2016

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 5 — Possible mechanisms involved in the effect of the CB receptor agonist CP55940 topically administered to the paraventricular nucleus (PVN) on the sympathetic outflow and cardiovascular parameters. Activation of presynaptic inhibitory CB₁ receptors on glutamatergic (Glu) neurones leads to a decrease in the sympathetic outflow (mainly to resistance vessels and heart) and a fall in blood pressure. Activation of presynaptic inhibitory CB₁ receptors on GABAergic (γ-aminobutyric acid) neurons leads to an increase in the sympathetic outflow (mainly of the adrenal medulla) and in blood pressure. Activation of presynaptic facilitatory (i) angiotensin II (Ang II) AT₁, (ii) thromboxane A₂ (TXA₂) TP and (iii) adrenaline (Adr) β₂-adrenergic receptors increases whereas activation of GABA_A receptors decreases the release of glutamate. Nitric oxide (NO) stimulates GABA release. For the sake of clarity, only interactions examined in the present study have been shown in this scheme. An inhibitory effect of Ang II and a facilitatory effect of CP55940 on NO production although opposite in direction to the effects usually obtained by AT₁ and CB₁ receptor activation, respectively, are also indicated. stimulatory inputs; inhibitory inputs. RVLM rostral ventrolateral medulla, IML intermediolateral column

Inline graphic — Possible mechanisms involved in the effect of the CB receptor agonist CP55940 topically administered to the paraventricular nucleus (PVN) on the sympathetic outflow and cardiovascular parameters. Activation of presynaptic inhibitory CB₁ receptors on glutamatergic (Glu) neurones leads to a decrease in the sympathetic outflow (mainly to resistance vessels and heart) and a fall in blood pressure. Activation of presynaptic inhibitory CB₁ receptors on GABAergic (γ-aminobutyric acid) neurons leads to an increase in the sympathetic outflow (mainly of the adrenal medulla) and in blood pressure. Activation of presynaptic facilitatory (i) angiotensin II (Ang II) AT₁, (ii) thromboxane A₂ (TXA₂) TP and (iii) adrenaline (Adr) β₂-adrenergic receptors increases whereas activation of GABA_A receptors decreases the release of glutamate. Nitric oxide (NO) stimulates GABA release. For the sake of clarity, only interactions examined in the present study have been shown in this scheme. An inhibitory effect of Ang II and a facilitatory effect of CP55940 on NO production although opposite in direction to the effects usually obtained by AT₁ and CB₁ receptor activation, respectively, are also indicated. stimulatory inputs; inhibitory inputs. RVLM rostral ventrolateral medulla, IML intermediolateral column