Inhibition of norepinephrine release by presynaptic alpha2-adrenoceptors in mesenteric vasculature preparations from chronic DOCA-salt hypertensive rats.

Tsuda, Kazushi; Tsuda, Seiko; Nishio, Ichiro; Masuyama, Yoshiaki

doi:10.1536/ihj.30.231

Cited by 12 publications

(17 citation statements)

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“…By contrast, presynaptic α 2 - [22,31,34,44] and β 2 -adrenoceptors [30] and adenosine A 1 heteroreceptors [37] rather increase hypertension. The differential behaviour of α 2 (or A 1 ) as opposed to CB 1 receptors is indeed surprising since each of the three receptors is G i/o proteincoupled [1].…”

Section: Function Of Presynaptic Cannabinoid Cb 1 Receptors In Doca-smentioning

confidence: 88%

“…The higher sympathetic tone is at least partially due to an impaired function of inhibitory presynaptic α 2 -adrenoceptors [22,31,34,44] and adenosine A 1 heteroreceptors [37] and an increased function of facilitatory presynaptic β 2 -adrenoceptors [30]. We can exclude the possibility that a reduction of renal mass affects our results, since unilateral nephrectomy was performed both in the hypertensive and normotensive animals.…”

Section: Characterization Of Cardiovascular Parameters In Doca-salt Hmentioning

confidence: 91%

“…This also holds true for the strongly reduced responses of femoral or renal arteries to sympathetic nerve stimulation (but unaltered or only slightly decreased responses to noradrenaline) in anaesthetised DOCA-salt dogs [13] and rats [16] in comparison to control animals. The evidence is, however, not unequivocal, since the maximum neurogenic response was greater in arteries from DOCAsalt hypertensive than from normotensive rats (e.g., [23,34,44]). …”

Section: Characterization Of Cardiovascular Parameters In Doca-salt Hmentioning

confidence: 95%

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Enhanced function of inhibitory presynaptic cannabinoid CB1 receptors on sympathetic nerves of DOCA–salt hypertensive rats

et al. 2015

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Section: Function Of Presynaptic Cannabinoid Cb 1 Receptors In Doca-smentioning

confidence: 88%

Section: Characterization Of Cardiovascular Parameters In Doca-salt Hmentioning

confidence: 91%

Section: Characterization Of Cardiovascular Parameters In Doca-salt Hmentioning

confidence: 95%

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Enhanced function of inhibitory presynaptic cannabinoid CB1 receptors on sympathetic nerves of DOCA–salt hypertensive rats

et al. 2015

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“…Clodronate was incorporated into liposomes as previously described (60,61). Control groups received liposome-encapsulated PBS (Lipo-PBS).…”

Section: Doca-salt Hypertensionmentioning

confidence: 99%

“…These data indicate that NE released from sympathetic nerves supplying MAs contributes to blood pressure regulation. Impaired function of ␣ 2 ARs in the mesenteric circulation will increase NE release, MA constriction, and blood pressure (61). Identification of the mechanism by which ␣ 2 AR function is disrupted will help elucidate the pathophysiology of salt-sensitive hypertension.…”

mentioning

confidence: 99%

Macrophage depletion lowers blood pressure and restores sympathetic nerve α₂-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats

Thang

Demel

Crawford

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Thang LV, Demel SL, Crawford R, Kaminski NE, Swain GM, Van Rooijen N, Galligan JJ. Macrophage depletion lowers blood pressure and restores sympathetic nerve ␣ 2-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats. Am J Physiol Heart Circ Physiol 309: H1186 -H1197, 2015. First published August 28, 2015; doi:10.1152/ajpheart.00283.2015.-We tested the hypothesis that vascular macrophage infiltration and O 2 Ϫ release impairs sympathetic nerve ␣ 2-adrenergic autoreceptor (␣2AR) function in mesenteric arteries (MAs) of DOCA-salt hypertensive rats. Male rats were uninephrectomized or sham operated (sham). DOCA pellets were implanted subcutaneously in uninephrectomized rats who were provided high-salt drinking water or high-salt water with apocynin. Sham rats received tap water. Blood pressure was measured using radiotelemetry. Treatment of sham and DOCA-salt rats with liposome-encapsulated clodronate was used to deplete macrophages. After 3-5, 10 -13, and 18 -21 days of DOCA-salt treatment, MAs and peritoneal fluid were harvested from euthanized rats. Norepinephrine (NE) release from periarterial sympathetic nerves was measured in vitro using amperometry with microelectrodes. Macrophage infiltration into MAs as well as TNF-␣ and p22 phox were measured using immunohistochemistry. Peritoneal macrophage activation was measured by flow cytometry. O 2 Ϫ was measured using dihydroethidium staining. Hypertension developed over 28 days, and apocynin reduced blood pressure on days 18 -21. O 2 Ϫ and macrophage infiltration were greater in DOCA-salt MAs compared with sham MAs after day 10. Peritoneal macrophage activation occurred after day 10 in DOCA-salt rats. Macrophages expressing TNF-␣ and p22 phox were localized near sympathetic nerves. Impaired ␣2AR function and increased NE release from sympathetic nerves occurred in MAs from DOCA-salt rats after day 18. Macrophage depletion reduced blood pressure and vascular O 2 Ϫ while restoring ␣2AR function in DOCA-salt rats. Macrophage infiltration into the vascular adventitia contributes to increased blood pressure in DOCA-salt rats by releasing O 2 Ϫ , which disrupts ␣2AR function, causing enhanced NE release from sympathetic nerves.salt-sensitive hypertension; immune activation; sympathetic nervous system; ␣2-adrenergic autoreceptors; amperometry NEW & NOTEWORTHYWe have identified a novel mechanism by which salt-sensitive hypertension disrupts normal function of the sympathetic nervous system. Antioxidants may be helpful in treating some forms of hypertension.INCREASED SYMPATHETIC nerve activity contributes to high blood pressure in some animal models of hypertension, including the DOCA-salt model (10, 57). Hypertension in the DOCA-salt model is driven by reduced renal mass (removal of one kidney), high circulating mineralocorticoid levels, and high salt intake (57). Elevated salt increases central sympathetic drive to the cardiovascular system (17, 48), but there are also alterations in the local mechanisms that modulate sympathetic neurotransmiss...

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New Insights into the Contribution of Arterial NCX to the Regulation of Myogenic Tone and Blood Pressure

Zhang

2012

Advances in Experimental Medicine and Biology

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Plasma membrane protein Na(+)/Ca(2+) exchanger (NCX) in vascular smooth muscle (VSM) cells plays an important role in intracellular Ca(2+) homeostasis, Ca(2+) signaling, and arterial contractility. Recent evidence in intact animals reveals that VSM NCX type 1 (NCX1) is importantly involved in the control of arterial blood pressure (BP) in the normal state and in hypertension. Increased expression of vascular NCX1 has been implicated in human primary pulmonary hypertension and several salt-dependent hypertensive animal models. Our aim is to determine the molecular and physiological mechanisms by which vascular NCX influences vasoconstriction and BP normally and in salt-dependent hypertension. Here, we describe the relative contribution of VSM NCX1 to Ca(2+) signaling and arterial contraction, including recent data from transgenic mice (NCX1(smTg/Tg), overexpressors; NCX1(sm-/-), knockouts) that has begun to elucidate the specific contributions of NCX to BP regulation. Arterial contraction and BP correlate with the level of NCX1 expression in smooth muscle: NCX1(sm-/-) mice have decreased arterial myogenic tone (MT), vasoconstriction, and low BP. NCX1(smTg/Tg) mice have high BP and are more sensitive to salt; their arteries exhibit upregulated transient receptor potential canonical channel 6 (TRPC6) protein, increased MT, and vasoconstriction. These observations suggest that NCX is a key component of certain distinct signaling pathways that activate VSM contraction in response to stretch (i.e., myogenic response) and to activation of certain G-protein-coupled receptors. Arterial NCX expression and mechanisms that control the local (sub-plasma membrane) Na(+) gradient, including cation-selective receptor-operated channels containing TRPC6, regulate arterial Ca(2+) and constriction, and thus BP.

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Inhibition of norepinephrine release by presynaptic alpha2-adrenoceptors in mesenteric vasculature preparations from chronic DOCA-salt hypertensive rats.

Cited by 12 publications

References 17 publications

Enhanced function of inhibitory presynaptic cannabinoid CB1 receptors on sympathetic nerves of DOCA–salt hypertensive rats

Enhanced function of inhibitory presynaptic cannabinoid CB1 receptors on sympathetic nerves of DOCA–salt hypertensive rats

Macrophage depletion lowers blood pressure and restores sympathetic nerve α₂-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats

New Insights into the Contribution of Arterial NCX to the Regulation of Myogenic Tone and Blood Pressure

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Inhibition of norepinephrine release by presynaptic alpha2-adrenoceptors in mesenteric vasculature preparations from chronic DOCA-salt hypertensive rats.

Cited by 12 publications

References 17 publications

Enhanced function of inhibitory presynaptic cannabinoid CB1 receptors on sympathetic nerves of DOCA–salt hypertensive rats

Enhanced function of inhibitory presynaptic cannabinoid CB1 receptors on sympathetic nerves of DOCA–salt hypertensive rats

Macrophage depletion lowers blood pressure and restores sympathetic nerve α2-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats

New Insights into the Contribution of Arterial NCX to the Regulation of Myogenic Tone and Blood Pressure

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Macrophage depletion lowers blood pressure and restores sympathetic nerve α₂-adrenergic receptor function in mesenteric arteries of DOCA-salt hypertensive rats