Hypertension alters the function of nitrergic and sensory innervation in mesenteric arteries from female rats

Campo, Lara del; Ferrer, Mercedes; Balfagón, Gloria

doi:10.1097/hjh.0b013e32832531e6

Cited by 18 publications

(24 citation statements)

References 40 publications

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“…However, we have observed that sensory innervation might increase its participation in several pathological conditions such as hypertension and diabetes [28,29]. Indeed, the participation of peptidergic innervation was not observed in any of the experimental groups when CGRP was used, suggesting that HgCl 2 treatment did not affect this innervation.…”

Section: Discussionmentioning

confidence: 79%

“…We have reported previously that rat mesenteric arteries possess adrenergic, nitrergic and sensory innervation, whose role may change depending on the pathophysiological situation [28][29][30]. EFS (electrical field stimulation) produces a vasoconstrictor response, which is the integrated result of neurotransmitter release, mainly of NA (noradrenaline), NO and CGRP (calcitonin gene-related peptide) [31,32].…”

Section: Introductionmentioning

confidence: 99%

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Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

et al. 2011

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In the present study, we have investigated the possible changes in rat mesenteric artery vascular innervation function caused by chronic exposure to low doses of HgCl(2) (mercuric chloride), as well as the mechanisms involved. Rats were divided into two groups: (i) control, and (ii) HgCl(2)-treated rats (30 days; first dose, 4.6 μg/kg of body weight; subsequent dose, 0.07 μg·kg-1 of body weight·day-1, intramuscularly). Vasomotor response to EFS (electrical field stimulation), NA (noradrenaline) and the NO donor DEA-NO (diethylamine NONOate) were studied, nNOS (neuronal NO synthase) and phospho-nNOS protein expression were analysed, and NO, O(2)- (superoxide anion) and NA release were also determined. EFS-induced contraction was higher in the HgCl(2)-treated group. Phentolamine (1 μmol/l) decreased the response to EFS to a greater extent in HgCl(2)-treated rats. HgCl(2) treatment increased vasoconstrictor response to exogenous NA and NA release. L-NAME (N(G)-nitro-L-arginine methyl ester; 0.1 mmol/l) increased the response to EFS in both experimental groups, but the increase was greater in segments from control animals. HgCl(2) treatment decreased NO release and increased O(2)- production. Vasodilator response to DEA-NO was lower in HgCl(2)-treated animals. Tempol increased DEA-NO-induced relaxation to a greater extent in HgCl(2)-treated animals. nNOS expression was similar in arteries from both experimental groups, whereas phospho-nNOS was decreased in segments from HgCl(2)-treated animals. HgCl(2) treatment increased vasoconstrictor response to EFS as a result of, in part, reduced NO bioavailability and increased adrenergic function. These findings offer further evidence that mercury, even at low concentrations, is an environmental risk factor for cardiovascular disease.

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Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

et al. 2011

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“…In certain experimental conditions, such as hyperaldosteronism and hypertension, alterations in sensory function play a key role in the regulation of mesenteric vascular tone (Balfagón et al, 2004;del Campo et al, 2009). Exogenous CGRP produced a mild vasodilatory response, which was comparable in the three groups.…”

Section: Figurementioning

confidence: 82%

“…NO release was measured as previously described (del Campo et al, 2009). Endothelium-denuded segments from control, HFD and HFD + rosuvastatin rats were subjected to a resting tension of 0.5 g as indicated for reactivity experiments.…”

Section: Release Of Nomentioning

confidence: 99%

Rosuvastatin restored adrenergic and nitrergic function in mesenteric arteries from obese rats

Blanco-Rivero

Heras

Martín-Fernández

et al. 2010

British J Pharmacology

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BACKGROUND AND PURPOSEWe investigated whether high-fat diet (HFD)-induced obesity was associated with changed function of components of the mesenteric innervation (adrenergic, sensory and nitrergic), the mechanisms involved and the possible effects of rosuvastatin on these changes. EXPERIMENTAL APPROACHMale Wistar rats were divided into three groups. (i) rats fed a standard diet (control group); (ii) rats fed a HFD (33.5% fat) for 7 weeks; and (iii) rats fed a HFD and treated with rosuvastatin (15 mg·kg) for 7 weeks. Segments of isolated mesenteric arteries were exposed to electric field stimulation (EFS) with or without tetrodotoxin, phentolamine, 7-nitroindazole (7NI) or N w nitro-L-arginine methyl ester (L-NAME). Noradrenaline, ATP and NO release, and nNOS expression were also measured. KEY RESULTSEFS induced a greater frequency-dependent contraction in obese than in control rats. In HFD rats, phentolamine reduced contractions elicited by EFS, but noradrenaline release was greater and ATP release decreased. L-NAME and 7NI increased contractions to EFS in segments from control rats, but not in those from HFD rats. NO release and nNOS expression were lower in arterial segments from HFD rats than in control rats. All these changes in HFD rats were reversed by treatment with rosuvastatin. CONCLUSIONS AND IMPLICATIONSNeural control of mesenteric vasomotor tone was altered in HFD rats. Enhanced adrenergic and diminished nitrergic components both contributed to increased vasoconstrictor responses to EFS. All these changes were reversed by rosuvastatin, indicating novel mechanisms of statins in neural regulation of vascular tone.

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“…We have previously reported that in this strain sensory innervation does not participate in vasomotor response induced by EFS in control animals, but that the participation of this innervation is increased in several pathological conditions such as hypertension, cirrhosis and diabetes [12,15,40,41]. In the present study, we observed that pre-incubation with the CGRP antagonist CGRP-(8-37) did not modify the vasoconstrictor response to EFS in mesenteric rings from SO rats, confirming CGRP non-participation in vasoconstriction in healthy Wistar rats [10,36,42].…”

Section: Short-term Phmentioning

confidence: 98%

Effect of short- and long-term portal hypertension on adrenergic, nitrergic and sensory functioning in rat mesenteric artery

et al. 2011

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In the present study, we analysed possible alterations in adrenergic, nitrergic and sensory functioning in mesenteric arteries from rats at 1 and 21 months after partial portal vein ligation, and the mechanisms involved in these alterations, if any. For this purpose, we analysed the vasoconstrictor response to EFS (electrical field stimulation) and the effect of the α-antagonist phentolamine, the NOS (nitric oxide synthase) inhibitor L-NAME (N(G)-nitro-L-arginine methyl ester) and the CGRP (calcitonin gene-related peptide) receptor antagonist CGRP-(8-37) in mesenteric segments from ST (short-term; 1 month) and LT (long-term; 21 months) SO (sham-operated) and pre-hepatic PH (portal hypertensive) rats. The vasomotor responses to NA (noradrenaline), the NO donor DEA-NO (diethylamine NONOate) and CGRP were analysed. NA, NO and CGRP releases were measured. Phospho-nNOS (neuronal NOS) expression was studied. The vasoconstrictor response to EFS was decreased in STPH animals. Phentolamine decreased this vasoconstrictor response more strongly in SO animals. Both L-NAME and CGRP-(8-37) increased vasoconstrictor response to EFS more strongly in PH than SO segments. PH did not modify vasomotor responses to NA, DEA-NO or CGRP, but it decreased NA release while increasing those of NO and CGRP. Phospho-nNOS expression was increased by PH. In LTPH, no differences were observed in vasoconstrictor response to EFS, vasomotor responses or neurotransmitter release when compared with age-matched SO animals. In conclusion, the mesenteric innervation may participate in the development of the characteristic hyperdynamic circulation observed in STPH through the joint action of decreased adrenergic influence, and increased nitrergic and sensory innervations influences. The participation of each innervation normalizes under conditions of LTPH.

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Hypertension alters the function of nitrergic and sensory innervation in mesenteric arteries from female rats

Cited by 18 publications

References 40 publications

Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

Rosuvastatin restored adrenergic and nitrergic function in mesenteric arteries from obese rats

Effect of short- and long-term portal hypertension on adrenergic, nitrergic and sensory functioning in rat mesenteric artery

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