Alterations in Perivascular Sympathetic and Nitrergic Innervation Function Induced by Late Pregnancy in Rat Mesenteric Arteries

Abstract

Background and PurposeWe investigated whether pregnancy was associated with changed function in components of perivascular mesenteric innervation and the mechanism/s involved.Experimental ApproachWe used superior mesenteric arteries from female Sprague-Dawley rats divided into two groups: control rats (in oestrous phase) and pregnant rats (20 days of pregnancy). Modifications in the vasoconstrictor response to electrical field stimulation (EFS) were analysed in the presence/absence of phentolamine (alpha-adrenoceptor antagonist) or L-NAME (nitric oxide synthase-NOS- non-specific inhibitor). Vasomotor responses to noradrenaline (NA), and to NO donor DEA-NO were studied, NA and NO release measured and neuronal NOS (nNOS) expression/activation analysed.Key ResultsEFS induced a lower frequency-dependent contraction in pregnant than in control rats. Phentolamine decreased EFS-induced vasoconstriction in segments from both experimental groups, but to a greater extent in control rats. EFS-induced vasoconstriction was increased by L-NAME in arteries from both experimental groups. This increase was greater in segments from pregnant rats. Pregnancy decreased NA release while increasing NO release. nNOS expression was not modified but nNOS activation was increased by pregnancy. Pregnancy decreased NA-induced vasoconstriction response and did not modify DEA-NO-induced vasodilation response.Conclusions and ImplicationsNeural control of mesenteric vasomotor tone was altered by pregnancy. Diminished sympathetic and enhanced nitrergic components both contributed to the decreased vasoconstriction response to EFS during pregnancy. All these changes indicate the selective participation of sympathetic and nitrergic innervations in vascular adaptations produced during pregnancy.

Decompensated liver cirrhosis and neural regulation of mesenteric vascular tone in rats: role of sympathetic, nitrergic and sensory innervations

“…However, a direct relationship between both neurotransmitters does not always appear, since we have also observed increased ATP together with decreased NO release 62 . Additionally, we have previously reported that modifications in NO release are independent of alterations in NA vasoconstriction 37 63 64 72 . Once again, these results seem to confirm that the possible interaction between the different components of perivascular innervation depends on the pathophysiological situation under study, and highlight the need for studying innervation function in different PH and cirrhosis models.…”

“…Both results indicate a greater participation by the sympathetic co-transmitter ATP in LC rats. Purinergic contribution has been reported to depend on previous vascular tone, and is higher when tone is increased 37 57 59 62 63 64 . Taking this into account, the increased vasoconstrictor response to EFS in LC rats could be responsible for the enhanced ATP release observed in these animals.…”

Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A

“…Similarly to observed with endothelial NO [16,36], here we have shown that the supplementation of MtS rats with synbiotics restore neuronal NO release, reaching levels comparable in the CT group. NO released from nitrergic nerve terminals is able to decrease in a great extent the maximal arterial tone elicited by the sympathetic neurotransmitter noradrenaline [23,50]. In situations where the vascular resistance is increased, we have previously observed either a potentiation in nitrergic function, which aims to compensate the greater vascular resistance [23,51], or a blunted nitrergic role, thereby participating in the enhancement of peripheral vascular resistance a consequently, in the development of hypertension [47,49].…”

Proteolytic degradation of regulator of G protein signaling 2 facilitates temporal regulation of Gq/11 signaling and vascular contraction

“…We tested this prediction by using submaximal electrical field stimulation (EFS) (40 V at 15 Hz) of MAs to release endogenous norepinephrine and ATP from sympathetic nerve terminals embedded in the vessel wall, thereby activating G q/11 -coupled ␣ 1 -adrenergic and P2Y2 purinergic GPCRs in vascular smooth muscle cells and triggering vasoconstriction (51)(52)(53). If the proteolytic half-life of RGS2 in MAs is similar to that of transfected RGS2 (ϳ30 min), then treating wild-type MAs 1 h with CHX would be sufficient for most of the preexisting pool of RGS2 to be degraded.…”