Abstract

ObjectivesThe aim of this study was to investigate in rat mesenteric artery whether breast feeding (BF) affects the vasomotor response induced by electrical field stimulation (EFS), participation by different innervations in the EFS-induced response and the mechanism/s underlying these possible modifications.MethodsExperiments were performed in female Sprague-Dawley rats (3 months old), divided into three groups: Control (in oestrous phase), mothers after 21 days of BF, and mothers that had recovered their oestral cycle (After BF, in oestrous phase). Vasomotor response to EFS, noradrenaline (NA) and nitric oxide (NO) donor DEA-NO were studied. Neuronal NO synthase (nNOS) and phosphorylated nNOS (P-nNOS) protein expression were analysed and NO, superoxide anion (O2 .–), NA and ATP releases were also determined.ResultsEFS-induced contraction was higher in the BF group, and was recovered after BF. 1 µmol/L phentolamine decreased the response to EFS similarly in control and BF rats. NA vasoconstriction and release were similar in both experimental groups. ATP release was higher in segments from BF rats. 0.1 mmol/L L-NAME increased the response to EFS in both control and BF rats, but more so in control animals. BF decreased NO release and did not modify O2 .– production. Vasodilator response to DEA-NO was similar in both groups, while nNOS and P-nNOS expressions were decreased in segments from BF animals.ConclusionBreast feeding increases EFS-induced contraction in mesenteric arteries, mainly through the decrease of neuronal NO release mediated by decreased nNOS and P-nNOS expression. Sympathetic function is increased through the increased ATP release in BF rats.

Highlights

  • Breast feeding is characterised by strict hormonal control mediated by oestrogen, progesterone, prolactin and oxytocin, associated with increases in gastrointestinal blood flow and cardiac output [1,2] to provide the udder with nutrients and hormones that regulate milk synthesis and secretion

  • Vascular tone is mediated by the integrated action of different neurotransmitters, mainly noradrenaline (NA) and ATP from sympathetic nerve terminals, neuronal nitric oxide (NO) from nitrergic innervation and calcitonin gene-related peptide (CGRP) from sensory nerves [7,8,9,10]

  • In endothelium-intact mesenteric segments, the vasoconstrictor response to 75 mmol/l KCl was similar in all experimental groups (Control: 1393689.65 mg; breast feeding (BF): 14456164.85 mg; After BF: 14126120.54 mg; P.0.05)

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Summary

Introduction

Breast feeding is characterised by strict hormonal control mediated by oestrogen, progesterone, prolactin and oxytocin, associated with increases in gastrointestinal blood flow and cardiac output [1,2] to provide the udder with nutrients and hormones that regulate milk synthesis and secretion. Some hormones implicated in the lactation process (prolactin, oxytocin) have been reported to alter vascular function [3,4]. Vascular tone is determined by an equilibrium among several mechanisms, including hormonal, metabolic and neuronal factors. This neural regulation involves sympathetic, cholinergic, nitrergic, peptidergic and/or sensory innervations that are specific to the vascular bed considered [5,6]. Vascular tone is mediated by the integrated action of different neurotransmitters, mainly noradrenaline (NA) and ATP from sympathetic nerve terminals, neuronal nitric oxide (NO) from nitrergic innervation and calcitonin gene-related peptide (CGRP) from sensory nerves [7,8,9,10]. Several experimental and pathophysiological circumstances including ageing, hypertension and diabetes, have been shown to alter the functional role of these components [11,12,13]

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