Maternal high-fat diet changes breathing pattern and causes excessive sympathetic discharge in juvenile offspring rat.

Early life over-nutrition, as experienced in maternal obesity, is a risk factor for developing cardiorespiratory and metabolic diseases. Here we investigated the effects of high-fat diet (HFD) consumption on the breathing pattern and sympathetic discharge to blood vessels in juvenile offspring from dams fed with HFD (O-HFD). Adult female Holtzman rats were given a standard diet (SD) or HFD from 6 wk before gestation to weaning. At weaning (P21), the male offspring from SD dams (O-SD) and O-HFD received SD until the experimental day (P28-P45). Nerve recordings performed in decerebrated in situ preparations demonstrated that O-HFD animals presented abdominal expiratory hyperactivity under resting conditions and higher vasoconstrictor sympathetic activity levels. The latter was associated with blunted respiratory-related oscillations in sympathetic activity, especially in control animals. When exposed to elevated hypercapnia or hypoxia levels, the O-HFD animals mounted similar ventilatory and respiratory motor responses as the control animals. Hypercapnia and hypoxia exposure also increased sympathetic activity in both groups but did not reinstate the respiratory-sympathetic coupling in the O-HFD rats. In freely behaving conditions, O-HFD animals exhibited higher resting pulmonary ventilation and larger variability of arterial pressure levels than the O-SD animals due to augmented sympathetic modulation of blood vessel diameter. Maternal obesity modified the functioning of cardiorespiratory systems in offspring at a young age, inducing active expiration and sympathetic overactivity under resting conditions. These observations represent new evidence about pregnancy-related complications that lead to the development of respiratory distress and hypertension in children of obese mothers.NEW & NOTEWORTHY Maternal obesity is a risk factor for developing cardiorespiratory and metabolic diseases. This study highlights the changes on the breathing pattern and sympathetic discharge to blood vessels in juvenile offspring from dams fed with HFD. Maternal obesity modified the functioning of cardiorespiratory systems in offspring, inducing active expiration and sympathetic overactivity. These observations represent new evidence about pregnancy-related complications that lead to the development of respiratory distress and hypertension in children of obese mothers.

Cardiovascular and hidroelectrolytic changes in rats fed with high-fat diet.

Obesity activates the renin-angiotensin and sympathetic systems facilitating hypertension and changes in the hydroelectrolytic balance. In the present study, in rats fed with high-fat diet (HFD), we investigated daily water intake and urinary excretion, prandial consumption of water and the changes in blood pressure and water intake to intracerebroventricular (icv) angiotensin II (ANG II). Male Holtzman rats (290-320 g) were fed with standard diet (SD, 11% calories from fat) or HFD (45% calories from fat) for 6 weeks. Part of the animals received a stainless steel cannula in the lateral ventricle (LV) at the 6th week after the beginning of the diets and the experiments were performed at the 7th week. The pressor effect, but not the dipsogenic response to acute icv injection of ANG II, was potentiated in the HFD rats. Daily water intake and urinary volume were reduced in rats fed with HFD with no significant changes in sodium excretion. Prandial water consumption was also reduced in rats ingesting HFD, an effect almost totally reverted blocking salivation with atropine. These results show a potentiation of the pressor response to icv ANG II in HFD-fed rats, without changing icv ANG II-induced water intake. In addition, prandial and daily water intake and urinary volume were reduced in HFD-fed rats, without changing sodium excretion. Salivation in rats ingesting HFD may play a role in the reduced prandial and daily water intake.

Endogenous hydrogen peroxide affects antidiuresis to cholinergic activation in the medial septal area.

Cholinergic activation of the medial septal area (MSA) with carbachol produces thirst, natriuresis and antidiuresis. Hydrogen peroxide (H2O2) injected into the medial septal area (MSA) impairs behavioral and renal responses induced by carbachol at the same site, suggesting the exogenous H2O2 may modulate the responses to cholinergic activation in the MSA. In the present study, we investigated if the accumulation of endogenous H2O2 in the MSA after the injection of the catalase inhibitor 3-amino-1,2,4-triazole (ATZ) also affects cholinergic responses. In addition, the effects of the combination of ATZ with a non-effective dose of H2O2 in the MSA were also tested. Male Holtzman rats (280-320 g) with stainless steel cannulas implanted in the MSA were used. The treatment with ATZ (10 nmol) into the MSA partially reverted the antidiuretic effect of carbachol (10.5 ± 0.7, vs. saline + carbachol: 7.3 ± 0.6 ml/120 min), without changing carbachol-induced water intake (9.5 ± 1.9, vs. saline + carbachol: 10.7 ± 1.6 ml/60 min). The combination of a low dose of ATZ (2.5 nmol) with an ineffective dose of H2O2 (0.5 µmol) into the MSA reduced carbachol-induced thirst (7.5 ± 2.0, vs. saline + carbachol: 14.9 ± 1.2 ml/15 min) and reverted the antidiuresis (8.1 ± 1.1, vs. saline + carbachol: 5.3 ± 0.9 ml/120 min). Sodium and potassium excretion were not modified regardless the treatment. Although exogenous H2O2 injected in the MSA may affect most of the responses to cholinergic activation of the MSA, the antidiuresis is the response clearly modulated by endogenous H2O2.