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Parkinson’s disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra, causing motor changes. In addition to motor symptoms, non-motor dysfunctions such as psychological, sensory and autonomic disorders are recorded. Manifestations related to the autonomic nervous system include the cardiovascular system, as postural hypotension, postprandial hypotension, and low blood pressure. One of the mediators involved is the nitric oxide (NO). In addition to the known roles such as vasodilator, neuromodulator, NO acts as an important mediator of the immune response, increasing the inflammatory response provoked by PD in central nervous system. The use of non-specific NOS inhibitors attenuated the neurodegenerative response in animal models of PD. However, the mechanisms by which NO contributes to neurodegeneration are still not well understood. The literature suggest that the contribution of NO occurs through its interaction with superoxides, products of oxidative stress, and blocking of the mitochondrial respiratory chain, resulting in neuronal death. Most studies involving Parkinsonism models have evaluated brain NO concentrations, with little data available on its peripheral action. Considering that studies that evaluated the involvement of NO in the neurodegeneration in PD, through NOS inhibitors administration, showed neuroprotection in rats, it has prompted new studies to assess the participation of NOS isoforms in cardiovascular changes induced by parkinsonism, and thus to envision new targets for the treatment of cardiovascular disorders in PD. The aim of this study was to conduct a literature review to assess available information on the involvement of nitric oxide (NO) in cardiovascular aspects of PD.

Aim: Autonomic modulation responds to ovarian hormones and estrogen increases nitric oxide bioavailability. Also, females have minor susceptibility to sepsis and a higher survival rate. However, few studies have evaluated the role of estrogen in cardiovascular, autonomic, and oxidative parameters during initial endotoxemia and under inducible nitric oxide synthase (iNOS) inhibition in female rats.Methods: Female wistar rats were subjected to ovariectomy and divided into three groups: OVX (ovariectomized), OVX+E (OVX plus daily estradiol) and SHAM (false surgery). After 8 weeks, mean arterial pressure (MAP) and heart rate (HR) were recorded in non-anesthetized catheterized rats, before and after intravenous LPS injection, preceded by S-methylisothiourea sulfate (SMT) injection, or sterile saline. Cardiovascular recordings underwent spectral analysis for evaluation of autonomic modulation. Two hours after LPS, plasma was collected to assess total radical-trapping antioxidant (TRAP), nitrite levels (NO2), lipoperoxidation (LOOH), and paraoxonase 1 (PON1) activity.Results: Two hours after LPS, females treated with SMT presented a decrease of MAP, when compared to saline-LPS groups. At this same time, all SMT+LPS groups presented an increase of sympathetic and a decrease of parasympathetic modulation of HR. Two hours after saline+LPS, OVX presented decreased total radical-trapping antioxidant (TRAP) compared to SHAM. When treated with SMT+LPS, OVX did not altered TRAP, while estradiol reduced LOOH levels.Conclusion: iNOS would be responsible for sympathetic inhibition and consumption of antioxidant reserves of females during endotoxemia, since iNOS is inhibited, treatment with estradiol could be protective in inflammatory challenges.

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