Nitric Oxide Release in the Nucleus Tractus Solitarius During and After Bilateral Common Carotid Artery Occlusion

Abstract

1. The purpose of the present study was to investigate the effect of bilateral common carotid artery occlusion (BCCAO) on cardiovascular responses and nitric oxide (NO) formation in the nucleus tractus solitarius (NTS). 2. Twenty-three adult cats were anaesthetized intraperitoneally with urethane (400 mg/kg) and alpha-chloralose (40 mg/kg). The femoral artery was cannulated to allow monitoring of systemic arterial pressure (SAP) and heart rate (HR). The femoral vein was cannulated for intravenous drug administration. 3. Extracellular NO levels in the NTS were measured by in vivo voltammetry using an NO microsensor combined with a microcomputer-controlled apparatus. 4. Microinjection of l-arginine (30 nmol) into the NTS produced hypotension and NO release. This effect of l-arginine was not changed by 2 min of BCCAO. 5. Bilateral common carotid artery occlusion produced increases in SAP and NO levels. These effects were more apparent in vagotomized than in intact animals. 6. The onset latency of BCCAO-induced changes in SAP levels (8.4 +/- 2.5 s) was longer than that for changes in NO (4.7 +/- 1.7 s). 7. Bilateral common carotid artery occlusion induced hypertension and NO release in the NTS of intact and vagotomized animals. These cardiovascular and NO responses to BCCAO were significantly attenuated by NG-nitro-l-arginine methyl ester (10 mg/kg, i.v.) and MK-801 (2.5 mg/kg, i.v.). These data suggest that NO synthase and activation of N-methyl-d-aspartate receptors are involved in the cardiovascular and NO responses to BCCAO.

Neurokinin-1 receptor inhibition reverses ischaemic brain injury and dementia in bilateral common carotid artery occluded rats: possible mechanisms

“…BCCAO-induced hypoperfusion also increases the nitrite level that increases leakiness or permeability of blood vessels and consequently inflammation (Wu and Chai 2004). Administration of aprepitant significantly decreased the level of nitrite.…”

N‐Methyl‐D‐aspartate Glutamate Receptor Modulates Cardiovascular and Neuroendocrine Responses Evoked by Hemorrhagic Shock in Rats

“…Accordingly, GABAergic neurotransmission activation inhibits the firing activity of neurosecretory neurons in the hypothalamus [60,61]. 6 BioMed Research International Although the evidence presented above strongly indicates the PVN as a site involved in the effect of MK801 reported in the present study, previous studies have demonstrated that systemic administration of MK801 can act in several other brainstem and forebrain structures controlling vasopressin release [45,62,63]. Therefore, the involvement of NMDA receptors in hemorrhagic shock is potentially a general brain mechanism mediated by other regions in addition to the PVN.…”

Potential of carnosine, a histamine precursor in rat model of bilateral common carotid artery occlusion‐induced vascular dementia

“…Endogenously formed NO is highly unstable and gets converted to nitrate and nitrite . Therefore, serum nitrite concentration has been employed as specific marker of endothelial dysfunction . According to the cholinergic hypothesis, memory impairment in senile dementia patients is due to selective and irreversible deficiency in the cholinergic function of the brain .…”