Methyl palmitate modulates the nicotine‐induced increase in basilar arterial blood flow

Abstract

It has been well established that cerebral blood vessels in several species receive vasoconstrictor and dilator nerves. 1,2 Norepinephrine (NE) released from sympathetic adrenergic nerves originating from the superior cervical ganglion (SCG) and acetylcholine (ACh) released from parasympathetic cholinergic nerves originating from the sphenopalatine ganglion were first suggested to be the respective transmitters for vasoconstriction and dilation. 3 Pharmacological and morphological studies have shown that activation of nicotinic acetylcholine receptors (nAChRs) located on the perivascular sympathetic nerve terminals of basilar arteries (BAs) increases the release of NE. This released NE then acts on β 2 -adrenoceptors located on neighboring parasympathetic nitrergic nerves to facilitate nitric oxide (NO) release, resulting in vasorelaxation 4,5 and increased blood flow. 6 These findings indicate that activation of cerebral perivascular sympathetic nerves of BAs causes dilation via a sympathetic/parasympathetic interaction mechanism (Figure 6). However,

The Acute Effects and Mechanism of Ketamine on Nicotine-Induced Neurogenic Relaxation of the Corpus Cavernosum in Mice

“…Nicotine-induced relaxation of the corpus cavernosum was suppressed by pretreatment with mecamylamine (a non-selective, non-competitive antagonist of the nAChRs), lidocaine (a nerve blocker), and guanethidine (an adrenergic neuronal blocker) ( Figure 4 ). These findings are consistent with previous research showing that activation of the sympathetic nerves of the superior cervical ganglion origin induced by electrical depolarization and topical nicotine increased the basilar arterial blood flow [ 48 , 49 ] via activation of nicotinic agonists of nAChR located on the perivascular sympathetic nerves. Therefore, nicotine-induced neurogenic relaxation in the corpus cavernosum is similar to that in the cerebral artery.…”

Role of Phenylethanolamine‐N‐methyltransferase on Nicotine‐Induced Vasodilation in Rat Cerebral Arteries

“…Our recent study demonstrated that topical application of the nicotinic agonist choline induced an increase in BABF, and this effect was significantly diminished by tetrodotoxin (a neurotoxin) and α‐bungarotoxin (a selective α7‐nAChR inhibitor) [6]. These results suggest that α7‐nAChRs are present on BAs and meditate nicotinic agonist‐induced neurogenic vasorelaxation in the rat brainstem.…”

“…Our previous studies demonstrated that the activation of sympathetic nerves originating in the SCG was induced by electrical depolarization, and that topical nicotine increased the BABF [3, 6] via activation of nicotinic agonists of nAChR located on the perivascular sympathetic nerves. In the current study, nicotine‐induced neurogenic vasorelaxation was suppressed by pretreatment with guanethidine (an adrenergic neuronal blocker).…”

Phytochemistry, GS-MS analysis, and heavy metals composition of aqueous and ethanol stem bark extracts of Ximenia americana

“…MP was reported as an inflammatory cell inhibitor by decreasing the plasma levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) [34]. MP was reported to act as a neuromodulator by activating the protein kinase C pathway subsequently leading to decrease in blood flow in brainstem partly attributed to the vasorelaxative effect of MP [35]. Stigmasterol was previously reported to exert anti-inflammatory effect by stabilizing the membranes of human red blood cells by lowering hemolysis with amplification of the membrane stability in a dose-dependent manner [36].…”