Disease relevance of Neosynephrine

• With hypoxia during baroreflex activation with PE, SNA did not increase (50 +/- 23 U/min) [1].
• Hypercapnia during baroreflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05) [1].
• Combined CBRX and ABRX eliminated all reflex responses except for a small bradycardia and a biphasic change in perfusion pressure (constrictor-dilator) during PE [2].
• Sustained hypertension induced by a moderate dose of PE provoked patterns of c-fos mRNA and protein expression that conformed in the nucleus of the solitary tract (NTS) to the termination patterns of primary baroreceptor afferents and in the caudal ventrolateral medulla (CVLM) to a physiologically defined depressor region [3].
• Activation of Ras by PMA, ET-1, or PE was reduced by inhibition of protein kinase C (PKC), and that induced by ET-1 or PE was partly sensitive to pertussis toxin [4].

High impact information on Neosynephrine

• All three women were positive for human leukocyte antigen (HLA) B7 expression (P = .011) [5].
• During PE alone, mean blood pressure increased and SNA decreased to 87 +/- 45 U/min (P less than 0.05) [1].
• Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation) [6].
• During PE plus NP, the baroreflex slope was reduced by 30% to 14.1 +/- 2.8 ms/mmHg (P less than 0.02 vs. during PE alone) [6].
• Basal pulmonary vascular resistance was NO dependent because L-NMMA infusion resulted in a dose-dependent decrease in local flow velocity (P < .005), with flow decreasing 33% at the highest dose of L-NMMA [7].

Chemical compound and disease context of Neosynephrine

• 17Beta-estradiol (10 microM) caused a 48.7+/-5.0% (n=11) relaxation of the PE contracture, which was significantly reduced to 25.1+/-5.3% (n=7) by L-NAME [8].
• MATERIALS AND METHODS: Isolated renal cell carcinoma feeder vessels were perfused in an organ bath with the alpha(1)-adrenoceptor agonist phenylephrine (PE) [9].
• Glibenclamide infusion did not influence the pressor or vasoconstrictor responses to PE in either group of animals during normoxia or acute hypoxia [10].

Biological context of Neosynephrine

• During PE alone, the baroreflex slope was 20.2 +/- 2.9 ms/mmHg (n = 10) [6].
• Pulmonary vascular resistance increased 39.8 +/- 9.4% (P < .01), whereas mean pulmonary artery pressure did not change [11].
• Administration of L-NMMA also reduced cardiac output by 27.8 +/- 2.9% and stroke volume by 15.4 +/- 3.5% (each P < .01) [11].
• Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units [12].
• Extensive colocalization of PE-induced Fos-IR and markers for the nitric oxide phenotype were seen in a circumscribed, rostral, portion of the baroreceptor afferent zone of the NTS, whereas only a small proportion of PE-sensitive neurons in the NTS were found to be GABAergic [3].

Anatomical context of Neosynephrine

• PE increased mean arterial pressure (MAP) by 13 +/- 2 mmHg (mean +/- SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors [6].
• NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone [12].
• m-Synephrine: normal occurrence in adrenal gland [13].
• 2 We examined the effect of Phe on nitric oxide synthase (NOS) activity by measuring the conversion of [(3)H]L-arginine to [(3)H]L-citrulline in rat aorta or in endothelial cells isolated from rat aorta [14].
• To examine the role of CO in reduced reactivity, small mesenteric arteries (100-200 microm intraluminal diameter) from control and 48-h CH rats were isolated and mounted on glass cannulas, pressurized to 60 mmHg and superfused with increasing concentrations of PE under normoxic conditions [15].

Associations of Neosynephrine with other chemical compounds

• Baroreflex activation was achieved by raising mean blood pressure by greater than 10 mmHg with intravenous infusion of phenylephrine (PE) [1].
• Progesterone also abolished PHE potentiation of vasoactive intestinal polypeptide-stimulated cAMP accumulation [16].
• Recordings were obtained at resting, reduced (nitroglycerin infusion), and elevated (metaoxedrin infusion) blood pressure [17].
• Vasoconstriction elicited by angiotensin II (Ang II) or phenylephrine (PE), G-protein-coupled receptor (GPCR) agonists, but not that elicited by arachidonic acid or KCl, was greater in eNOS KO mice [18].
• Data suggest that estrogen facilitation of baroreflex responses to PE and ANG II is predominantly mediated by ERalpha subtype [19].

Gene context of Neosynephrine

• However, in comparison with ET-1 and PE, BK was only weakly hypertrophic as assessed by cell morphology and patterns of gene expression [20].
• 11 beta-HSD1 antisense oligomers also enhanced the ability of B to amplify the contractile response to PE [21].
• In aortic rings incubated (24 h) with corticosterone (B) (10 nmol/l) and 11 beta-HSD2 antisense (3 micromol/l), the contractile response to graded concentrations of PE (PE: 10 nmol/l - 1 micromol/l) were significantly (P < 0.05) increased compared to rings incubated with B and 11 beta-HSD2 nonsense [21].
• Immunohistochemical staining experiments also showed that expression of eNOS increased in endothelial cells after Phe exposure of the aortas [14].
• 4. Prolonged incubation (16 h) with endotoxin (3 microg ml(-1)) did not alter the response to PE, however incubation with IFN-gamma (10 ng ml(-1)), TNF-alpha (5 ng ml(-1)) and interleukin-1beta (20 ng ml(-1)) for 16 h increased PE log EC(50) from -6.44+/-0.09 to -6 [22].

Analytical, diagnostic and therapeutic context of Neosynephrine

• In small pressurized mesenteric arteries (inner diameter = 177 +/- 5 mum), PE constriction was decreased in untreated HET arteries compared with WT (P < 0.05). l-NNA (100 muM) augmented PE constriction more in HET arteries than in WT arteries, and responses were not different between groups in the presence of l-NNA [23].
• However, the isolated cardiac-aortic baroreflex gains (i.e., delta HR/delta MAP) were significantly less in the HF (0.16 +/- 0.02 and 0.14 +/- 0.03 beats.min-1.mmHg-1) than in the AF (0.52 +/- 0.08 and 0.59 +/- 0.07 beats.min-1.mmHg-1) subjects at PE + NP and PE + NP + lower body negative pressure [24].
• The rank order of maximal behavioral responses to EPI, 6FNE, and PE in DCMB-treated mice was the same as the rank order of their maximal stimulation of hydrolysis of phosphatidylinositol at cloned alpha(1B)-adrenoceptors in cell culture [25].
• Intraperitoneal injection of m-synephrine into rats gave: unconjugated MHMA (5%), MHPG sulphate (35%), unconjugated m-synephrine (7%) and conjugates of m-synephrine (9%:4% as the glucuronide and 5% as the sulphate) [26].
• Baroreflex gain was evaluated by intravenous injection of phenylephrine (PE: 15-18 microg/kg) and sodium nitroprusside (SNP: 46-50 microg/kg) in WT and nNOS-/- anesthetized mice [27].

References