Both nitric oxide and prostaglandin-mediated responses are impaired in skeletal muscle arterioles of hypertensive rats.

摘要: OBJECTIVE To investigate the role played by endothelium-derived dilator factors in regulation of peripheral vascular resistance determining whether dysfunction endothelium contributes to reduced responsiveness skeletal muscle arterioles hypertension. METHODS The endothelial function isolated, cannulated, pressurized (at 80 mmHg) gracilis (45-50 microns diameter) normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive (SHR) was compared utilizing vasoactive agents known action. RESULTS Acetylcholine (ACh, 10(-9), 10(-8) 5 x mol/l) sodium nitroprusside (SNP, 10(-8), 10(-7) 10(-6) elicited similar dilations WKY SHR. Substance P (10(-9), caused significantly less dilation (by approximately 70%) SHR with rat arterioles. calcium ionophore A23187 (5 (9.1 +/- 1.1, 24.0 1.5, 39.0 3.4%, respectively), whereas it evoked constrictions (6.5 14.9 25.5 1.6%, respectively) Removal endothelium, inhibition prostaglandin synthesis (indomethacin) or blockade H2 (PGH2) receptors SQ 29548) eliminated A23187-induced nitric oxide synthase blocker, NG-nitro-L-arginine a greater substance P-induced reduction basal diameter than did those from CONCLUSIONS These data suggest that, arterioles, and/or action is, are, impaired metabolism arachidonic acid is altered, resulting an enhanced production PGH2. simultaneous these two pathways arteriolar could contribute observed