The endothelium partially obscures enhanced microvessel reactivity in DOCA hypertensive rats.
This study examined the contribution of the endothelium to pressor and depressor responses in the isolated, perfused mesentery of mineralocorticoid hypertensive rats. Following uninephrectomy, adult male rats were made hypertensive by subcutaneous implantation of deoxycorticosterone acetate (DOCA; 200 mg/kg); control rats were sham-treated. All rats received drinking water that contained 1.0% NaCl and 0.2% KCl. Following 4 to 6 weeks of treatment, the rats were anesthetized and the mesenteric vasculature was isolated and pump-perfused (constant flow with buffer) to evaluate changes in perfusion pressure. Vascular responses were determined before and after disruption of endothelial function by perfusion with oxygen free radicals generated in the buffer by electrical stimulation. Vasodilator responsiveness to acetylcholine and nitroprusside in the intact mesentery of hypertensive rats did not differ from that in the intact mesentery of normotensive rats, whereas pressor responses to norepinephrine in the intact mesentery of hypertensive rats were greater than normotensive values. Following disruption of endothelial function, depressor responses to acetylcholine were greatly attenuated whereas those to nitroprusside were unaltered or increased. Pressor responses to norepinephrine were potentiated in mesentery that had undergone endothelial disruption, and this potentiation was greater in hypertensive rats than in control rats. The slopes of pressure-flow curves in the presence of norepinephrine were less steep in mesentery with intact endothelium. The flow-modified component of these pressure-flow curves that was related to the endothelium was greater in mesenteric vascular beds of hypertensive rats. These results indicate that a factor released from the endothelium partially masks the enhanced vascular reactivity characteristic of this animal model of mineralocorticoid hypertension.
King
C M
CM
Department of Physiology, University of Michigan Medical School, Ann Arbor.
Webb
R C
RC
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D003900:Desoxycorticosterone / Q000494:pharmacology; D004727:Endothelium / Q000502:physiology*; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D051381:Rats; D012965:Sodium Chloride / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D009599:Nitroprusside; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D000109:Acetylcholine; D009638:Norepinephrine