Effect of sodium loading and depletion on vascular reactivity and prostacyclin generation.
In order to estimate the modulatory activity of Prostacyclin (PGI2) to the vascular reactivity, pressor responses to angiotensin II (A II) and noradrenaline (NA) and PGI2 generation aorta were measured using the rats of sodium loading or of sodium depletion. On the sodium loading, the blood pressure increased gradually and plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were decreased. The pressor responses to A II and NA were enhanced by sodium loading. The PGI2 generation of aorta was enhanced at the initial stage of sodium loading and decreased thereafter. The increased generation of PGI2 may represent the adaptive mechanism for the attenuation of the sustained elevation in blood pressure. It sodium depletion, the pressor responses to A II and NA were decreased, and PRA and PAC were elevated. PGI2 generation of aorta was also increased. These findings suggested that PGI2 could participate in blood pressure control mechanism on sodium loading and depletion.
D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D011464:Epoprostenol / Q000096:biosynthesis* / Q000502:physiology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D011945:Receptors, Angiotensin / Q000187:drug effects; D012083:Renin / Q000097:blood; D012964:Sodium / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
D011453:Prostaglandins; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D011464:Epoprostenol; D012083:Renin; D000254:Sodium-Potassium-Exchanging ATPase; D009638:Norepinephrine