title: Alteration in the sarcolemmal Na(+)-K+ pump of hindquarters resistance arteries in DOCA-salt rats.
abstract: It has been suggested that a circulating inhibitor of the Na(+)-K+ pump contributes to the development and maintenance of DOCA-salt hypertension. However, the discordant results have been reported as to whether the sarcolemmal Na(+)-K+ pump in DOCA-salt hypertension is inhibited. Furthermore, no study has examined alteration in the sarcolemmal Na(+)-K+ pump of the true resistance arteries. We examined hindquarters vasoconstriction induced by ouabain (10(-3) M) in the vascularly isolated hindquarters of the DOCA-salt treated or control rats, which were perfused with Krebs-Henseleit solution. Hindquarters vasoconstriction induced by ouabain (10(-3) M) was greater in the prehypertensive and hypertensive DOCA-salt rats than in the corresponding control rats (p less than 0.01). We also examined hindquarters vasoconstriction induced by ouabain (10(-3) M) in the vascularly isolated hindquarters of the normal assay rats which were perfused by the plasma obtained from the DOCA-salt or control rats. The plasma of the prehypertensive and hypertensive DOCA-salt rats attenuated ouabain-induced hindquarters vasoconstriction in the assay rats (p less than 0.01). The plasma of the DOCA-salt rats did not alter nonspecific vasoconstriction caused by barium chloride. These results suggest that the plasma of the prehypertensive and hypertensive DOCA-salt rats had an inhibitor of the sarcolemmal Na(+)-K+ pump of the resistance arteries, but the sarcolemmal Na(+)-K+ pump molecules of the resistance arteries of those rats were increased. The in vivo activity of the sarcolemmal pump of the resistance arteries of the DOCA-salt rats would be determined by the relative influence of increased pump molecules and a circulating pump inhibitor.
authors: Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
authors: K
authors: K
authors: Yamamoto
authors: A
authors: A
authors: Takeshita
authors: T
authors: T
authors: Ashihara
authors: T
authors: T
authors: Imaizumi
authors: M
authors: M
authors: Nakamura
mesh_terms: D000818:Animals; D001464:Barium / Q000494:pharmacology; D017609:Barium Compounds; D001693:Biological Transport, Active; D001790:Blood Physiological Phenomena; D001808:Blood Vessels / Q000187:drug effects; D002712:Chlorides; D003900:Desoxycorticosterone / Q000494:pharmacology*; D006614:Hindlimb / Q000098:blood supply*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000493:pharmacokinetics*; D051381:Rats; D012508:Sarcolemma / Q000378:metabolism*; D012964:Sodium / Q000493:pharmacokinetics*; D012965:Sodium Chloride / Q000494:pharmacology*; D014462:Ultrafiltration; D014655:Vascular Resistance; D014664:Vasodilation
chemical_list: D017609:Barium Compounds; D002712:Chlorides; C024986:barium chloride; D001464:Barium; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D010042:Ouabain; D012964:Sodium; D011188:Potassium