Pulmonary vascular efflux of norepinephrine in Dahl rats susceptible or resistant to salt-induced hypertension.
The purpose of these studies was to determine whether the accumulation of norepinephrine by the pulmonary circulation is altered in the Dahl model of genetic hypertension. Pulmonary norepinephrine accumulation was evaluated by performing a compartmental analysis of the efflux of L-[3H]norepinephrine from perfused lungs after inhibition of the norepinephrine-metabolizing enzymes. The lungs were isolated from Dahl salt-hypertension-susceptible (S) and salt-hypertension-resistant (R) rats that had been on a high sodium diet for 3 weeks. In both S and R rats, norepinephrine was accumulated into a single compartment with an efflux half-time of approximately 23 min, in addition to its distribution in the extracellular space. The size of the extracellular space was significantly increased in the S rats, but there was no difference in the size of the compartment of L-[3H]norepinephrine efflux between S (6.4 +/- 1.2 ml/g) and R (3.7 +/- 0.7 ml/g) rats. These data indicate that impaired accumulation and efflux of norepinephrine by the lungs does not contribute to the pathogenesis of hypertension in Dahl S rats.
Metting
P J
PJ
Department of Physiology, Medical College of Ohio, Toledo 43699.
Duggan
J M
JM
D000818:Animals; D004351:Drug Resistance; D006973:Hypertension / Q000097:blood* / Q000139:chemically induced / Q000235:genetics; D008168:Lung / Q000098:blood supply*; D008297:Male; D009638:Norepinephrine / Q000097:blood*; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride; D013012:Sorbitol / Q000097:blood
D012965:Sodium Chloride; D013012:Sorbitol; D009638:Norepinephrine