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(Hypertension. 1995;26:1030-1034.)
© 1995 American Heart Association, Inc.

Articles

Nitric Oxide Synthase Isoform Activities in Kidney of Dahl Salt-Sensitive Rats

Yoshihiro Ikeda; Komei Saito; Jong-Il Kim; Mitsuhiro Yokoyama

From The First Department of Internal Medicine, Kobe (Japan) University School of Medicine.

Correspondence to Komei Saito, MD, The First Department of Internal Medicine, Kobe University School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650, Japan.

Abstract An abnormal L-arginine–nitric oxide axis has been suggested to be relevant to the genesis of salt-sensitive hypertension. In the present study we investigated the activities of three isoforms of nitric oxide synthase (NOS) in the kidney of Dahl salt-sensitive and salt-resistant rats. Five-week-old Dahl Iwai salt-sensitive (n=9) and salt-resistant (n=10) rats were maintained on a high salt diet (4% sodium chloride) for 4 weeks. We measured calcium-dependent and calcium-independent NOS activities in each particulate and soluble fraction of kidney by conversion of L-[³H]arginine to L-[³H]citrulline. Systolic blood pressure was elevated significantly (P<.001) in salt-sensitive but not salt-resistant rats. Calcium-dependent NOS activity in the soluble fraction was significantly lower in salt-sensitive rats than in salt-resistant rats (25.8±9.0 versus 48.2±19.2 disintegrations per microgram protein, respectively; P<.01). There were no differences in calcium-dependent NOS activity in the particulate fraction and calcium-independent NOS activity in the soluble fraction between groups. Renal norepinephrine content was lower in salt-sensitive rats than in salt-resistant rats (P<.05) and was positively correlated with calcium-dependent NOS activity in the soluble fraction (P<.01). Although no differences in endothelial and inducible-type NOS activity were observed a significant reduction in calcium-dependent NOS activity in the soluble fraction of the kidney of salt-sensitive rats suggests that the decreased neural-type NOS activity may in part be involved in the mechanism of salt-sensitive hypertension, possibly through alterations in renal sympathetic nervous activity and sodium handling.

Key Words: sodium • kidneys • norepinephrine • nitric oxide • rats, inbred strains

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