To know the role played by the kidney in the genesis of deoxycorticosterone acetate (DOCA)-saline hypertension, the arterial pressure-urinary output (AP-UO) relationship was compared in unanesthetized, unrestrained uninephrectomized (1-K) control and normal Wistar-Imamichi (W-I) rats according to the method of Norman et al. [Am. J. Physiol. 234 (Regulatory Integrative Comp. Physiol. 3): R98-R103, 1973]. The gradient of AP-UO relationship was slightly decreased in 1-K control rats compared with that in W-I rats. However, the AP-UO relationship of DOCA-saline hypertensive rats underwent only a parallel shift to higher blood pressure ranges compared with that of 1-K control rats. There was no significant change in the urinary volume, urinary sodium excretion, and urinary osmolarity. Furthermore, the AP-UO relationship was shifted back to the lower pressure range under the influence of hydralazine, a preferential renal arteriolar dilator, suggesting that constriction of the renal artery caused the rise of the arterial pressure in DOCA-saline hypertensive rats.
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