Arterial pressure-urinary output relationship in DOCA-saline hypertensive rats.
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.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003900:Desoxycorticosterone / Q000633:toxicity; D006339:Heart Rate / Q000187:drug effects; D006830:Hydralazine / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000633:toxicity; D014556:Urine
D006830:Hydralazine; D003900:Desoxycorticosterone; D012965:Sodium Chloride