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To determine whether renal interleukin-6 was produced constitutively under the normal physiological conditions and to evaluate the influence of hypertension development on interleukin-6 production in two different hypertensive models, the spontaneously hypertensive rat (SHR) and the two-kidney, one clip (2-K, 1C) hypertensive rat.In a chronic study, Wistar rats and SHR, aged 4, 5, 7 and 9 weeks, and 2-K, 1C Goldblatt hypertensive rats, at 2 and 4 weeks after applying the clip, were anaesthetized, their blood pressures were measured and the kidneys were collected and renal interleukin-6 production estimated.The rats were lightly anaesthetized with halothane and prepared for blood pressure measurement via a carotid artery cannula. Interleukin-6 production was estimated from the interleukin-6 messenger RNA (mRNA) present in the kidney tissue. The mRNA species (interleukin-6, β-actin and renin) were measured by densitometric analysis of the autoradiographs following Northern blot hybridization.The blood pressure was approximately 100 mmHg at all ages in the Wistar rats, but rose from 101 ± 3 mmHg at age 4 weeks to 154 ± 2 mmHg at age 9 weeks in the SHR (means ± SEM, P<0.01). Constitutive production of renal interleukin-6 could not be detected in either the Wistar rats or the SHR. In 2-K, 1C rats the blood pressure was increased significantly at 2 and 4 weeks after clipping to 129 ± 3 and 140 ± 4 mmHg (means ± SEM, both P<0.01), respectively, and the renal renin mRNA concentration was increased significantly in the clipped and decreased in the non-clipped kidneys at 2 and 4 weeks after clipping. The renal interleukin-6 mRNA could not be measured in either clipped or non-clipped kidneys at either 2 or 4 weeks after clipping.These findings demonstrate that renal interleukin-6 was not produced constitutively under normal physiological conditions. Moreover, in spite of the development of hypertension from two causes, genetic and renin-dependent, renal interleukin-6 was not expressed even though there is a deficit in immunological function in the SHR and damage to the renal tissue of the 2-K, 1C rats.