Macula densa (MD) cells of the juxtaglomerular apparatus (JGA) synthesize type 1 nitric oxide synthase (NOS1) and type 2 cyclooxygenase (COX-2). Both nitric oxide (NO) and prostaglandins have been considered to mediate or modulate the control of renin secretion. Reactive oxygen species (ROS) produced locally by NADPH oxidase may influence NO bioavailability. We have tested the hypothesis that in hypertension elevated ROS levels may modify the expression of NOS1 and COX-2 in the JGA, thereby interacting with juxtaglomerular signaling. To this end, spontaneously hypertensive rats (SHR) and Wistar-Kyoto control rats (WKY) received the specific NADPH oxidase inhibitor, apocynin, during 3 wk. Renal functional and histochemical parameters, plasma renin activity (PRA), and as a measure of ROS activity, urinary isoprostane excretion (IP) were evaluated. Compared with WKY, IP levels in untreated SHR were 2.2-fold increased, and NOS1 immunoreactiviy (IR) of JGA 1.5-fold increased, whereas COX-2 IR was reduced to 35%, renin IR to 51%, and PRA to 7%. Apocynin treatment reduced IP levels in SHR to 52%, NOS1 IR to 69%, and renin IR to 62% of untreated SHR, whereas renin mRNA, COX-2 IR, glomerular filtration rate, PRA, and systolic blood pressure remained unchanged. WKY revealed no changes under apocynin treatment. These data show that NADPH oxidase is an important contributor to elevated levels of ROS in hypertension. Upregulation of MD NOS1 in SHR may have the potential of blunting the functional impact of ROS at the level of bioavailable NO. Downregulated COX-2 and renin levels in SHR are apparently unrelated to oxidative stress, since apocynin treatment had no effect on these parameters.
De Smet HR, Menadue MF, Oliver JR, and Phillips PA. Increased thirst and vasopressin secretion after myocardial infarction in rats. In METHODS, in the section AVP Study, the groups were not described accurately at the beginning of the paragraph. The paragraph should have read: "The first six rats were randomly allocated to water ad libitum at 1 wk or water deprivation at 1 wk after infarct induction. The remaining rats (n ϭ 60) were allocated randomly to one of four treatment groups: 1) water ad libitum at 1 wk after infarct induction; 2) water deprivation at 1 wk; 3) water ad libitum at 8 wk; and 4) water deprivation at 8 wk. Rats were placed in metabolism cages for the same measurements as above. A 3-day acclimatization period was allowed before the 24-h treatment. Rats were killed at the end of the 24-h treatment period as described above."This has no impact on the important comparisons that are made between the water deprivation and water ad libitum results at each time point and the relationship between infarct size and AVP level within each individual time point. These remain unchanged.I acknowledged the contribution of L. Arnolda and D. McKitrick in the study design and teaching the snare technique for myocardial infarction to H. De Smet. I apologize for making this acknowledgement without the permission of L. Arnolda or D. McKitrick and the misrepresentation implied.While the research was conducted with the understanding that full Ethics Committee approval was in place for the project as reported, it has become clear that continuous approval of the project as reported was not in place because a change to the protocol involving the number of animals studied and the length of observations was not reported to the Ethics Committee due to an administrative oversight. . Effect of apocynin treatment on renal expression of COX-2, NOS1, and renin in Wistar-Kyoto and spontaneously hypertensive rats. . FAS inhibitor cerulenin reduces food intake and melanocortin receptor gene expression without modulating the other (an)orexigenic neuropeptides in chickens.
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