Peripheral vascular resistance and sensitivity to circulating pressor and vasoconstrictor agents are blunted during pregnancy. This has been mainly attributed to an increased production of endothelium-derived mediators. The objective of this work was to evaluate if pregnancy changes the relative participation of nitric oxide (NO) and prostaglandins (PG) in respect to the modulation of the increases in renal perfusion pressure induced by phenylephrine (Phe). Dose-response curves were made with gradually increasing doses of Phe using an isolated kidney preparation in the presence of a NO synthase (NOS) inhibitor (L-NAME, 1 microM), a PG-synthesis inhibitor (indomethacin, 1 microM), both, or neither. Also, renal cyclooxygenase (COX-1 and COX-2) and endothelial NOS (eNOS) expression was determined using PCR. The experiments were done in kidneys from nonpregnant and pregnant rats. Our results showed that the relative participation of renal vasoactive mediators seems to change during pregnancy. We found the presence of a COX-1-dependent vasoconstrictor in the middle of pregnancy that was not found in nonpregnant rats. Our results also suggest that there is increased participation of another renal vasodilator substance, the effect of which is observed when NO or PG synthesis is inhibited during late pregnancy. In addition, an apparent interaction between renal eNOS and COX-1 expression was observed: eNOS expression was diminished, while COX-1 was increased during the 2nd week of pregnancy. In contrast, in kidneys from the 3rd week of pregnancy, the expression of these two enzymes was similar.
Diabetic nephropathy is the first cause of end‐stage renal disease. The exact pathogenesis has not been described. Hypertrophy has been mentioned as one of the most earlier changes induced by diabetes mellitus (DM). Angiotensin II (Ang II) and prostaglandins (PG) have been involved in hypertrophic processes. The aim of this work was to study if Ang II and PG participate in early diabetes hypertrophy development. We induced DM with streptozotocin (65 mg/Kg) in Wistar rats. Four treatment groups were formed: Control; Celecoxib (Cel), a COX‐2‐specific inhibitor, 20 mg/Kg; Losartan (Los), an AT1 receptor antagonist, 40 mg/Kg, and Captopril (Cap), an ACE inhibitor, 20 mg/Kg. Treatments were given during one week after DM induction. Proteinuria, creatinine clearance, kidney weight, protein/DNA ratio and cellular area were measured. Cortex COX‐2 expression was determined using immunoblot. Cel did not modify kidney weight. Cap but not Los diminished kidney weight. All treatments improved proteinuria and none modified creatinine clearance. Cel, but neither Cap nor Los, decreased protein/DNA ratio and cellular area. Cel and Cap reverted COX‐2 increase in renal cortex, but Los augmented COX‐2 expression. Our results suggest that PG participate in developing of DM‐induced hypetrophy, while Ang II by itself does not, but probably another peptide in this system could be involved. PAPIIT IN210307 SIP 20080066 CONACYT 46217
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