RESUMO
Objective To evaluate the effects of 131 adrenoceptor anfisense on blood pressure and?1 adrenoceptor mRNA and protein levels in 2 kidney 1 clip(2K1C)rats.Method 2KIC hypertensive rots were produced by clipping renal artery of SD rats.Liposome/AS-ODNs 2.0 were tested intravenously in rats with 2KIC hypertension.Animals were divided into 5 groups(n=18 in each group):?1-AS-ODN group,?1-IN-ODN group,2K1C group,Sham group and SD group.Blood pressure was measured by tail-cuff method,the levels of myocardial?adreneceptor mRNA and protein were tested by RT-PCR and binding assay.Results On the basis of the magnitude and duration of hypotension,?1-AS-ODN decreased blood pressure by 39 mmHg at the most for 4 weeks.Compared with the 2KIC group,?1-AS-ODN did not significantly change the levels of myocardial?1 adrenoceptor mRNA but significantly decreased the levels of myocardial?1 adrenoceptor protein at 2,7,30 days (P
RESUMO
The present study was aimed to explore an interaction between endothelium-derived nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in normotensive and hypertensive states. Rats were made two-kidney, one clip (2K1C) hypertensive and supplemented with either N-G-nitro-L-arginine methyl ester (L-NAME, 5 mg/100 ml drinking water) or L-arginine hydrochloride (400 mg/100 ml drinking water). One group supplied with normal tap water served as control. Sham-clipped rats were also divided into the L-NAME, L-arginine, and control groups. The plasma levels and atrial contents of ANP were determined at day 28 following clipping the renal artery. In 2K1C rats, the plasma level of ANP was higher and the atrial content was lower than in the sham-clipped control. L-Arginine increased the atrial content of ANP in association with a decreased plasma ANP, whereas L-NAME significantly affected neither parameter. The increase of blood pressure in 2K1C rats was not affected by L-arginine or L-NAME. In sham-clipped rats, the plasma level of ANP was significantly increased by L-NAME along with an increase in blood pressure. On the contrary, L-arginine did not affect the blood pressure or plasma ANP. The atrial content of ANP was significantly altered neither by L-arginine nor by L-NAME. These results suggest that NO plays a tonic inhibitory role on the ANP release with concomitant increases of the atrial tissue content. In addition, hypertension is suggested to modify the release and tissue storage of ANP.
Assuntos
Animais , Ratos , Arginina , Fator Natriurético Atrial , Pressão Sanguínea , Ingestão de Líquidos , Hipertensão , NG-Nitroarginina Metil Éster , Óxido Nítrico , Plasma , Artéria Renal , ÁguaRESUMO
A long-term effect of pentobarbital on the atrial natriuretic peptide (ANP) system was investigated. The experimental group of rats (Sprague-Dawley, male) was one week previously treated with pentobarbital (50 mg/kg, intraperitoneal), and the control was an age-matched group of rats which had never been anesthetized. ANP reaponse to volume-expansion (VE) induced by intravenous infusion of iso-oncotic saline over 30 min (total volume infused amounted up to 5% body weight) was examined under thiopental anesthesia (50 mg/kg, intraperitoneal). Basal plasma ANP level did not significantly differ between the experimental and control groups. Following VE, while the plasma ANP five-fold increased in the control, it rather decreased in the experimental group. Despite the different ANP responses, the magnitude of urinary responses (volume and sodium excretion) to VE did not differ between the two groups. Right and left atrial tissue contents of ANP were significantly lower in the experimental group than in the controL In another series of experiments, the two-kidney, one clip rats were made under either pentobarbital or ether anesthesia and the blood pressure and ANP responses were compared. While the magnitude of blood pressure increases did not differ, the plasma ANP level measured on Day 12 after the clipping was lower in the pentobarbital group than in the ether group. These results suggest that pentobarbital has a long-term inhibitory effect on the ANP system. Its physiological significance in blood pressure and body fluid homeostasis remains to be determined.