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V Cachofeiro

Publications and source records attributed to V Cachofeiro.

42 records · Page 3Linked to original sources

Glomerular and vascular atrial natriuretic factor receptors in adrenalectomized rats.

The renal and vascular responses to atrial natriuretic factor (ANF) and glomerular and vascular ANF receptors were studied in adrenalectomized (ADR) rats with or without deoxycorticosterone (DOC) or dexamethasone (Dexa) replacement therapy. As expected, adrenalectomy elicited hypotension, hemoconcentration, and increased plasma renin activity, but no changes in plasma levels of either ANF-(1-98) or ANF-(99-126) were detected. Dexa treatment decreased both ANF-(1-98) and ANF-(99-126), whereas DOC treatment increased only ANF-(1-98). The acute renal response to ANF and furosemide was reduced in ADR rats and partially restored either by steroid replacement or by raising blood pressure. The blunted natriuretic response to ANF in ADR rats was associated with an increased density of glomerular receptors. Norepinephrine-precontracted vascular strips from ADR rats were more sensitive to ANF (ED50: 1.7 x 10(-8) M) than those from sham-operated animals (ED50: 1.5 x 10(-7) M). However, vascular ANF receptor density in mesenteric vessels from ADR animals was decreased. Dexa treatment restored vascular response to that observed in sham-operated animals without a concomitant change in vascular receptor density. Because the presence of guanylate cyclase-coupled and noncoupled ANF receptor subtypes have been described in different tissues, we conclude that the apparent lack of correlation between the biological response to ANF and total binding of ANF to glomeruli or mesenteric artery membranes in ADR rats may be in part caused by a differential regulation of both receptor subtype populations.

Adrenalectomy↗

Effect of a chronic infusion of atrial natriuretic factor on glomerular and vascular receptors in spontaneously hypertensive rats.

To investigate the effect of a prolonged infusion of atrial natriuretic factor (ANF) on its vascular and glomerular receptors, ANF (Ser 99-Tyr 126) was chronically administered (100 ng/h) for 7 days by osmotic minipumps to spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Blood pressure in the SHR fell from 149 +/- 5 to 119 +/- 3 mmHg 5 days after the ANF infusion was initiated, whereas no changes were observed in ANF-infused WKY rats. The SHR had higher plasma levels of both ANF (1-98) and (99-126) than the normotensive controls, but the ANF infusion did not modify these values in either group. Diuresis, natriuresis and haematocrit remained unchanged during the infusion. The higher plasma ANF levels noted in the SHR were associated with a decreased density (Bmax) and enhanced affinity (Kd) of ANF-binding sites in the mesenteric vessels. This pattern was not modified by the ANF infusion. The hypertensive animals had glomerular ANF receptors with a higher affinity than the WKY rats. The Bmax of these receptors was decreased significantly in ANF-infused SHR and WKY rats compared with non-infused animals. We conclude that the lack of change in vascular ANF receptors, during chronic ANF infusion in the SHR, could be associated with the hypotensive response.

Animals↗

Acute effect of potassium canrenoate administration on renin-angiotensin, kallikrein-kinin and prostaglandin systems.

1. To investigate the possible effects of potassium canrenoate (PC) on plasma renin activity (PRA) and on renal prostaglandins (PGS) and kinins under elevated sodium and/or potassium intakes, a single dose of PC was administered to four groups of Wistar male rats. 2. They were fed a normal diet (C), a diet supplemented with 4% of NaCl, (Na), with 1% of KCl: (K) or both supplements (NaK). 3. PRA and urinary PGS excretion did not show changes after PC administration, but total urinary kinins showed higher values after the treatment in all groups. 4. A diuretic but not natriuretic effect was observed only in C animals. 5. In conclusion, the single dose of PC was able to stimulate urinary kinins and to spare potassium independently of dietary electrolyte supplements that were able to block the diuretic effect of the drug.

Animals↗

Effect of ZK 36 374 on blood pressure, diuresis, plasma renin activity and urinary excretion of prostaglandin E2 and sodium.

ZK 36 374 is a chemically stable prostacyclin analogue which has been demonstrated to be a potent vasodilator. The effects of the drug on blood pressure, plasma renin activity, diuresis and urinary excretion of prostaglandin E2 and sodium, were studied on the 1st and 7th days of treatment and a week after the end of the administration to rats submitted to the following experimental situations: Goldblatt 2k-1c, Goldblatt 2k-1c + 5% NaCl loading, 5% NaCl loading, and controls. ZK 36 374 was continuously administered during one week by an osmotic pump subcutaneously implanted and connected to the right jugular vein. Twenty four hours after the pump implantation, blood pressure decreased in the three experimental groups. At the 7th day, pressure remained at similar levels except in NaCl loaded rats where an increase was observed. At the 15th day pressure levels returned to pretreatment values. On the 7th day of treatment urinary PGE2 showed higher values than pretreatment ones, to return to pretreatment at the 15 day. Sodium excretion showed an increase on the 7th day and was even higher on the 15th day. Plasma renin activity levels remained unchanged during the treatment except in the Goldblatt 2k-1c group which showed a significant fall at the 7th day. All the changes described on the 1st day of treatment might be related to counteraction of the blood pressure decrease on the same day.

Animals↗

Different excretion pattern of urinary PGE2 and 6-keto-PGF1 alpha in two kidney-one clip Goldblatt rats.

Changes in blood pressure and 24 hour urinary excretion of PGE2 and 6-keto-PGF1 alpha have been studied during ten weeks after renal artery clipping or sham operation in rats. From the second week on, systolic blood pressure was significantly increased in the two kidney-one clip rats as compared to controls. Maximal differences were reached in the 10th week after the operation (145 +/- 8 vs 116 +/- 3.2 mm Hg; p less than 0.001). Urinary PGE2 levels showed markedly elevated values versus controls from the 6th week on (p less than 0.001). However, no significant changes in urinary 6-keto-PGF1 alpha excretion were observed between the groups during the whole experimental period. These findings suggest that renal PGE2 may be involved in the pathophysiology of blood pressure control in the two kidney-one clip model, whereas, 6-keto-PGF1 alpha seems not to be altered after renal artery clipping.

6-Ketoprostaglandin F1 alpha↗

Simple radioimmunological method for urinary 6-keto-PGF1 alpha measurement.

A radioimmunoassay for the determination of 6-keto-PGF1 alpha (stable metabolite of Prostacyclin) in urine using a specific antiserum, is described. The antibody used, showed no significant cross-reactivity with other PGS. (3H)-6-keto-PGF1 alpha has been used as tracer and a 30% Hydroxyapatite suspension was utilized for the separation of bound and free fractions. Standard curve ranges between 2 and 1000 pg thus allowing measurements in urine. Aliquots of 0.2 to 1 ml of 24 hours urinary samples were submitted to a preextraction step with Hexane in order to eliminate neutral fats. After acidifying with 0.1 N HCl to pH = 3.5-4, an Ethyl Ether extraction step was performed showing a recovery of 66%. Repeated analysis of a rat urine pool, showed 7.7 intraassay and 9.8 interassay variation coefficients. Values obtained amounted to 38.3 +/- 4.6 ng/24 h in normal rats and 133 +/- 32 ng/24 h in 5% NaCl loaded rats (p less than 0.001). The values obtained in healthy men were 508 +/- 94 ng/24 h and in women 375 +/- 136 (p less than 0.05).

6-Ketoprostaglandin F1 alpha↗