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Query: UMLS:C0004135 (ATM)
 13,001 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats drinking 1% NaCl. The acute pressure-natriuresis relationship was studied under Inactin anesthesia in volume-expanded rats with fixed neurohumoral influences on the remaining kidney. Renal interstitial hydrostatic pressure (RIHP) was measured using a catheter implanted into the renal cortex. Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6) and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min, respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for the respective control rats. Compared with values in control rats, ANG II-infused rats had significantly (P < 0.05) lower urine flow and absolute and fractional sodium excretion at renal artery pressures of 115-150 mmHg. There were no significant differences between RIHP measured in control and ANG II-hypertensive rats. The shift in the pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium excretion relationships was similar with both doses of ANG II and was reversed by the acute administration of losartan (10 mg/kg iv). In all groups of rats, renal blood flow was autoregulated, whereas glomerular filtration rate was not autoregulated in ANG II-infused rats and was significantly lower than that in control rats at the lower level of renal artery pressure. The data indicate that rats with ANG II-induced hypertension have a rightward shift of the pressure-natriuresis curve caused primarily by a decrease in fractional excretion of sodium. The lack of effect of chronic ANG II infusion on filtration fraction and RIHP suggests that the increased tubular reabsorption was due to a direct action of ANG II on renal tubules. The reversal of these effects by losartan suggests that the shift in the pressure-natriuresis curve in ANG II-induced hypertension is mediated by the AT1-receptor subtype.
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PMID:Altered pressure natriuresis in chronic angiotensin II hypertension in rats. 816 Aug 66

1. The effects of the specific angiotensin II receptor type I (AT1) antagonist candesartan on renal proximal tubular sodium transport were studied using lithium clearance. The effects of candesartan on mean arterial blood pressure (MABP), renal plasma flow (RPF), glomerular filtration rate (GFR) and sodium and potassium excretion were also investigated. 2. Male Wistar rats were anaesthetized with Inactin (thiobutabarbital sodium; Sigma, St Louis, MO, USA). Clearance markers (8% polyfructosan, 1% para-aminohippuric acid and 4 mmol/l lithium chloride) were given into a jugular vein at the rate of 1.6 mL/h per 100 g bodyweight. Candesartan was given as bolus injection (0.01, 0.1, 0.2, 0.5 and 1.0 mg/kg) followed by 60 min continuous infusion at a rate of 0.5, 5, 10, 25 and 50 microg/min per kg, respectively. 3. The non-depressor dose of candesartan (0.01 mg/kg) did not alter RPF or GFR, whereas diuresis, natriuresis and kaliuresis were observed. The higher doses of candesartan reduced MABP, RPF and GFR, although diuresis, natriuresis and kaliuresis were still observed. 4. Renal tubular sodium and water reabsorption were inhibited after intravenous administration of candesartan independently of an alteration in arterial pressure. Lithium clearance data indicate that the site of inhibition was in the proximal nephron segment.
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PMID:Acute effects of candesartan on rat renal haemodynamics and proximal tubular reabsorption. 1617 27