Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of losartan and the endothelin A and B receptor antagonist, bosentan was assessed on the alterations in renal hemodynamic and function as well as urinary albumin excretion (taken as an index of renal lesions) associated with L-NAME hypertension. L-NAME was given for 4 weeks (20 mg/100 mL in the drinking (fluid) followed by a 2-week period of concomitant treatment with L-NAME and losartan or bosentan (30 and 30 mg/kg, gavage). A group of rats received L-NAME without additional treatment and a group of rats were not given L-NAME and served as normotensive controls. Systolic arterial pressure (SAP) was measured before L-NAME, and before and every 5 days of losartan or bosentan treatment period. Urinary excretion of albumin (UAlb) was determined before and at the end of treatment period. Under anesthesia, glomerular filtration rate (GFR) and renal plasma flow (RPF) were estimated by the clearance method and the filtration fraction was calculated [FF = 100* (GFR/RPF)].
Arch Mal Coeur Vaiss 1998 Aug
PMID:[Renal alterations in L-NAME hypertension: influence of losartan and bosentan]. 974 61

Renal NaCl reabsorption is increased in Dahl "salt-sensitive" (DS) rats, due to an increased activity of the Na-K-Cl cotransporter NKCC2. On the other hand, nitric oxide (NO) is an inhibitor of NKCC2 and a deficient nitric oxide synthase (NOS) seems to play an important role in salt-sensitivity of DS rats. Here, we investigated the hypothesis that NKCC2 hyperactivity in DS rats is due to a deficient NOS, via the interactions cyclic GMP (cGMP)/cyclic AMP (cAMP) at the level of the thick ascending Henle's loop (TAL). DS rats DS (males, 250-300 g) and their normotensive controls DR ("salt-resistant") are sacrificed, the kidneys removed and NKCC2 activity is measured in medullary TAL (mTAL) as previously described. Medullary contents of NO are measured with a NitroFlux analyser by heat-reduction of nitrates and nitrites to NO. AMPc levels in mTAL are measured by an EIA immunotest. Neither L-NAME (3 mM), nor L-arginine were able to modify NKCC2 activity in mTAL from DS (pre-hypertensive) or DR rats. Levels of NO in the medullary interstitium and AMPc in mTAL were not significantly different between DS and DR rats. Conversely, in DS rats charged with 2% salt (in the food) during 7 weeks, L-arginine significantly inhibited NKCC2 in DS (35.6 +/- 6.8 vs 25.3 +/- 4.9 nmoles/mg protein/min; p<0.05 non-paired Student's t-test), but not in DR rats. In conclusion, NKCC2 in our mTAL preparation of prehypertensive DS and DR rats is insensitive to L-NAME and L-arginine. This suggests the absence of a functional NOS. NKCC2 hyperactivity of prehypertensive DS is therefore not due to a deficient NOS. This was confirmed by the normal levels of interstitial NO and mTAL cAMP in prehypertensive DS rats. Finally, a salt-load seems to induce NOS expression in mTAL of DS rats. This last observation deserves further investigation.
Arch Mal Coeur Vaiss
PMID:[Role of nitric oxide in the NKCC2 hyperactivity of Dahl "salt-sensitive" rats]. 1550 55

Hypertension is frequently associated with the development of renal fibrosis leading to chronic renal failure. The objective of the present study was to evaluate the role of blood pressure and renal hemodynamics on the development of renal lesions during hypertension. To this end, rats were treated with a NO synthase inhibitor, L-NAME, for 4 weeks. At this time point, systolic blood pressure reached 170 mmHg, renal blood flow dropped to 3.3 +/- 0.7 ml/min and kidneys displayed glomerular and tubulo-interstitial lesions as evidenced by histological analysis. Thereafter, L-NAME treatment was combined with an AT1 receptor antagonist, losartan (30 mg/kg/d), for an additional period of 4 weeks. Treatment with losartan for 4 additional weeks did not significantly modify hypertension (168 mmHg) either the degree of tubulo-interstitial lesions; in contrast, a significant regression of ischemic and sclerotic glomerular lesions was observed. In parallel, renal blood flow was significantly improved by losartan (5.2 +/- 0.8 ml/min). In addition a negative correlation was observed between renal blood flow and index of glomerulosclerosis (r = -0.82), whereas tubulo-intarstitial damage was positively correlated to systemic pressure (r = 0.93). In conclusion, inhibition of the local effects of angiotensin II alleviates the fall of renal blood flow consecutive to NO deficiency and reduces the morphological and functional lesions of glomeruli, independently of the changes in blood pressure. In contrast, tubulo-interstitial lesions are not correlated with the levels of renal blood flow and do not regress with the blockade of AT1 receptors when rats remain hypertensive.
Arch Mal Coeur Vaiss
PMID:[Renal hemodynamics and development of renal fibrotic lesions during hypertension]. 1706 47

Among the primitive cardiac tumours, myxoma is the most common. This benign tumour is sometimes described in the context of Carney's syndrome, in which cardiac myxoma, cutaneous myxoma, lentigo and pigmentary nevus cutaneous lesions, endocrine disorders, and testicular, thyroid and hypophyseal tumours are associated. The cardiac myxomata observed are multiple, recurrent, and involve the four cardiac chambers, with a peak incidence at 25 years of age. These observations may exist in a familial context, linked to an autosomal dominant genetic factor, localized on the 17q2 chromosome with polymorphism of the PRKAR1a gene. As in the case of sporadic myxoma, rapid surgical treatment with cardio-pulmonary bypass is indicated, bearing in mind the increased risk of thromboembolic phenomena and sudden death from valvular encroachment. We report a case of bi-atrial myxoma observed in the context of Carney's syndrome.
Arch Mal Coeur Vaiss 2007 Oct
PMID:[Multiple myxomata: about one case]. 1803 20


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