Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors demonstrated that isradipine reduces the blood pressure assessed at rest in patients with mild to medium severe hypertension. The antihypertensive action was enhanced by administration of beta-blockers. In a loading test the pressor response to strain was reduced in particular as regards diastolic pressure; from this in may be concluded indirectly that a vasodilatating effect is involved. The authors recorded a rise of plasma renin activity which may be associated with previous vasodilatation. Parameters of lipid metabolism were influenced by isradipine. The indifference of isradipine as regards the effect on functions indicated by biochemical screening was again confirmed in the present investigation. The undesirable effects typical for calcium antagonists were manifested in a very small percentage of the investigated subjects and in a small number of repeated examinations. The reason for discontinuation of treatment in one patient was an effects which does not threaten the patient (flush). Isradipine is an effective antihypertensive drug with very good tolerance.
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PMID:[The antihypertensive effect of isradipine and additional pharmacodynamic effects]. 850 74

The 8-month-old patient was hospitalized after a few days of apathy and feeding difficulty with moderate exsiccation. Severe hypokalemia, hyponatremia, hypochloremia associated with alkalosis were found, which were accompanied by the decreased urinary electrolytes and elevated serum renin and aldosterone, therefore the condition corresponded to a pseudo-Bartter syndrome. The diagnosis of cystic fibrosis was arisen, which was established by the elevated sweat chloride levels. Sequencing of the 27 exons of the cystic transmembrane regulator gene two rare mutations were detected in compound heterozygous form: in the exon 10 a C1529G transversion, whereas in the exon 20 a G3978A transition was verified, both of them result in development of premature stopcodons (S466X and W1282X, respectively). Carriage of first mutation could be found in the asymptomatic mother, while the other one was identified in the father. In the proband and in the mother a G3341A mutation was also detected in exon 17, which causes an R1070Q amino acid change. However, this likely cannot associate with pathology since the existing premature stopcodon on the same allele does not allow synthesis of protein. These mutations have been described in combination with delta F508 mutation, however, their simultaneous presence in the same subject has not been reported. During the one and half year follow-up the clinical picture appeared benign.
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PMID:[Pseudo-Bartter syndrome in a case of cystic fibrosis caused by C1529G and G3978A compound heterozygosity]. 1825 63