Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared blood pressure, hindquarter vascular resistance properties, left ventricular weight, and norepinephrine kinetics, in spontaneously hypertensive rats (SHR) and weight-matched normotensive Wistar-Kyoto (WKY) rats at 4, 9, 14, 20, 30, and 50 weeks of age. At 4 weeks, systolic and mean blood pressure measurements were the same in both strains, but the vascular resistance of the fully dilated hindquarter bed was significantly higher in SHR than in WKY rats, with a much larger difference during maximum constriction. Plots of resistance at maximum dilatation and at maximum constriction against body weight suggest that a component of the increase in vascular muscle mass in SHR occurred in the neonatal period preceding hypertension followed by a later component related to the rise in blood pressure. By contrast, left ventricular hypertrophy was minimal at 4 weeks and most of its development paralleled the rise in blood pressure. Sympathetic activity, assessed by norepinephrine fractional rate constant, was higher in SHR than in WKY rats in the left ventricle and kidney through most of the period between 4 and 50 weeks, but was similar in both strains in the muscle bed. This pattern of sympathetic activity will accentuate hypertension once cardiac and vascular hypertrophy are fully established. In all regions, norepinephrine tissue concentration was higher in young SHR and could potentiate the trophic effects of growth factors in early vascular hypertrophy. We suggest that the initial (primary) component of vascular hypertrophy precedes the rise in blood pressure and may be critical in the pathogenesis of hypertension. Possible reasons for the short delay in the rise in blood pressure in young SHR, once the vascular "amplifier" has been established, include high vascularity, immaturity of smooth muscle, and delay in the development of left ventricular hypertrophy.
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PMID:Differential development of vascular and cardiac hypertrophy in genetic hypertension. Relation to sympathetic function. 252 1

The present study describes an association between adverse outcome in the twin-to-twin transfusion syndrome (TTTS) and pulmonary stenosis or reactive right ventricular hypertrophy. Six discordant monozygotic twin pregnancies with TTTS are described. Ventricular hypertrophy and atrioventricular valvular regurgitation occurred in all the recipient twins with pulmonary valvular stenosis in three cases and infundibular stenosis in one case. The recipient twin in one pair and both twins in another pregnancy died as a consequence of immaturity but the remaining twins all survived. Surgical intervention was required in one baby for valvular pulmonary stenosis. Our observations suggest that elevated blood pressure in the transfusion recipient may play an important role in pathogenesis. We hypothesise that both pulmonary stenosis and right chamber hypertrophy are secondary to hemodynamic changes. Although we have found valvular pulmonary stenosis in three recipients and infundibular stenosis in only one, this (obstruction to outflow) could be due to right chamber hypertrophy.
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PMID:Pulmonary stenosis and reactive right ventricular hypertrophy in the recipient fetus as a consequence of twin-to-twin transfusion. 1143 48