Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension occurs in 50% of the elderly persons in industrialized societies. This disorder of the regulation of the arterial blood pressure has different manifestations in different age groups. The young hypertensive usually has an increase in cardiac output and a normal peripheral vascular resistance. The elderly patient with hypertension exhibits a decreased cardiac output and an increased peripheral vascular resistance. In the elderly hypertensive there is a progressive anteriolar narrowing and there is hardening of the largest arteries. The vascular disease that contributes to the hypertension in the elderly also causes hypoperfusion of the target organs. During the aging process there is a decrease in cardiac output, glomerular filtration rate, vital capacity, renal plasma flow and maximal cardiac rate. There are changes in the kidneys and the liver that influence the way different medications are handled by the body. The main findings of the Australian, EWPHE, Coope & Warrender, SHEP, STOP-HYP and MRC studies of hypertension in the elderly have been summarized. The intervention studies have proven that the treatment of hypertension in the elderly patient is efficacious and decreases the mortality and morbidity due to coronary and cerebrovascular events. The pharmacologic agents available for the treatment of hypertension in the elderly are the diuretics, beta blockers, vasodilators, calcium-channel blockers, adrenergic blockers and angiotensin converting enzyme inhibitors. The morbidity and mortality benefits derived from antihypertensive trials are greater for the older than for the younger patients. The pharmacologic antihypertensive agents to be used in older patients will also depend upon the presence or not of associated illnesses in which some agents might be harmful or contraindicated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypertension in old age]. 858 23

This study investigated whether increased muscle acetylcarnitine provision (acetate infusion) or hyperoxia (100% O(2)) would increase the rate of oxidative phosphorylation and reduce the reliance on muscle substrate phosphorylation after the onset of moderate exercise. Eight subjects completed three randomized trials, each separated by 1 wk: 1) saline infusion for 1 h before exercise, while breathing room air for 20 min before exercise and during 120 s of cycling at 65% maximal exercise (VO(2 max)) (CON), 2) saline infusion with 4 mmol/kg body wt sodium acetate, while breathing room air before and during exercise (ACE), and 3) saline infusion and breathing 100% O(2) before and during exercise (HYP). Muscle biopsies were sampled at rest and after 30 and 120 s of exercise. ACE increased muscle acetyl-CoA and acetylcarnitine contents at rest vs. CON and HYP [22.9 +/- 2.8 vs. 8.9 +/- 2.4 and 10.5 +/- 1.8 micromol/kg dry muscle (dm); 11.0 +/- 1.2 vs. 3.5 +/- 1.3 and 4.0 +/- 1.2 mmol/kg dm]. Acetate had no effect on resting pyruvate dehydrogenase activity in the active form (PDH(a)) among CON, ACE, and HYP. During exercise, acetyl-CoA and acetylcarnitine were unchanged in ACE but increased over time in the CON and HYP trials, and PDH(a) increased similarly in all trials. Muscle phosphocreatine use, lactate accumulation, and substrate phosphorylation energy provision after 30 or 120 s of exercise were similar in all trials. In summary, increased acetylcarnitine availability did not accelerate the rate of oxidative phosphorylation at the onset of exercise, suggesting that this is not a site of extra substrate. Hyperoxia had no effect on substrate phosphorylation, suggesting that O(2) availability does not limit oxidative phosphorylation at the onset of moderate exercise.
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PMID:Effects of acetate infusion and hyperoxia on muscle substrate phosphorylation after onset of moderate exercise. 1170 27

Hypertension has been anecdotally reported in children with familial hypophosphatemic rickets (XLH). To better identify and characterize the clinical and laboratory features of hypertensive XLH children, we reviewed the medical records of 41 XLH children, all treated with phosphate and vitamin D analogues. Eight children, who were originally normotensive, developed hypertension during the 2nd decade of life. At diagnosis of hypertension all had persistent secondary/tertiary hyperparathyroidism (HPTD), defined as high serum parathyroid hormone (PTH) for 12 months or longer. Seven had nephrocalcinosis (NC). Analysis of data showed that of 11 children with HPTD, 8 developed hypertension compared with 0 among 30 without HPTD (P<0.001). Of 40 children studied, 18 had NC that was significantly associated with both HPTD (P<0.01) and hypertension (P<0.025). At diagnosis of hypertension, serum calcium was elevated in 2. Plasma renin activity was high in 3 of 4 patients in whom it was measured. Doppler ultrasonography or renal scan was normal in the 5 children studied. Early echocardiography showed left ventricular hypertrophy in only 2 of 5 children studied. In 3 patients who underwent parathyroidectomy, hypertension persisted and 1 progressed to renal failure. Serum creatinine remained normal in all others. Successful treatment of hypertension consisted of beta-adrenergic blockers, angiotensin converting enzyme inhibitors, and Ca channel blockers as monotherapy or in combination. We conclude that hypertension in treated XLH children is closely associated with HPTD. Emphasis should therefore be placed on prevention of the development of HPTD as a complication of XLH treatment, and close monitoring for hypertension in those who do develop HPTD.
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PMID:Hypertension in hypophosphatemic rickets--role of secondary hyperparathyroidism. 1257 6