Although the arrhythmia occurs at rest, the constellation of findings in idiopathic VT that is characterized by RMVT is consistent with the mechanism of cAMP-mediated triggered activity. Therefore, the spectrum of VT resulting from this mechanism includes not only paroxysmal exercise-induced VT but also RMVT.

smaller rise in serum [K ϩ ], 0.12 mEq/L above baseline (P ϭ ACE inhibition or angiotensin receptor blockade: Impact on 0.1), a 43% lower value when compared with the change in potassium in renal failure. those who received lisinopril. This blunted rise in [K ϩ ] in people Background. Inhibition of the renin-angiotensin system is taking valsartan was not associated with a significant decrease known to raise serum potassium [K ϩ ] levels in patients with in plasma aldosterone (P ϭ 0.14). renal insufficiency or diabetes. No study has evaluated the Conclusions. In the presence of renal insufficiency, the ARB comparative effects of an angiotensin-converting enzyme valsartan did not raise serum [K ϩ ] to the same degree as the (ACE) inhibitor versus an angiotensin receptor blocker (ARB) ACE inhibitor lisinopril. This differential effect on serum [K ϩ ] on the changes in serum [K ϩ ] in people with renal insufficiency. is related to a relatively smaller reduction in plasma aldoste-Methods. The study was a multicenter, randomized, double rone by the ARB and is not related to changes in GFR. This crossover design, with each period lasting one month. A total study provides evidence that increases in serum [K ϩ ] are less of 35 people (21 males and 14 females, 19 African Americans likely with ARB therapy compared with ACE inhibitor therapy and 16 Caucasian) participated, with the mean age being 56 Ϯ in people with renal insufficiency. 2 years. Mean baseline serum [K ϩ ] was 4.4 Ϯ 0.1 mEq/L. The glomerular filtration rate (GFR) was 65 Ϯ 5 mL/min/1.73 m 2 , and blood pressure was 150 Ϯ 2/88 Ϯ 1 mm Hg. The main outcome measure was the difference from baseline in the level Drug-induced hyperkalemia, that is, serum potassium of serum [K ϩ ], plasma aldosterone, and GFR following the Ͼ5.5 mEq/L, is an important but often overlooked probinitial and crossover periods. Results. For the total group, serum [K ϩ ] changes were not lem encountered commonly in clinical practice. Medicasignificantly different between the lisinopril or valsartan treattions generally produce hyperkalemia either by causing ments. The subgroup with GFR values of Յ60 mL/min/1.73 redistribution of potassium (␤ 2-adrenergic blockers, sucm 2 who received lisinopril demonstrated significant increases cinylcholine, digitalis overdose, hypertonic mannitol) or in serum [K ϩ ] of 0.28 mEq/L above the mean baseline of by impairing renal potassium excretion. Drugs such as 4.6 mEq/L (P ϭ 0.04). This increase in serum [K ϩ ] was also accompanied by a decrease in plasma aldosterone (P ϭ 0.003). nonsteriodal anti-inflammatory drugs (NSAIDs), inhibi-Relative to the total group, the change in serum [K ϩ ] from tors of the renin-angiotensin-aldosterone (RAA) system, baseline to post-treatment in the lisinopril group was higher heparin, and cyclosporine impair renal potassium excreamong those with GFR values of Յ60 mL/min/1.73 m 2. The tion by interfering with the production and/or secretion lower GFR group taking valsartan, however, demonstrated a of aldosterone [1]. Renal in...

In the presence of renal insufficiency, the ARB valsartan did not raise serum [K(+)] to the same degree as the ACE inhibitor lisinopril. This differential effect on serum [K(+)] is related to a relatively smaller reduction in plasma aldosterone by the ARB and is not related to changes in GFR. This study provides evidence that increases in serum [K(+)] are less likely with ARB therapy compared with ACE inhibitor therapy in people with renal insufficiency.

A comprehensive review of physiological and molecular biological evidence refutes claims for synthesis of renin by cardiac and vascular tissues. Cardiovascular tissue renin completely disappears after binephrectomy. Residual putative reninlike activity, where investigated, has had the characteristics of lysosomal acid proteases. Occasional reports of renin or renin mRNA in vascular and cardiac tissues can be ascribed to failure to remove the kidneys 24 hours beforehand, overloading of detection systems, problems with stringency in identification, and illegitimate transcripts after more than 25 cycles of polymerase chain reaction. Others, using more stringent criteria, have failed to detect cardiac and vascular renin mRNA. Accordingly, a growing number of investigators have concluded that the kidneys are the only source of cardiovascular tissue renin. Although prorenin is secreted from extrarenal tissues as well as from the kidneys, there is no evidence that it is ever converted to renin in the circulation. The kidney is the only tissue with known capacity to convert prorenin to renin and to secrete active renin into the circulation. Accordingly, renin of renal origin determines plasma and hence, extracellular fluid renin levels. In these loci, angiotensin (Ang) I, formed by renin cleavage of circulating and interstitial fluid angiotensinogen, is in turn cleaved by angiotensin converting enzyme, located in plasma and extracellular fluids and on the luminal surface of pulmonary and systemic vascular endothelial cells, to Ang II, which perfuses and bathes the heart and vasculature. Consistent with this model, plasma renin and angiotensin and the antihypertensive action of renin inhibitors, converting enzyme inhibitor, or Ang II antagonists all disappear after binephrectomy. Thus, the plasma renin level, via Ang II formation, determines renin system vasoconstrictor activity, the antihypertensive potential of anti-renin system drugs, and the risk of heart attack in hypertensive patients. This analysis redirects renin research to renal mechanisms that create the plasma renin level, to renal prorenin biosynthesis and its processing to renin, and to their regulated secretion, extracellular distribution, and possible binding to by target tissues. In this context, it is still possible that changes in circulating and interstitial renin substrate or available converting enzyme might exert subtle modulating influences on Ang II formation. However, this analysis redefines the importance of plasma renin measurements to assess clinical situations, because plasma renin is the only known initiator driving the cardiovascular renin-angiotensin system, and its strength can be measured.