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PubMed1986

Circulatory basis for the use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure.

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect; it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency, and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these should be more specific in action than the presently available and very successful converting enzyme inhibitors.

Administration, Oral↗
PubMed1987

Converting enzyme inhibitors in the treatment of hypertension.

The renin-angiotensin system has a wide range of physiological actions, and thus interference with the system has attractive therapeutic potential. The orally active angiotensin converting enzyme (ACE) inhibitors have so far been the most successful drugs in this area. They lower arterial pressure both in renovascular and essential hypertension, and their effects are enhanced by concomitant diuretic therapy or dietary salt restriction. Since, in renovascular hypertension, the affected kidney depends on enhanced local generation of angiotensin II to help preserve its function, the circulation and excretory capacity of this kidney may be compromised with ACE inhibition. ACE inhibitors can improve exercise tolerance and diminish cardiac ventricular arrhythmias in patients with heart failure. Because these drugs lower plasma aldosterone, they tend to correct potassium deficiency and hypokalemia, which may have been induced by diuretic treatment. Hypotension can occur with the first dose of ACE inhibitor, especially in sodium-depleted subjects; in patients on prior antihypertensive therapy, particularly if this includes a diuretic; and in the elderly. Not all of the actions of ACE inhibitors are necessarily due to lowering of plasma angiotensin II: accumulation of kinins may be responsible for some of the effects and side effects. Common to all ACE inhibitors are occasional rashes, cough, and, more rarely, angioedema. Apparently peculiar to captopril, and less often seen with the lower doses now employed, are taste disturbance, proteinuria, and marrow depression. ACE inhibitors, should not be used in pregnant women.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1968

Effects of Potassium Nutrition on Ribonucleic Acid and Ribonuclease in Zea mays L.

Potassium deficiency decreased the total RNA per shoot in corn (Zea mays L.) seedlings due to the reduced sizes of the plant, but increased the ratio of RNA to dry matter as much as 40%. Total base composition of RNA was unaffected by K(+) deficiency. Thus K(+) deficiency does not appear to alter RNA metabolism to such an extent that a lack of RNA becomes a factor limiting growth. The RNA contents of leaves were followed as deficiency developed or as the plant recovered from deficiency. Such time-course studies, although extremely useful in microbial work, did not yield as much information with higher plants. The ratio of RNA to dry matter in younger leaves was much higher than that in older leaves. The ribonuclease level in corn shoots was increased as much as threefold by K(+) deficiency.

Journal Article↗
PubMed1986

The electrogenic Na-pump and spontaneous contraction of the hypokalemic rat duodenum.

The effects of the electrogenic Na-pump on spontaneous contraction in the isolated, longitudinal muscle of the duodenum of rats which had been on a potassium-deficient diet for 7 weeks, have been investigated. Intracellular levels of Na+ are increased by this diet. The spontaneous contraction of the duodenal muscle was stopped, transiently, by 0.5 to 120 mM-K+ Krebs solution. The period of decrease of tone and amplitude occurring immediately after adding K+ was shortened when the external K+ concentration ([K]o) was increased from 0.5 to 120 mM. The decrease in tone and amplitude induced by K+ was abolished by exposure of the tissue to 0 mM [K]o, by exposure to a temperature below 14 degrees C, and in the presence of ouabain (3 X 10(-5)-10(-4) M). The spontaneous contraction of 'Na-rich' duodenum in bathing medium containing 15 mM K+ and following inhibition of the electrogenic Na-pump with cooling or ouabain was much the same as in the duodenum from rats fed balanced diets: i.e., increase of contractile tone immediately after adding K+. To activate the Na-pump in 'Na-rich' duodenum, the external K+ could be replaced by Rb+, Cs+, NH4+ and Tl3+. The effectiveness was in the order K+ greater than Rb+ greater than Cs+ greater than NH4+ greater than Tl3+. The possible existence of a neuronal or hormonal inhibitory mechanism affecting the active Na-K transport in rat smooth muscle in situ, under conditions of hypokalemia, is discussed.

Animals↗
PubMed1969

Potassium depletion in severe heart disease.

Exchangeable sodium and potassium, total body water, and sulphate space were measured in 42 patients with severe valvular heart disease who were free of oedema. Compared with normal subjects of the same height, no increase in exchangeable sodium was found but a mean potassium depletion of 27% was shown. This depletion was not related to diuretic therapy, and no relationship between the degree of depletion and postoperative arrhythmias was found. It is concluded that the major cause of the low exchangeable potassium is the reduction in cell mass that occurs in chronic heart disease, and that there is no significant fall in the intracellular potassium concentration.

Adult↗
PubMed1974

Total body potassium in long-term frusemide therapy: is potassium supplementation necessary?

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.

Administration, Oral↗
PubMed1984

Myocardial damage due to hypokalaemia and hypophosphataemia.

A case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed.

Echocardiography↗
PubMed2002

Potassium depletion increases potassium clearance capacity in skeletal muscles in vivo during acute repletion.

Muscular K uptake depends on skeletal muscle Na-K-ATPase concentration and activity. Reduced K uptake is observed in vitro in K-depleted rats. We evaluated skeletal muscle K clearance capacity in vivo in rats K depleted for 14 days. [(3)H]ouabain binding, alpha(1) and alpha(2) Na-K-ATPase isoform abundance, and K, Na, and Mg content were measured in skeletal muscles. Skeletal muscle K, Na, and Mg and plasma K were measured in relation to intravenous KCl infusion that continued until animals died, i.e., maximum KCl dose was administered. In soleus, extensor digitorum longus (EDL), and gastrocnemius muscles K depletion significantly reduced K content by 18%, 15%, and 19%, [(3)H]ouabain binding by 36%, 41%, and 68%, and alpha(2) isoform abundance by 34%, 44%, and 70%, respectively. No significant change was observed in alpha(1) isoform abundance. In EDL and gastrocnemius muscles K depletion significantly increased Na (48% and 59%) and Mg (10% and 17%) content, but only tendencies to increase were observed in soleus muscle. K-depleted rats tolerated up to a fourfold higher KCl dose. This was associated with a reduced rate of increase in plasma K and increases in soleus, EDL, and gastrocnemius muscle K of 56%, 42%, and 41%, respectively, but only tendencies to increase in controls. However, whereas K uptake was highest in K-depleted animals, the K uptake rate was highest in controls. In vivo K depletion is associated with markedly increased K tolerance and K clearance despite significantly reduced skeletal muscle Na-K-ATPase concentration. The concern of an increased risk for K intoxication during K repletion seems unwarranted.

Animals↗
PubMed1982

Stimulation of aldosterone biosynthesis by sodium sequestration: role of angiotensin II.

The role of angiotensin II in the stimulation of aldosterone biosynthesis by sodium sequestration in potassium-deficient rats was assessed by experiments involving 1-day angiotensin II infusion, converting enzyme inhibition, and bilateral nephrectomy. In intact rats, only an extremely high dose of exogenous angiotensin II imitated the stimulatory effects of polyethylene glycol-induced edema on the conversions of deoxycorticosterone and corticosterone to 18-hydroxycorticosterone and aldosterone. Treatment with the converting enzyme inhibitor captopril as well as bilateral nephrectomy blocked the aldosterone-stimulating action of edema. This inhibition was prevented by the simultaneous infusion of angiotensin II in captopril-treated rats but not in nephrectomized animals. According to these results, angiotensin II is an essential mediator in the stimulation of aldosterone biosynthesis by sodium sequestration. However, the role of the kidneys appears to be twofold. First, they act through the secretion of renin. In addition, a second yet unknown kidney factor is necessary for a full response of the zona glomerulosa to the stimulatory action of angiotensin II.

Adrenal Glands↗
PubMed1987

Acidification is inhibited in late proximal convoluted tubule during chronic metabolic alkalosis.

In vivo microperfusion was used to assess the changes in the active and passive components of bicarbonate absorption in the rat late proximal tubule during chronic metabolic alkalosis. In tubules perfused with 40 mM bicarbonate, net bicarbonate absorption was inhibited and normal flow dependence was attenuated during alkalosis, compared with values in normal tubules perfused with 40 or even 25 mM bicarbonate concentrations. Under all conditions, bicarbonate back leak was small and contributed little to alterations in net bicarbonate transport, even though bicarbonate permeability was reduced by approximately 75% during chronic metabolic alkalosis and was flow dependent. Suppression of net bicarbonate absorption during chronic metabolic alkalosis was instead attributable to inhibition of proton secretion as a function of both luminal bicarbonate concentration and flow rate. At the highest level of bicarbonate delivery to yield maximal acidification rates, proton secretion during alkalosis was diminished by 38% (from 216 +/- 15 to 133 +/- 10 peq X mm-1 X min-1, P less than 0.001). In conclusion, despite extracellular volume contraction, potassium deficiency, and reduction in bicarbonate permeability during chronic metabolic alkalosis, net bicarbonate absorption in the late proximal convoluted tubule is depressed as a function of luminal bicarbonate concentration and flow rate because acidification is inhibited by hyperbicarbonatemia/alkalemia.

Absorption↗
PubMed2004

Plasticity of mouse renal collecting duct in response to potassium depletion.

Plasticity of mouse renal collecting duct in response to potassium depletion.--Renal collecting ducts are the main sites for regulation of whole body potassium balance. Changes in dietary intake of potassium induce pleiotropic adaptations of collecting duct cells, which include alterations of ion and water transport properties along with an hypertrophic response. To study the pleiotropic adaptation of the outer medullary collecting duct (OMCD) to dietary potassium depletion, we combined functional studies of renal function (ion, water, and acid/base handling), analysis of OMCD hypertrophy (electron microscopy) and hyperplasia (PCNA labeling), and large scale analysis of gene expression (transcriptome analysis). The transcriptome of OMCD was compared in mice fed either a normal or a potassium-depleted diet for 3 days using serial analysis of gene expression (SAGE) adapted for downsized extracts. SAGE is based on the generation of transcript-specific tag libraries. Approximately 20,000 tags corresponding to 10,000 different molecular species were sequenced in each library. Among the 186 tags differentially expressed (P < 0.05) between the two libraries, 120 were overexpressed and 66 were downregulated. The SAGE expression profile obtained in the control library was representative of different functional classes of proteins and of the two cell types (principal and alpha-intercalated cells) constituting the OMCD. Combined with gene expression analysis, results of functional and morphological studies allowed us to identify candidate genes for distinct physiological processes modified by potassium depletion: sodium, potassium, and water handling, hyperplasia and hypertrophy. Finally, comparison of mouse and human OMCD transcriptomes allowed us to address the question of the relevance of the mouse as a model for human physiology and pathophysiology.

Acid-Base Equilibrium↗
PubMedDate not supplied

What makes cells grow larger and how do they do it? Renal hypertrophy revisited.

Hypertrophy, defined as an increase in cell size without an increase in cell number, occurs in a number of conditions, including compensatory renal growth, diabetes mellitus, protein feeding, chronic metabolic acidosis, and chronic potassium deficiency. In vitro cell culture studies have been used to characterize the mechanisms involved in the development of hypertrophy. Two mechanisms have been identified and characterized. One mechanism involves regulation of processes that are also associated with the initial events of the hyperplastic growth process, and is referred as a cell cycle-dependent mechanism. The other mechanism occurs independently of these particular cell cycle processes, but involves regulation of protein degradation by lysosomal enzymes. This latter mechanism is referred to as a cell cycle-independent mechanism. In vivo studies suggest that both compensatory renal hypertrophy following uninephrectomy and diabetes mellitus-induced hypertrophy involve the cell cycle-dependent mechanism.

Animals↗
PubMed1998

Micronutrients, minerals and growth control.

(1) Dietary deficiencies of Zn, Mg and K lead to a rapid drop in serum concentrations, with no change (Zn) or a slow decline (Mg and K) in the concentrations in skeletal muscle. (2) These deficiencies all lead to inhibition of growth and protein synthesis in muscle. (3) The inhibition of protein synthesis is faster in onset than the loss of Zn, Mg and K from muscle and therefore unlikely to result from cellular mineral deficiency. (4) The deficiencies are likely to be detected by the early drop in serum concentration, but the mechanism is unknown. (5) Possible mediators of growth inhibition are anorexia, GH and IGF-I. (6) Early detection of mineral deficiencies allows the organism to minimize wasteful protein synthesis and the formation of functionally inadequate tissues.

Animals↗
PubMed1998

Regulation of Na+, K(+)-ATPase in the rat outer medullary collecting duct during potassium depletion.

Because in outer medullary collecting ducts (OMCD) of K(+)-depleted rats, K+ secretion is abolished, whereas Na+, K(+)-ATPase, which energizes this secretion, is markedly stimulated, it has been proposed that Na+, K(+)-ATPase was mislocated to the apical cell membrane and energized K+ reabsorption. This hypothesis has been supported by paradoxical effects of ouabain in K(+)-depleted compared with normal rats. However, we have recently shown that ouabain inhibits not only Na+, K(+)-ATPase but also apical H+, K(+)-ATPase in the OMCD of K(+)-depleted rats. Therefore, this study was designed to evaluate whether previous observations were accounted for by Na+, K(+)-ATPase or by ouabain-sensitive H+, K(+)-ATPase. Na+, K(+)-ATPase was distinguished from H+, K(+)-ATPase by its insensitivity to Sch-28080. Results indicate that the hydrolytic and transport activities of Na+, K(+)-ATPase, the number of its functional units, and the expression of mRNA of its alpha 1 and beta 1 subunits were increased threefold or more in the OMCD of rats fed a K(+)-depleted diet for 2 wk. By immunofluorescence, Na+, K(+)-ATPase staining was strongly increased in K(+)-depleted rats but remained localized to the basolateral pole of OMCD principal cells. In conclusion, K+ depletion is associated with marked induction of functional Na+, K+ pumps at the basolateral pole of rat OMCD. Therefore, reduced K+ secretion might result from inhibition of apical K+ conductances and stimulation of basolateral K+ recycling. It is proposed that increased Na+, K(+)-ATPase participates in the increased Na+ reabsorption prevailing in collecting ducts of K(+)-depleted rats.

Animals↗