Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study focuses on the interaction between cadmium (Cd) and the Na, K-ATPase system in in vitro grown vascular smooth muscle cells (VSMCs) derived from the rat carotid artery. In disrupted VSMCs rendered permeable by osmotic shock, Cd inhibited Na, K-ATPase; I50 was reached at 10(-5) M Cd. Mg-ATPase was also inhibited by Cd; I50 was attained at concentrations of 10(-4) M Cd. Cd inhibition of Na,K-ATPase in the VSMCs was noncompetitive with respect to Na, K, and ATP. Rubidium transport experiments performed with intact VSMCs demonstrated that within an incubation period of 150 minutes, a concentration of 10(-4) M Cd in the extracellular fluid exerted no acute effect on the Na-K pump. Within this time interval, intracellular Cd attained a concentration eightfold higher than the extracellular Cd concentration. Thus, it appears that under acute conditions Cd exerts its inhibitory effect on Na, K-ATPase only in disrupted VSMCs. The data further suggest that, in the VSMC, conditions under which Cd inhibits Na, K-ATPase are consistent with inhibition from the cytoplasmic side of the cell membrane.
Hypertension
PMID:Cadmium effect on the Na,K-ATPase system in cultured vascular smooth muscle cells. 614 Nov 42

It has been demonstrated in experiments on cats and rabbits that a single and chronic administration of pentamine (1 mg/kg) produced a distinct variation in carbohydrate-energy metabolism in the tissue of different blood vessels, enhancing the glycolytic formation of ATP. Chronic administration of pentamine corrected metabolic disorders in rabbit vascular tissue in experimental pituitrin-induced hypertension.
 ...
PMID:[Effect of pentamine on vascular tissue metabolism in experimental vascular pathology]. 620 Mar 58

Sodium pumps of cardiac plasma membranes were studied in young, spontaneously hypertensive rats (SHR) and in their normotensive controls (Wistar-Kyoto; WKY) using the two following methods. The enzymatic activity and its sensitivity to ouabain were measured as the Na+, K+ -dependent ATP hydrolysis, and the number of pumps was estimated by [3H] ouabain binding. The main results of this study were the observations that (a) concentrations of ouabain as low as 10(-10) M inhibited 10-15% of the enzyme activity in both strains; (b) Na+, K+- adenosine triphosphatase (ATPase) activity in membranes from SHR was double that in membranes from WKY (16.5 +/- 3.2 mumol Pi/h/mg protein vs. 8.2 +/- 1.2 mumol Pi/h/mg protein for 10(-7) M ouabain; p less than 0.01); (c) sensitivity to three different cardiac glycosides, ouabain, digoxin, and digitoxigenin, was identical in SHR and WKY vesicles; and (d) the binding capacity of [3H] ouabain was significantly higher in SHR than in WKY vesicles, but the dissociation constant (KD) did not appear to differ between the two substrains. These studies, performed on 3-week-old rats before the appearance of hypertension, showed, on the one hand, the existence of a Na+, K+ -ATPase of very high affinity in the rat heart, and, on the other, that cardiac sarcolemmal membranes from SHR had a greater number of sodium pumps than those from WKY and thus a greater ability to extrude sodium.
 ...
PMID:Quantitative changes in cardiac Na+, K+ -adenosine triphosphatase of spontaneously hypertensive rats. 620 Jul 16

Age-related changes in the myocardial energy metabolism were studied in spontaneously hypertensive (SHR) rats of 5-15 weeks of age. Systolic blood pressure increased rapidly during 5 to 10 weeks of age (developing phase) and attained a plateau level at 10 to 15 weeks (sustained phase). Even during the developing phase, the heart was hypertrophic, as assessed by an increase in the ratio of the ventricular weight to body weight. However, myocardial contents of glycolytic intermediates and high energy phosphate compounds and thus, the myocardial energy state (phosphorylation potential) in SHR rats did not differ from those in age-matched normotensive Wistar-Kyoto (WKY) rats. The lactate/pyruvate ratio was significantly lower in SHR rats. On the other hand, during the sustained phase, cardiac hypertrophy progressed only gradually, and myocardial contents of creatine phosphate and ATP were lower, while the lactate content was higher than in WKY rats. The lactate/pyruvate ratio was elevated, while phosphorylation potential was lowered. These findings suggest that the energy state is normal during the developing phase of hypertension despite the presence of cardiac hypertrophy and the increased pressure load, whereas the energy state is at a lower level during the sustained phase of hypertension.
 ...
PMID:Myocardial energy metabolism in the hypertrophied hearts of spontaneously hypertensive rats. 621 80

Protein content, enzymatic activites and Ca2+ accumulation capacities were studied in plasma membrane fractions isolated from mesenteric arteries of rats made hypertensive by renal artery stenosis with and without contralateral nephrectomy, i.e., one-kidney, one clip (1-KHR) and two-kidney, one clip (2-KHR) hypertension, respectively. Both types of renovascular hypertension showed similar vascular plasma membrane abnormalities which included increased total protein contents, enhanced alkaline phosphatase activities and reduced ATP-dependent Ca2+ accumulation compared to control values. The altered alkaline phosphatase activity and ATP-dependent Ca2+ accumulation appeared to be associated with blood pressure elevation in both types of hypertension and may be related to the elevation of blood pressure insensitive to captopril (SQ 14,225) in 1-KHR and 2-KHR. These results are consistent with the current concept of biochemical abnormalities of arterial smooth muscle in the development ostem.
 ...
PMID:Characteristics of arterial plasma membrane in renovascular hypertension in rats. 624 53

Recently it has been claimed that the active potassium influx in erythrocytes of patients with essential hypertension would be increased. In view of the diagnostic and possibly therapeutic potential of this claim, we have determined the Na+-K+ activated ATPase activity and the affinity of the enzyme for Na+, K+, and ATP in membranes isolated from erythrocytes of hypertensive (with and without medication) and normotensive subjects. Subsequently, the active (ouabain-sensitive) sodium and potassium fluxes and their ratios have been determined after treatment of intact erythrocytes either with cold or with p-chloromercuribenzene-sulfonate (PCMBS). Finally, in view of a subsequent claim that the furosemide-sensitive, ouabain-insensitive cation fluxes would be greatly reduced in erythrocytes of patients with essential hypertension, we have determined these fluxes in choline chloride medium containing ouabain with and without furosemide. For none of these parameters has any significant difference between hypertensive and normotensive subjects been found except for a decrease in the ouabain-sensitive K+ influx after cold treatment in hypertensives. This is also true for the hypertensive subjects who had a known hypertensive parent. It is concluded that the results do not support a role of Na+-K+ activated ATPase or the furosemide-sensitive cation carrier in the pathogenesis of essential hypertension, and that ouabain-sensitive and furosemide-sensitive cation flux determinations in erythrocytes do not seem to be useful for the diagnosis of this condition.
Hypertension
PMID:Cation fluxes and Na+-K+-activated ATPase activity in erythrocytes of patients with essential hypertension. 627 69

To study the relative roles of sodium (Na+) and calcium ions (Ca2+) in the response of adrenal glomerulosa cells, we investigated the effects of different Na+ concentrations in the incubation media and the actions of substances that interfere with Ca2+ fluxes. Basal aldosterone secretion and response to angiotensin II (AII), adrenocorticotropic hormone (ACTH), or potassium (K+) were dependent on extracellular Na+ concentration. Veratridine, a Na+ channel opener that dissipates Na+ gradients, blocked the stimulated steroidogenic response. Mersalyl acid and tetracaine, which are potent Ca2+ antagonists, blocked the effects of aldosterone secretagogues. Divalent cations with Ca2+ antagonistic action such as manganese M(n2+), nickel (Ni2+), and cobalt (Co2+) blocked the aldosterone secretory response to AII, ACTH, and K+. Barium (Ba2+) and strontium (Sr2+), known to mimick Ca2+ effects, increased or did not affect responses of the glomerulosa cells. Sodium vanadate, an inhibitor of ATP-dependent Ca2+ translocation, did not alter the stimulated aldosterone responses. Trifluoperazine (10(-6) M), an inhibitor of calmodulin, blocked AII and K+-induced aldosterone secretion, but was partially effective on ACTH-stimulated aldosterone output only at a concentration of 10(-5) M. The actions of ouabain on aldosterone biosynthesis were similarly affected by all these drugs. Thus, both extracellular Na+ and Ca2+ appear to play a role in the steroidogenic response of isolated glomerulosa cells. The intracellular action of Ca2+ may involve a calmodulin-like protein. The effects of ACTH are only partially dependent on Ca2+ as a second intracellular messenger.
Hypertension
PMID:Relative roles of sodium and calcium ions in the steroidogenic response of isolated rate adrenal glomerulosa cells. 627 6

Effects of CV-2619 (10 and 30 mg/kg/day, p.o.) or ubiquinone-10 (Q-10, 10 mg/kg/day, p.o.) treatment for 5 weeks on systolic blood pressure (SBP) and myocardial energy metabolism were studied in spontaneously hypertensive rats of 20 weeks of age. The systolic blood pressure was about 205 mmHg at the start of the experiment, and a slight increase was noted thereafter in the control (vehicle) group. CV-2619, but not Q-10, inhibited the increase in the blood pressure. At 25 weeks of age, cardiac hypertrophy was noted to the same extent in either treated group. Myocardial contents of glycolytic intermediates (glycogen, glucose, pyruvate and lactate) and creatine phosphate (Cr-P), ATP, ADP, and AMP were not significantly influenced by CV-2619 or Q-10 treatment. CV-2619, however, significantly increased the energy charge, an index of myocardial energy state, with higher dose and lowered the lactate/pyruvate ratio with either dose. These results suggest that CV-2619 has a mild antihypertensive effect and improves the myocardial energy state in the hypertrophied heart during the sustained phase of hypertension in SHR rats.
 ...
PMID:[Effects of 2,3-dimethoxy-5-methyl-6-(10'-hydroxydecyl)-1,4-benzoquinone (CV-2619) on myocardial energy metabolism in the hypertrophied heart of spontaneously hypertensive rats]. 629 97

Considerable experimental as well as clinical evidence has now accumulated to indicate that Mg2+ and K+ deficiencies have probably been overlooked as important causal factors in the etiology of hypertensive disease. Mg2+ ions are important for the regulation of Na+ and K+ transport across cell membranes, including those found in cardiac and vascular smooth muscle cells. Mg2+ activates a Na+-K+-ATPase pump which in turn plays a major role in regulating Na+-K+ transport. Loss of cellular Mg2+ results in the loss of critically important phosphagens: Mg ATP and creatine phosphate. Thus, under conditions where cellular Mg2+ is depleted (e.g. hypoxia, anoxia, ischemia, Mg deficiency, errors in Mg metabolism and/or binding, and transport), the Na+-K+ pump and phosphagen stores will be compromised, leading to alterations in resting membranes (e.g. membrane depolarization). Cellular Mg2+ depletion has been found to result in concomitant depletion of K+ in a number of cells, including cardiac and vascular muscles. Myocardial and vascular injury thus results in an uptake of Na+ and Ca2+, Mg2+ and K+ being lost first. The available evidence indicates that Mg2+ is important in the control of arteriolar tone and blood pressure, primarily via the regulation of vascular membrane Mg2+-Ca2+ exchange sites. A reduction in extracellular Mg2+ (or K+) can produce hypertension, vasospasm and potentiation of vasoconstrictor agents by allowing excess entry of Ca2+, concomitantly the potency of vasodilators is reduced. Alterations in vascular membrane Mg2+ result in 'leaky' arterial and arteriolar membranes thus contributing to the cellular reduction in K+ and the gain of Ca2+ and Na+. These factors seem all-important in the production and etiology of hypertension. Both clinical and experimental forms of hypertension are associated with tissue and plasma deficits of Mg2+. The arterial blood pressure elevation appears to be inversely related to the level of ionized intracellular and plasma Mg2+.
 ...
PMID:Interactions of Mg and K on blood vessels--aspects in view of hypertension. Review of present status and new findings. 639 41

To study the hitherto unknown long-term effects of ethanol on the contractile activity of wall cells of coronary microvessels (mv.), 21 experimental and 21 control animals were investigated, using a new histomorphometric method. The pair-fed rats of the experimental group were given a diet containing ethanol which replaced 36% of the total calories for 4 weeks. This resulted in an increase of wall thickness of mv. in all segments of the microvasculature and an augmentation of the number of ATP-hydrolyzing small-calibered mv. The increase of wall thickness of muscularized mv. was interpreted as a structural adaptation to a long-term predominance of vasotonic influences, which were apparently likewise responsible for the increase of ATP-hydrolysis in the smallest mv. The possible reasons for this predominance are discussed and the necessity to include myocardial metabolic factors in pathogenic considerations on ethanol-induced coronary affections is indicated. Such mv. reactions as observed may be considered as a potential contributive pathogenic factor in ethanol-induced cardiomyopathies and hypertension.
 ...
PMID:Long-term effects of ethanol on coronary microvessels of rats. 640 Apr 31


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>