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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific atrial natriuretic factor (ANF) analogues have been found to have inhibitory activity in vitro in a calmodulin-dependent, human red blood cell membrane Ca2+-adenosine triphosphatase (ATPase) model. Studied at 10(-8) to 10(-6) M concentrations, atriopeptin I (residues 127-147 of rat prepro-ANF sequence) and atriopeptin III (residues 127-150) progressively inhibited Ca2+-ATPase activity by up to 20% (p less than 0.001). This degree of inhibition was consistent with activities of other (calmodulin-independent) enzyme inhibitors in this model. Therefore, the C-terminal Phe-Arg-Tyr sequence (residues 148-150) is unnecessary for atriopeptin action on Ca2+-ATPase. Human and rat atrial peptides with amino acids 123-150 were inactive, indicating that the 123-126 sequence (Ser-Leu-Arg-Arg) must be cleaved to activate atriopeptins in this system. Human ANF fragment 129-150 also had no effect on Ca2+-ATPase, defining the importance of residues 127-128 (Ser-Ser) proximal to the disulfide bridge (joining 129 to 145). The addition of purified calmodulin to red blood cell membranes in the presence of inhibitory ANF did not restore Ca2+-ATPase activity to normal levels, indicating that the ANF effect on this enzyme is calmodulin-independent. Atriopeptin I and atriopeptin III had no effect on red blood cell Na+, K+-ATPase activity in vitro. Thus, the structure-activity relationships of ANF analogues in this novel human cell membrane model are highly specific. Although the inhibitory action of ANF analogues on Ca2+-ATPase, a calcium pump-associated enzyme, may be unique to the red blood cell, the calcium dependence of the gluconeogenic effects of ANF in the kidney would be supported by inhibition of this ATPase.
Hypertension 1988 Oct
PMID:Analogue-specific action in vitro of atrial natriuretic factor on human red blood cell Ca2+-ATPase activity. 284 69

Maternal endoxin (digoxinlike substance) is proposed as arising in the fetal area of the fetal adrenal cortex. Its function may be to sensitize the uterus for labor, much as does cortisol in the sheep fetus. Because endoxin is a sodium-potassium-adenosine triphosphatase inhibitor, however, it may also induce maternal vasoconstriction. On our service, normal pregnant women have detectable endoxin after 35 weeks with increasing amounts at term. Specimens of cord blood often have "digoxin" in the therapeutic range. We find that about 40% of women in premature labor and 65% of pregnant women with hypertension have elevated levels of serum endoxin. Postdate gravid women sometimes have very low endoxin levels. Pregnant women with complications and elevated digoxin (endoxin) levels could have specific antidigoxin therapy if endoxin proves to be a modulator of their symptoms. Digoxinlike substances are also sometimes elevated in ill nonpregnant persons, such as those with renal, liver, or heart failure, or hypertension.
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PMID:Fetal endoxins and complications of pregnancy. 284 75

Inhibition of vascular smooth muscle sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) has been postulated as a central mechanism in enhancing vascular contractility. In the present study, kinetics of inhibition of Na-K-ATPase by lead, ouabain, and natriuretic hormone (NH) was studied in a purified hog cerebral cortex enzyme preparation. Determination of I50 values for lead, ouabain, and NH revealed that NH is the most potent inhibitor of the enzyme system (0.8 x 10(-6) M ouabain equivalents). Kinetic analyses indicated that lead and NH exhibited different inhibitory mechanisms. The inhibition by lead was noncompetitive with respect to potassium and competitive with respect to sodium and MgATP. Natriuretic hormone was noncompetitive with respect to potassium, uncompetitive with respect to MgATP, and exhibited no inhibitory effect with respect to sodium. Synergism between lead and NH in the inhibition of Na-K-ATPase raises the possibility that lead may be a contributory factor in hypertension via this mechanism.
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PMID:Effects of lead and natriuretic hormone on kinetics of sodium-potassium-activated adenosine triphosphatase: possible relevance to hypertension. 284 38

Several operationally defined adenosine triphosphatase (ATPase) activities were determined in vitro in red blood cell lysates of normotensive or hypertensive humans: Mg2+-ATPase, Na+,K+-ATPase, and Ca2+ pump ATPase, the latter in the calmodulin-activated and basal states. Basal Ca2+ pump ATPase was defined as the Ca2+-activated ATPase resistant to 10(-4) M trifluoperazine. Subjects were part of a double-blind study in which treatment was divided into several phases: baseline (4 weeks), placebo or calcium (1 g elemental calcium/day, 8 weeks), placebo washout (4 weeks), placebo or calcium (1 g elemental calcium/day, 8 weeks). Irrespective of the phase of treatment, the basal Ca2+ pump ATPase activity in red blood cell lysates of 36 hypertensive subjects was significantly less than that in lysates from 18 normotensive subjects. Other ATPase activities did not differ significantly, although all ATPases tended to be decreased in hypertension. The data are consistent with previous reports of altered membrane Ca2+ binding and transport in hypertension, but the precise changes are not elucidated.
Hypertension 1986 Nov
PMID:Decreased calcium pump adenosine triphosphatase in red blood cells of hypertensive subjects. 294 85

Fourteen reports have identified an association between lower dietary calcium consumption and higher blood pressure in adults. The relationship between dietary calcium and blood pressure status of humans may be modified by a wide variety of demographic, environmental, life-style, and nutritional factors. Reduced dietary calcium intake may be a proximate cause of several of the reported biochemical abnormalities of Ca2+ metabolism including the reductions in serum ionized Ca2+ concentrations and increases in circulating parathyroid hormone levels. The paradoxical increases in intracellular free Ca2+ observed in hypertension on low dietary Ca2+ intake suggest that a primary defect in the cellular handling of Ca2+ may exist, possible mediated through defective Ca2+ adenosine triphosphatase pump activity.
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PMID:Epidemiological evidence associating dietary calcium and calcium metabolism with blood pressure. 295 Jul 55

These studies were designed to investigate whether the antihypertensive effects of high potassium or low sodium diets are related to changes in vascular Na+,K+-adenosine triphosphatase (ATPase) activity. Vascular Na+,K+-ATPase was measured as ouabain-sensitive rubidium uptake in aorta incubated in buffer or plasma from spontaneously hypertensive rats (SHR) fed either a high potassium, a low sodium, or a normal diet for 2 weeks. The high potassium diet significantly increased Na+,K+-ATPase activity, whereas the low sodium diet significantly decreased activity. There was no evidence of a ouabainlike factor in plasma. The increased pump activity on the high potassium diet appeared to be due to an increase in maximum activity (Vmax) of the enzyme, rather than to an increased affinity for potassium. Potentially, an increase in Na+,K+-ATPase activity could contribute to the antihypertensive effect of potassium by hyperpolarizing the cell membrane. The decrease in vascular Na+,K+-ATPase activity on a low sodium diet probably is unrelated to its depressor effect, but it may be a homeostatic mechanism for maintaining sodium balance in the animal.
Hypertension 1987 Jun
PMID:Effects of high potassium or low sodium diet on vascular Na+,K+-ATPase activity and blood pressure in young spontaneously hypertensive rats. 295 81

The plasma membrane calcium-activated adenosine triphosphatase (Ca2+-ATPase) is known to regulate intracellular calcium levels. This enzyme was localised in intracerebral cortical vessels of normotensive and acutely hypertensive rats. Of interest was whether the arterioles that develop increased permeability to horseradish peroxidase (HRP) in acute hypertension demonstrate any alteration in localisation of Ca2+-ATPase as compared to normotensive controls. Rats were injected with HRP intravenously and acute hypertension was induced by a 2-min infusion of angiotensin amide. Following perfusion of fixative, brains were sliced and reacted for demonstration of HRP reaction product and Ca2+-ATPase. Normotensive rats showed discontinuous distribution of Ca2+-ATPase on the outer plasma membranes of endothelial, smooth muscle and adventitial cells of arterioles. The localisation of Ca2+-ATPase in pinocytotic vesicles present in endothelial and smooth muscle cells was quite striking. Focal cortical areas of hypertensive rats showed increased arteriolar permeability to HRP. Permeable arterioles showed marked reduction of Ca2+-ATPase on the outer plasma membranes of endothelium and smooth muscle cells as compared to nonpermeable arterioles of the same animals and arterioles of normotensive controls. The latter finding suggests that calcium may be involved in increased cerebrovascular permeability mechanisms in acute hypertension.
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PMID:Localisation of calcium-activated adenosine-triphosphatase (Ca2+-ATPase) in intracerebral arterioles in acute hypertension. 296 18

Sodium pump activity of blood vessels has been reported to decrease in several animal models of hypertension. We studied sodium-potassium-adenosine triphosphatase (Na-K-ATPase) activity of renal tubular segments in 12-week-old spontaneously hypertensive rats and in age-matched Wistar-Kyoto normotensive rats. The enzyme activity of the individual nephron segments was determined by a microfluorometric assay in which ATP hydrolysis is coupled with NADH oxidation. In the spontaneously hypertensive rats, systolic blood pressure was significantly higher (181 +/- 3 mm Hg) than in the Wistar-Kyoto rats (134 +/- 2 mm Hg). However, there was no difference in mean Na-K-ATPase activity in any of the nephron segments from the spontaneously hypertensive compared with the Wistar-Kyoto group. It is concluded that Na-K-ATPase activity does not change in any of the nephron segments with spontaneous hypertension.
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PMID:Sodium-potassium-adenosine triphosphatase in nephron segments of spontaneously hypertensive rats. 298 96

Material extracted and partially purified from plasma of the Sabra hypertension prone rats was found to be capable of 1) inhibiting the binding of 3H-ouabain to rat brain synaptosomes, 2) inhibiting the activity of rat brain microsomal Na, K activated adenosine triphosphatase, and 3) increasing the contractile force of rat heart muscle. The results demonstrate the presence of a ouabainlike compound in the plasma of these rats. The plasma concentration of this compound in Sabra hypertension prone rats was 698 +/- 199 nmol/ml in ouabain equivalents (SEM; n = 11) versus 2543 +/- 1140 nmol/ml (n = 9) in the Sabra normotensive strain. The presence of ouabainlike compound in the plasma is consistent with the hypothesis that this compound functions as a hormone that regulates Na, K activated adenosine triphosphatase activity and the physiological processes in which this enzyme is involved.
Hypertension
PMID:Demonstration of a ouabainlike plasma compound in hypertension prone and hypertension resistant rats. 299 63

Ion metabolism in obesity-associated hypertension is reviewed. A hypothesis is presented which proposes that ion imbalances in obesity may play an etiological role in obesity-associated diabetes mellitus as well. It is suggested that the rise in intracellular calcium--secondary to reduced sodium, potassium-activated adenosine triphosphatase (Na,K-ATPase) activity--may aid in the development of increased vascular tone and decreased glucose tolerance.
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PMID:Hypertension and diabetes in obesity: a review and new ideas on the contributing role of ions. 301 58


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