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

We determined whether the rate of metabolic recovery and electrophysiological deficit after incomplete cerebral ischemia is related to intracellular pH (pHi) achieved at the end of ischemia in a dose-dependent manner. End-ischemic pHi was varied by employing two ischemic durations, 12 and 30 min, and by setting preischemic plasma glucose to approximately 80 or 400 mg/dl. Incomplete global ischemia was produced in anesthetized dogs by transient intracranial hypertension followed by 4 h of reperfusion, and pHi, ATP, and phosphocreatine (PCr) were measured with 31P magnetic resonance spectroscopy. Cerebral blood flow was reduced to approximately 6 ml.min-1.100 g-1 during ischemia. End-ischemic pHi was greater than 5.7 in all animals from various treatment groups except for four of seven dogs treated with 30-min hyperglycemic ischemia. When end-ischemic pHi remained greater than 5.7, there was nearly complete recovery of ATP, PCr, pHi, intracellular bicarbonate concentration [( HCO3-]i), and O2 consumption. Partial recovery of somatosensory-evoked potentials (SEP) occurred in most of these animals. In the 30-min hyperglycemic animals in which pHi fell below 5.5, ATP, PCr, and O2 consumption recovered by only one-half over 60 min of reperfusion and then declined to near-zero levels without SEP recovery. In addition, pHi remained less than 6.0, and [HCO3-]i remained less than 2 mM throughout reperfusion. We conclude that there is an apparent in vivo pHi threshold of approximately 5.5-5.7 during incomplete cerebral ischemia that is associated with an inability to significantly restore pHi and [HCO3-]i and with secondary deterioration of high-energy phosphate levels.
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PMID:Dependence of cerebral energy phosphate and evoked potential recovery on end-ischemic pH. 199 96

Renomedullary interstitial cells cultured from the Dahl salt-resistant rat have higher levels of basal cytosolic calcium and prostaglandin E2 and are more responsive to vasopressin than interstitial cells from the Dahl salt-sensitive rat. We examined the potential role of inositol phospholipid hydrolysis in mediating these differences. Vasopressin-induced increases in labeled inositol phosphates were enhanced in renomedullary interstitial cells from Dahl salt-resistant compared with those from salt-sensitive rats. Addition of neomycin reduced basal production of labeled inositol phosphates and abolished the increase in inositol phosphates induced by vasopressin. Neomycin also prevented the peak decline pattern in cytosolic Ca2+ seen with vasopressin but did not influence basal cytosolic Ca2+. In the presence of neomycin, vasopressin induced a modest but prolonged increase in cytosolic calcium. In contrast to its marked effects on inositol phosphate production, neomycin was without effect on basal or vasopressin-responsive prostaglandin E2 production. Moreover, basal and vasopressin-induced increases in cytosolic Ca2+ remained higher in renomedullary interstitial cells from Dahl salt-resistant versus those from salt-sensitive rats exposed to neomycin. The results do not support a requirement for phospholipase C-induced inositol phospholipid hydrolysis in the mediation of vasopressin actions on prostaglandin E2 production by renomedullary interstitial cells and imply that the differences in cytosolic Ca2+ and prostaglandin E2 seen in these two cell lines are not related to differences in inositol phospholipid metabolism.
Hypertension 1991 Mar
PMID:Calcium and prostaglandin E2 in renomedullary interstitial cells. 199 61

The inhibition of angiotensin converting enzyme by ramipril, ramiprilat, enalapril, enalaprilat, and captopril was studied in the plasma and various tissues (lung, heart, renal cortex, renal medulla) of normotensive rats and spontaneously hypertensive rats. Displacement curves for [3H]ramiprilat were established on each tissue with the converting enzyme inhibitors, and their potencies were expressed as the concentration that inhibited 50% of the specific [3H]ramiprilat binding. In the plasma, lung, and heart, the order of activities was: ramiprilat greater than enalaprilat greater than captopril greater than ramipril greater than enalapril. This order was different in the kidney (cortex and medulla): ramiprilat greater than enalaprilat greater than ramipril greater than captopril greater than enalapril. For ramiprilat, enalaprilat, and captopril, there were no differences in their respective potencies between tissues or between rat strains. However, the two prodrugs ramipril and enalapril were 10-30 times more active in the kidney than in the other tissues in both groups of rats. This was due to the deesterification of the prodrugs: in the presence of an esterase inhibitor (diethyl nitrophenyl phosphate, 10 microM), the potencies of ramipril in the kidney were not different from that obtained in the lung, which was not affected by the presence of the esterase inhibitor. These results suggest that the variations in the tissue activities of an angiotensin converting enzyme inhibitor are probably not due to differences in tissue affinities of the angiotensin converting enzyme inhibitor but depend on the concentration of this angiotensin converting enzyme inhibitor in each tissue.
Hypertension 1991 Apr
PMID:In vitro tissue potencies of converting enzyme inhibitors. Prodrug activation by kidney esterase. 201 76

A prospective study on 1,482 adult members of 98 Utah pedigrees was carried out to determine which variables may be associated with an increased risk of hypertension incidence. After an average of 7 years of follow-up, 40 individuals had been placed on antihypertensive medications to lower blood pressure. Baseline study variables included anthropometrics, clinical chemistry measurements of blood and urine, socioeconomic and lifestyle variables, and detailed erythrocyte ion transport and concentration measurements. Age (relative risk of 4.28 for a 2 SD difference, p less than 0.0001) and baseline systolic and diastolic blood pressures (relative risks of 3.55 and 3.52, respectively, both p less than 0.0001) had the strongest associations with hypertension incidence. Controlling for age and baseline blood pressure, the following age- and sex-adjusted variables were associated with an increased risk of future hypertension (relative risks for a 2 SD difference, all p less than 0.10): family history of hypertension (2.35); height (1.97); body mass index (2.31); abdominal girth (2.66); subscapular, suprailiac, and triceps skinfold thicknesses (2.79, 2.52, and 2.28, respectively); percent ideal body weight (2.63); log triglyceride concentration (2.02); plasma uric acid (2.16); inorganic phosphate (0.50); and passive erythrocyte sodium permeability (1.59). The final model,which included all of the age- and sex-adjusted variables (p less than 0.10) in a backward elimination logistic regression analysis, consisted of age (4.78), systolic blood pressure (2.91), subscapular skinfold thickness (2.21), height (1.92), uric acid (2.06), inorganic phosphate (0.50), and family history of hypertension (1.82). None of the ion transport or concentration measurements ws associated with an increased risk of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Predictors of an increased risk of future hypertension in Utah. A screening analysis. 204 78

The carboxy terminal homologue of angiotensin II (Ang II), Ang-(3-8) or hexapeptide, was used as a model peptide to examine the types of receptor mechanisms involved in calcium mobilization in cultured vascular smooth muscle cells. Hexapeptide did not produce tachyphylaxis but did produce a sustained increase in intracellular calcium. Differences in the increase in intracellular calcium [( Ca2+]i) and the pattern of inositol phosphate production indicate that Ang-(3-8) and maximal concentrations of Ang II mobilize calcium through different mechanisms. The calcium-mobilizing mechanisms that predominate appear to depend on the concentration of angiotensin. Concentrations of Ang II greater than 10(-8) M produce sharp calcium transients in which the [Ca2+]i returns close to baseline within 1 minute after stimulation, but concentrations of Ang II equal to or less than 3 x 10(-9) M result in a plateau increase in calcium. Pretreatment with Bordetella pertussis toxin does not abolish either the calcium transient induced by Ang II or the plateau phase induced by Ang-(3-8), indicating that the GTP-transducing protein that couples the receptor to phospholipase C or, possibly, a receptor-operated calcium channel is not Bordetella pertussis toxin sensitive.
Hypertension 1990 Jun
PMID:Regulation of cytosolic calcium by angiotensins in vascular smooth muscle. 211 11

Cultured aortic smooth muscle cells from SHR proliferate more actively than cells normotensive control animals. This experimental data may be related to the hypertensive arteriopathy which mainly proceeds from media dystrophy made of hypertrophy, hyperplasia and excessive protein secretion of the smooth muscle cells. In order to precise the molecular cause of the phenomenon and the eventual action of calcium channel blockers on the development of this organic characteristic of hypertension, we have compared the responses of cultured cells from both SH and WKY rats to various agents in the absence or presence of verapamil. Cell proliferation, phospholipase C activation, and c-jun and c-fos oncogene expressions were measured in both cultures under the same conditions. The mitogenic actions of both foetal calf serum (FCS) and angiotensin II are two times more important on SH than on WKY rat cells. However, while inositol phosphate production elicited by angiotensin in also doubled in SHR cultures versus WKY ones. FCS-induced PLC activation is equivalent in both types of cells. The proto-oncogenes are more intensively expressed when WKY cells are stimulated by FCS than in the presence of angiotensin, but, contrarily to angiotensin, serum is not more active upon this parameter in SHR cultures. Verapamil (from 10(-8) M to 10(-5) M) decreases by 30% the proliferative effect of serum in both SH and WKY rat cells but is not significantly active on angiotensin stimulation. It also depresses in the same proportion the serum-induced inositol phosphate production and oncogene expressions without altering the responses to angiotensin. Nicardipine is less active than verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of external calcium on the growth of aortic smooth muscle cells in SHR]. 212 55

The concentration of serum inorganic phosphorus was determined in 162 patients with essential arterial hypertension (EAH) and in 71 control subjects. The serum phosphorus level was lower in patients with essential arterial hypertension than in the control subjects, and the differences were higher in the advanced stages of the disease. The lowest level of serum phosphate concentration was noted in overweight hypertensive patients, probably in relation to an enhanced insulin secretion. In control subjects the serum concentration of phosphate decreased with advancing age.
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PMID:Hypophosphatemia in patients with essential arterial hypertension. 213 90

Recent studies suggest that serotonergic receptor activation is coupled to phospholipase C-mediated phosphoinositide hydrolysis, which results in the release of intracellular second messengers. The purpose of this study was to determine whether altered phosphoinositide metabolism is the basis for augmented vascular responsiveness to serotonin in genetic hypertension. Thoracic aortic segments isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY) were labeled with myo-[3H]inositol and stimulated with serotonin in the presence of LiCl. Accumulation of [3H]inositol phosphates was then quantitated by column chromatography. Basal inositol phosphate accumulation and basal incorporation of myo-[3H]inositol into aortic cell membranes from SHRSP was not significantly different from WKY values. At 2.6 x 10(-7) to 2.6 x 10(-4) M serotonin, phosphoinositide metabolism was significantly augmented in aortae from SHRSP compared with WKY. Depolarization (100 mM KCl) did not increase phosphoinositide hydrolysis above basal levels in SHRSP or WKY. 2-Nitro-4-carboxyphenyl-N,N-diphenyl carbamate (NCDC), an inhibitor of phospholipase C, prevented the serotonin-induced phosphoinositide metabolism. NCDC also partially inhibited phasic contractions (responses in calcium-free solution) to serotonin in aortas from SHRSP and WKY. In conclusion, abnormal phosphoinositide metabolism may be one mechanism responsible for the characteristic increase in vascular reactivity to serotonin in hypertension.
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PMID:Augmented phosphoinositide metabolism in aortas from genetically hypertensive rats. 215 30

To study the effects of prolonged oral calcium loading on the development of hypertension in spontaneously hypertensive rats (SHR), 48 male animals (age 9 weeks) were divided into four groups according to the treatment: control, calcium, deoxycorticosterone (DOC) and calcium/DOC. Both calcium groups received 1.5% calcium chloride solution ad libitum as their drinking fluid. The animals in the DOC groups were treated with a mineralocorticoid, deoxycorticosterone trimethylacetate 25 mg kg-1 s.c. once a week. Systolic blood pressure (BP) was measured twice a week during the 4-week study period. Calcium loading alone lowered BP (p less than 0.01) after four weeks. Combined with DOC treatment, calcium administration had no significant effect on BP. Calcium loading increased the total plasma calcium concentration in the calcium group (p less than 0.05). Urinary excretions of sodium and potassium were augmented in both groups receiving calcium compared to DOC group. DOC treatment alone increased the excretion of calcium (P less than 0.05). Calcium supplementation decreased the plasma phosphate concentration in both groups (calcium p less than 0.05; calcium/DOC p less than 0.01) as well as the excretion phosphate (p less than 0.005) compared to control. The urinary excretion of cAMP remained unaffected by the calcium treatment. The present results indicate that mineralocorticoid treatment can prevent the BP-lowering effect of calcium in SHR. The mechanism of this action remains unclear, but it does not seem to depend on electrolyte or phosphate balance. The investigation of this action of DOC may provide a means for further exploration of the mechanisms by which increased calcium intake lowers BP in SHR.
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PMID:Deoxycorticosterone prevents the blood pressure-lowering effect of calcium in spontaneously hypertensive rats. 215 18

Phosphoinositide (PI) turnover, a major control mechanism of cellular function, was studied in erythrocytes of spontaneously hypertensive rats (SHR). After 32p (inorganic phosphate) incorporation in intact cells, release of inositol trisphosphate (IP3) and inositol bisphosphate (IP2) from membrane fractions was measured in SHR with or without prior Ca2+ stimulation. The present study revealed an increase of Ca2(+)-stimulated IP3 release in SHR, suggesting high polyphosphoinositide phosphodiesterase activity in this model of hypertension.
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PMID:Increased inositol trisphosphate in erythrocytes of spontaneously hypertensive rats. 216 73


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