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 possible role of endogenous sodium pump inhibitors was studied in salt-sensitive rats of Dahl strain which were influenced by high salt intake either in youth (from prepuberty) or only in adulthood. The aim of our study was to search for the relations between the age-dependent blood pressure response to high salt intake and the changes in volume or distribution of body fluids, red cell ion transport or Na+,K+-ATPase activity in various tissues of salt-sensitive (S/JR) and salt-resistant (R/JR) rats. Salt hypertension was especially pronounced in those S/JR rats which were maintained on a high-salt diet from prepuberty. This was accompanied by the moderate expansion of body fluids in young but not in adult hypertensive animals. Na+,K+-ATPase activity was suppressed in both kidney and heart of young S/JR rats with salt hypertension while this was not true in adult hypertensive animals. On the other hand, no inhibition of sodium pump was observed in brain microsomes and erythrocytes of severely hypertensive young S/JR rats. Moreover, no increased levels of endogenous sodium pump inhibitors were detected in plasma of salt hypertensive S/JR rats. Thus our study indicated the age-dependent suppression of sodium pump activity in some tissues of salt hypertensive Dahl rats but we failed to confirm increased levels of circulating sodium pump inhibitors in young salt hypertensive rats.
 ...
PMID:Sodium pump activity in young and adult salt hypertensive Dahl rats. 243 46

1. Salt restriction is recommended in the treatment of hypertension and is included in national dietary guidelines, but its effect on exercise in hot conditions has not been extensively studied. 2. The effects of 2 weeks on two levels of salt intake (50 and 150 mmol/day) on the ability to exercise (60% of maximal oxygen uptake) in a hot environment (35 degrees C) were studied in eight healthy normotensive subjects. 3. All subjects were able to complete the exercise load on the two levels of salt intake. No differences in mean oxygen uptake, heart rate or rectal temperature during exercise were observed between the two salt intakes. 4. Plasma sodium, potassium and osmolality were similar on the two salt intakes both before and during exercise. Plasma renin activity and aldosterone concentration were elevated after 2 weeks on the reduced salt intake and remained so during exercise. 5. The estimated sweat rate during exercise was similar on the two salt intakes but the loss of sodium was less on the low salt intake. 6. On the basis of these results it is concluded that moderate salt restriction does not impair the ability to exercise in a hot environment.
 ...
PMID:Exercise tolerance in the heat on low and normal salt intakes. 265 71

Salt intake in excess of body needs has long been considered a factor in the genesis and maintenance of human hypertension; the mechanism is salt retention due to faulty renal excretory efficiency. This discussion reviews clinical studies that make a case either for or against the salt hypothesis. Included is a summary of recent experiences with 4 days of salt depletion and 3 days of salt loading in 96 normotensive control subjects and 40 hypertensive patients. These studies were done to test the hypothesis that salt-sensitive blood pressure changes are quantitatively related to sodium balance. However, we found no statistically significant relation between arterial pressure changes and sodium lost during salt depletion or retained during salt loading. The failure of that hypothesis prompted a study of the known factors that control arterial pressure by using multidimensional response surface modeling for changes produced by salt loading. The analysis indicated that in these experiments salt-sensitive blood pressure changes of hypertensive patients were controlled differently than those of normotensive subjects. In the hypertensive group, the changes were highly predictable by combinations of variables, which featured plasma aldosterone, norepinephrine, and epinephrine. In the normotensive group, the changes were less predictable; fewer of the factors were involved, and plasma renin activity was the featured variable. These findings and results of studies done over the past 50 years indicate that salt-dependent hypertension is controlled by many factors and is not a strict correlate of salt intake.
Hypertension 1989 Jun
PMID:Corcoran lecture: the case for or against salt in hypertension. Arthur Curtis Corcoran, MD (1909-1965). Tribute and prelude to Corcoran Lecture of 1988. 266 26

Dahl Salt Sensitive (DS) rats rapidly develop high blood pressure when exposed to a high-salt diet. Recent studies suggest that DS rats have poorly functioning baroreceptor afferents and baroreflexes even when salt intake is restricted. This study examines baroreceptor pressure- and mechano-transduction in DS, Dahl Resistant (DR), and Sprague-Dawley (SD) rats during low- and high-salt conditions. Single unit, regularly discharging baroreceptors were studied using an in vitro aortic arch-aortic nerve preparation. Pressure thresholds and suprathreshold pressure sensitivities were determined from responses to slow ramps of pressure. Pressure-diameter relations measured in each rat were used to transform pressure threshold and pressure sensitivity values to their mechanical equivalents in terms of aortic wall strain. A total of 407 unit baroreceptors were studied from 49 rats. Tail systolic blood pressures were significantly higher only in DS during high salt. Pressure threshold was similar for all groups on low salt. Exposure to a high-salt diet increased the mean pressure threshold for all three groups. Pressure threshold for high-salt diet was highest in DS and lowest in DR. Pressure sensitivities were lowest in DS and highest in DR on low salt. High salt had no significant effect on pressure sensitivity. The differences in threshold apparent when expressed in terms of pressure were eliminated by conversion to their mechanical equivalents (strain threshold and strain sensitivity). The results suggest that baroreceptors in the two Dahl rat strains represent two extremes from normal baroreceptor function. DS tend to be less pressure responsive than normal (SD), and DR tend to be somewhat more responsive to pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:High-salt diet elevates baroreceptor pressure thresholds in normal and Dahl rats. 270 32

Dietary sodium and the myocardial alpha 1-receptor have been implicated in the hypertrophic response of myocardial tissue. Alterations in sodium homeostasis have been demonstrated to influence sympathetic nervous function, centrally and peripherally. In this investigation, we have examined the effect of dietary sodium on the development of myocardial hypertrophy; and the role of sympathetic neuroeffector mechanisms in the hypertrophic response. Studies were performed in three groups of uninephrectomized rats: A-regular diet; B-1% saline/regular diet; C-1% Saline/doca/regular diet. Groups A and B did not develop systemic hypertension (SHT). Saline treatment increased heart weight and the density of surface alpha 1-receptors; myocardial norepinephrine (NE) was reduced. Group C developed SHT. Heart weight was greatest in Group C; and myocardial NE was severely depleted. Downregulation of myocardial alpha 1-receptors, a finding consistent with the hyperadrenergic state, was observed in Group C. Our results suggest dietary sodium may modulate hypertrophic response in myocardial tissue, by altering sympathetic neuroeffector mechanisms.
 ...
PMID:Myocardial hypertrophy: the effect of sodium and the role of sympathetic nervous system activity. 283 63

Addition of dietary calcium exerts antihypertensive effects in spontaneously hypertensive rats (SHR), which can be intensified by a parallel increase of sodium in the diet. It was of interest to what extent calcium addition to a high salt diet might modify salt-dependent hypertension in salt-sensitive Dahl rats (S/JR). Groups of six S/JR and seven salt-resistant Dahl rats (R/JR) received, when 4 weeks old, diets containing differing sodium and calcium concentrations. A further group received a calcium-enriched diet supplemented with the calcium antagonist nitrendipine. A higher calcium content in the diet did not change the effects resulting from an 8% NaCl diet, with regard to heart weight and laboratory parameters. Salt-sensitive Dahl rats on a calcium-enriched NaCl diet had a more rapid development of hypertension than S/JR on a normal calcium/high salt diet or S/JR on a calcium-enriched diet supplemented with nitrendipine. Salt-resistant Dahl rats did not differ significantly with regard to blood pressure development on any diet. In contrast to the effect in SHR, dietary calcium has therefore no antihypertensive effect on salt-induced hypertension. A moderate increase in the calcium content of the diet does not alter blood pressure lowering effects of calcium antagonists.
 ...
PMID:Influence of a calcium-enriched diet on salt-induced hypertension in rats. 285 58

We evaluated the response to salt restriction in hypertensive patients receiving drugs. By restricting their salt intake to less than 80 mmol of sodium per day for 3 months, 50% of patients reaching goal compliance were able to discontinue diuretics. The literature also reveals responses to a low salt diet. Salt restriction augmented the hypotensive effect of chlorthalidone in two investigations, but not in another, and the hypotensive effect of beta-blockers in three trials. Sodium intake of 10 mmol/day caused a much greater decrease in blood pressure in response to a single dose of captopril than did a sodium diet of 200 mmol/day. In patients receiving various fixed regimens for 2 months, salt restriction decreased blood pressure in all but those receiving calcium blockers. A single dose of nifedipine lowered blood pressure more in patients receiving 350 mmol of sodium per day than in the same patients given 150 or 10 mmol/day. Verapamil for 3 days was more effective in patients receiving 212 mmol of sodium per day than in the same subjects receiving 9 mmol/day. Nitrendipine caused a greater decrease in diastolic blood pressure in patients who did not reduce salt intake compared to those who did. Salt restriction appears useful in salt-sensitive patients who receive beta-blockers, diuretics, converting enzyme inhibitors, or centrally acting drugs. Calcium channel entry blockers may not require salt restriction to maximize their effect.
Hypertension 1988 Feb
PMID:Review of salt restriction and the response to antihypertensive drugs. Satellite symposium on calcium antagonists. 289 58

Renal damage is systemic hypertension has traditionally been related to an ischemic glomerular injury secondary to arteriosclerosis and arteriolosclerosis of preglomerular vessels. The use of micropuncture techniques with histopathologic studies have suggested non ischemic mechanisms of renal damage in systemic hypertension. Indeed in experimental models of hypertension which include DOCA-Salt, Goldblatt hypertension or genetic hypertension, the development of glomerular damage is associated with hyperfiltration secondary to increases in flow and pressure to the glomerular capillary. Hyperfiltration as a mechanism of renal damage in human systemic hypertension has not been established. Recent studies from our group have demonstrated lack of renal functional reserve in patients with systemic hypertension, reserve which is reestablished after 3 days of antihypertensive treatment. These data suggest therefore the presence of hyperfiltration as a possible mechanism of renal damage in patients with essential hypertension.
 ...
PMID:[Is the kidney lesion caused by hypertension really ischemic?]. 294 50

The cardiac atria are known to play a role in blood volume homeostasis, secreting a peptide that induces a potent natriuresis and diuresis. This peptide is atrial natriuretic factor (ANF), and its primary site of storage is within atria-specific granules found in atrial cardiocytes. Since salt loading results in an increase in circulating levels of ANF, our aim was to determine if the atria-specific granule population in the cardiocytes of Dahl rats would decrease accordingly. To this end, the fractional volume of the atria-specific granules was determined by ultrastructural morphometric analysis in the Dahl salt model of hypertension. This analysis was performed on the right atria of Dahl Salt-resistant (DR) and salt-sensitive (DS) rats fed either a low-salt (0.4%) or high-salt (8%) diet for 12 weeks prior to sacrifice. DR and DS rats fed a low-salt diet had significantly reduced plasma sodium levels and osmolalities, and a significantly lower mean arterial blood pressure than did rats fed a high-salt diet. The fractional volume of atria-specific granules was significantly lower in salt-loaded DR (P less than 0.01) and DS (P less than 0.025) rats than in their respective low-salt controls. This significant decrease in atrial granules corresponds to the reported decrease in the storage of atrial ANF in salt-loaded rats, and provides a morphological verification of the biochemical studies. Moreover, these results, in combination with a growing body of physiological data, lend support to the hypothesized role of ANF in the regulation of water-electrolyte balance, which may play an important role in cardiovascular pathophysiological states related to hypertension.
 ...
PMID:Effects of salt loading on the fractional volume of atria-specific granules in Dahl salt-sensitive and salt-resistant rats. 295 6

Likelihood analysis was used to test for evidence that an allele at a major locus elevates rates of sodium-lithium countertransport (SLC) in a sample of 1,989 members of 89 Utah pedigrees. The pedigrees were ascertained through two or three sibs who died of stroke before age 74 years (stroke pedigrees), through hypertensive and normotensive probands of the Salt Lake Center of the Hypertension Detection and Followup Program (HDFP pedigrees), or through men who suffered a myocardial infarction before age 55 years (coronary pedigrees). Major-locus inheritance could be rejected in the total sample; transmission probability estimates of tau1 = .972, tau2 = .520, tau3 = .185 differed significantly from Mendelian transmission specified by tau1 = 1, tau2 = 1/2, tau3 = 0. However, heterogeneity between ascertainment groups was significant (chi2(18) = 40.06, P less than .01) and justified analysis within subsets of the sample. In the stroke pedigrees, evidence of major-locus inheritance was not found; polygenic heritability was estimated as .647. In the HDFP pedigrees, estimates of tau1 = .987, tau2 = .430, tau3 = .506 differed significantly from Mendelian transmission; the inferred model consisted of a mixture of two distributions incompatible with both Mendelian and environmental transmission but compatible with polygenic inheritance within distributions. In the coronary pedigrees, the hypothesis of Mendelian transmission could not be rejected. In the coronary pedigrees, the evidence supported an incompletely recessive allele with a frequency of .227 which elevated the level of SLC to a mean of .530 mmol/liter RBC/h.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hypertension and sodium-lithium countertransport in Utah pedigrees: evidence for major-locus inheritance. 316 87


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