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

The purpose of this study was to identify microvascular alterations that could contribute to increased peripheral vascular resistance in the Dahl salt-sensitive rat with salt-induced hypertension. Intravital microscopy was used to study the spinotrapezius muscle arteriolar network in anesthetized salt-sensitive rats fed either a high salt (7% sodium chloride) or low-normal salt (0.45% sodium chloride) diet for 4 weeks. Age-matched Dahl salt-resistant rats on high and low-normal salt diets served as controls. The high salt diet had no effect on arterial pressure in salt-resistant rats but increased arterial pressure in salt-sensitive rats. Mean resting diameter of arcade arterioles in salt-sensitive rats on high salt diet was reduced by 25% compared with salt-sensitive rats on low salt or salt-resistant rats on either diet. After abolition of vascular tone with 10(-3) M adenosine, arcade diameters were comparable in all groups. No difference among groups was found in either resting or passive diameter of the more distal transverse arterioles. Measurement of vessel lengths and numbers in cleared muscle specimens revealed no differences among groups in the anatomic density of either arcade or transverse arterioles. These data suggest that a reduction in the resting diameter of arcade, but not transverse, arterioles may increase spinotrapezius muscle vascular resistance in hypertensive salt-sensitive rats. The similarity in vascular densities among groups indicates that structural rarefaction of arterioles does not contribute to any increase in spinotrapezius muscle resistance at this stage of salt-induced hypertension.
Hypertension 1990 Apr
PMID:Effect of dietary salt on the skeletal muscle microvasculature in Dahl rats. 231 23

It has been reported that both sodium and chloride ions must be ingested to induce the elevated blood pressure of deoxycorticosterone acetate (DOCA)-salt-sensitive hypertension. This study was designed to determine the separate roles of the sodium and chloride ions in the altered hemodynamics underlying the high blood pressure. DOCA pellets (75 mg) were implanted in uninephrectomized rats and the animals were then fed one of four diets: (i) high sodium chloride, (ii) high sodium-low chloride, (iii) high chloride-low sodium, or (iv) low sodium chloride. Blood pressures were measured weekly by tail-cuff plethysmography for 5 weeks and the animals were then subjected to a terminal experiment to measure cardiac output by thermodilution technique, renal blood flow by electromagnetic flow probe, and direct arterial pressure. Blood pressure in the DOCA-high NaCl group was significantly greater (P less than 0.05) compared with that of the DOCA-low NaCl group (160 +/- 3 mm Hg vs 124 +/- 2 mm Hg, respectively) at 5 weeks after treatment; all other groups were not significantly different from the DOCA-low NaCl group. Cardiac output was significantly greater in DOCA-treated rats consuming diets high in sodium (44 +/- 2 ml/min/100 g) or sodium chloride (40 +/- 2 ml/min/100 g) compared with animals consuming low sodium chloride (31 +/- 2 ml/min/100 g; P less than 0.01 for each comparison). Direct intraarterial blood pressure and renal blood flow were used to calculate renal vascular resistance. Renal vascular resistance was increased in those DOCA-treated rats consuming diets high in chloride (42 +/- 3 mm Hg/ml/min/100 g) and high sodium chloride (54 +/- 3 mm Hg/ml/min/100 g) compared with rats consuming low sodium chloride (30 +/- 3 mm Hg/ml/min/100 g; P less than 0.01 for each). It appears that elevations in cardiac output are associated with increased dietary sodium and act in synergy with the elevations in renal vascular resistance associated with increased dietary chloride. Increases in both cardiac output and renal vascular resistance are involved in the maintenance of elevated blood pressure in the DOCA-salt-sensitive model of hypertension.
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PMID:Separate hemodynamic roles for chloride and sodium in deoxycorticosterone acetate-salt hypertension. 235 92

It has already been emphasized that salt-dependent hypertension might be especially sensitive to calcium antagonists, and it has recently been shown that binding at different receptor types might be altered by dietary sodium chloride. Therefore, it was of interest to find the extent to which the specific membrane-associated dihydropyridine (DHP) receptors are influenced by salt loading and/or nitrendipine treatment. Groups of 10-12 salt-sensitive (S/JR) or salt-resistant (R/JR) Dahl rats and spontaneously hypertensive rats (SHRSP) or normotensive Wistar-Kyoto rats (WKY) received diets containing low (0.4%) or high (8%) NaCl for 21 days; treated animals received 300 ppm nitrendipine additionally with the diet. Blood pressure of R/JR and WKY did not differ markedly on the different diets, whereas in hypertensive rat strains, salt loading increased blood pressure after 3 weeks. High salt resulted in an increased number of cardiac DHP receptors in SHRSP; the addition of nitrendipine enhanced DHP receptor capacity in the heart and brain membranes of both strains (SHRSP and S/JR). No major changes in affinity were observed. Augmentation in the number of DHP receptors as analyzed in a follow-up interim observation study on SHR occurred more rapidly in heart than in brain tissue. It can be concluded that an altered number of the DHP receptor sites, and not changes in affinity, might be essential during treatment with calcium antagonists. The DHP receptor sites, and not changes in affinity, might be essential during treatment with calcium antagonists. The DHP receptor density can be modified by high salt intake, as shown in salt-loaded SHRSP.
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PMID:Effects of salt loading and nitrendipine on dihydropyridine receptors in hypertensive rats. 245 36

Gordon's syndrome was diagnosed in a 19-year-old woman who had hypertension, hyperkalemia and hyperchloremic acidosis. In family screening, hyperkalemia and hyperchloremic acidosis were also found in the patient's mother and brother. The proband and her brother were studied and showed normal glomerular function with normal renal sodium conservation and urine acidification mechanisms. The levels of plasma aldosterone were normal in both subjects. The renin activity was low in the proband but normal in the brother. Both the basal and the volume-stimulated plasma concentration of atrial natriuretic peptide was low in the two patients. As compared with controls, the kaliuretic response to infusion of sodium chloride was not decreased in the patients. Hydrochlorothiazide promptly corrected the acidosis and the hyperkalemia as well as normalized the raised blood pressure of the proband. We suggest that a deficiency of atrial natriuretic peptide rather than an unusual avidity for sodium chloride reabsorption by the renal tubules plays a significant pathogenetic role in Gordon's syndrome.
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PMID:A deficient response of atrial natriuretic peptide to volume overload in Gordon's syndrome. 252 4

Studies were carried out in normal male subjects (n = 6, age 20-35 years) to determine the interaction of angiotensin II and plasma sodium on aldosterone secretion. These relations were quantified by elevation of plasma sodium with an infusion of 5% sodium chloride (4 ml/kg/30 min i.v.) with measurements of plasma aldosterone, atrial natriuretic factor (ANF), and arginine vasopressin (AVP) over 3 hours. Two hours before sodium chloride infusion, an intravenous infusion of angiotensin II was begun at 0.5 or 5.0 ng/kg/min and continued throughout the study. Plasma potassium was maintained constant by the addition of potassium to the infusate. NaCl/KCl infusion raised plasma sodium 4 meq/l with no decreases of plasma potassium. Plasma aldosterone averaged 7 +/- 1.8 ng/dl before NaCl infusion in subjects infused with 0.5 ng angiotensin II and was not significantly reduced with sodium chloride infusion. Angiotensin II infused at 5 ng/kg/min resulted in average plasma aldosterone levels of 31 +/- 3.6 ng/dl, which sodium chloride infusion decreased to 16.6 +/- 1.3 ng/dl (p less than 0.05) in 60 minutes. Plasma aldosterone remained depressed for the remaining period of study. Plasma ANF increased from 40 to 60 pg/ml with sodium chloride infusion. We conclude that small physiological elevations of plasma sodium concentrations can signal substantial decreases of plasma aldosterone in normal human subjects in situations where plasma angiotensin II is moderately elevated. The precise mechanisms of these responses remain to be determined.
Hypertension 1989 Aug
PMID:Effect of plasma sodium on aldosterone secretion during angiotensin II stimulation in normal humans. 252

Cigarette smoke is linked to many pathologies and also affects a very important aspect of human physiology that is taste. In fact already in the past years, researchers have worked on this phenomenon and have come to the conclusion that smoke influences the perception of bitter taste. In our study we researched the detection and identification threshold in thirty smokers, for the citric acid, quinine, sodium chloride and saccharose, and it turned out that smokers suffer a raise in quinine identification and sodium chloride detection and identification threshold. On the basis of the results obtained with sodium chloride, a theory on hypertension etiopathogenesis is suggested.
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PMID:[Variations in the taste function of smokers]. 262 19

Recently, food intake in Japan has been characterized by an increase in fat intake, especially animal-fat intake and the maintenance of excess salt (sodium chloride) intake. It is generally accepted that the increase in fat intake is closely related to atherosclerosis, and excess salt intake is a high risk factor for the development of hypertension and cerebrovascular lesions. So far, in almost all reports, the increase in fat intake and excess salt intake have been studied independently, and there have been few reports on the combined effects of these two factors. Taking the above things into consideration, it would seem to be very interesting to investigate the effect of excess salt intake on lipid metabolism. In this paper, we studied the effects of excess salt intake on lipoprotein and apolipoprotein metabolisms, using stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Kyo: Wistar rats (WKY) as model animals. The results obtained were as follows: A significant increase in the concentration of serum total cholesterol (TC) was observed in SHRSP and WKY, when the rats were given a regular diet (CE-2, Clea Japan Inc.) and 1% sodium chloride solution (1% NaCl) as drinking water for 4 weeks. This was accompanied by a tendency toward increases in the concentrations of serum apolipoproteins in both strains. These results suggest that excess salt intake could accelerate the production of serum total lipoproteins in SHRSP and WKY, when the rats are fed a regular diet. Next, 1% NaCl and a high-fat and high-cholesterol diet (HFC diet) were simultaneously given to SHRSP and WKY for 6 weeks. The effects of simultaneous administration on lipoprotein and apolipoprotein metabolisms were compared with those of HFC feeding. One percent NaCl did not markedly affect hypercholesterolemia in WKY, while it induced more marked hypercholesterolemia in SHRSP that was associated with extreme elevations of serum TC and the atherogenic index (A.I.). This deleterious effect of 1% NaCl in SHRSP was due to drastic elevations of cholesterol contents in the very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) fractions. This was also associated with marked increases in apo B contents in the VLDL, IDL and LDL fractions and significant increases in apo E contents in the VLDL and IDL fractions. These results indicate that 1% NaCl induced much larger increases in serum atherogenic beta-lipoproteins in SHRSP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-fat and high-cholesterol diet--effects of salt intake on serum lipoprotein and apolipoprotein metabolism]. 263 85

Environmental stress increases renal sympathetic nerve activity and decreases urinary sodium excretion to a greater degree in conscious hypertensive rats (spontaneously hypertensive rat; deoxycorticosterone-sodium chloride, Dahl salt-sensitive) than normotensive control rats. The dependence of the antinatriuretic response to environmental stress on the renal sympathetic nerves is indicated by the finding that renal denervation prevents the response. Central nervous system beta 2- and alpha 2-adrenoceptors mediated the renal sympathetic nerve activity and antinatriuretic responses to environmental stress in conscious spontaneously hypertensive rats. Increased renal sympathetic nerve activity and renal sodium retention may contribute to chronic stress hypertension.
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PMID:Effect of environmental stress on neural control of renal function. 264 27

In order to clarify the possible relationship between changes in blood pressure after salt loading, membrane sodium transport and renin profile, 19 patients with essential hypertension (8 patients with low renin hypertension and 11 patients with normal renin hypertension), admitted to our hospital, were studied. We also examined the correlation of changes in intracellular sodium concentration after salt loading between erythrocytes and lymphocytes. After a control period of one week, all subjects were placed on a low salt intake for one week followed by one week of a high salt intake. Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Percent changes in intracellular sodium concentration in erythrocytes inversely correlated with those in ouabain sensitive sodium efflux rate constant and positively correlated with those in intracellular sodium concentration in lymphocytes. These results suggest that an increase in sodium chloride sensitivity of blood pressure in patients with low renin hypertension may be due to the inhibition of Na+-K+ pump in vascular smooth muscle cell membrane.
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PMID:Sodium chloride sensitivity, intracellular sodium concentration in erythrocytes and lymphocytes, and renin profile in essential hypertension. 265 38

It has been postulated that endogenously produced dopamine (DA) may play a role in the regulation of renal sodium excretion. In the present study, experiments were designed to test the hypothesis that acute volume expansion with isotonic sodium chloride stimulates the production of DA within the kidney, which in turn acts on specific DA1 receptors to promote sodium excretion. In pentobarbital-anesthetized rats, acute volume expansion over a period of 1 hour evoked a pronounced increase in urine output and urinary sodium excretion. These diuretic and natriuretic effects were not accompanied by any significant changes in blood pressure or heart rate. However, there was a significant elevation in central venous pressure and a transient rise in glomerular filtration rate. The natriuretic and diuretic response was accompanied by a significant increase in urinary DA excretion, and this effect was clearly dissociated from the rise in glomerular filtration rate. In a separate group of rats, the effects of acute volume expansion were studied in the presence of selective DA1 receptor antagonist SCH-23390 (50 micrograms/kg i.v. bolus; 10 micrograms/kg/min). During DA1 receptor blockade, there was a marked attenuation in the diuretic and natriuretic response throughout the period of volume expansion, when compared with that in the control group. The changes in central venous pressure and glomerular filtration rate were identical in the two groups. In another group of rats, the renal effects of exogenously administered DA were studied. DA (0.5 micrograms/kg/min) produced significant increases in urine output and urinary sodium excretion, without causing any alterations in blood pressure or glomerular filtration rate, suggesting a tubular site of action.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jun
PMID:Role of kidney dopamine in the natriuretic response to volume expansion in rats. 266 32


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