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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Besides the duration and severity of hypertension, several other factors have been shown to be related to left ventricular hypertrophy (LVH) in essential hypertension. The present study was conducted to examine the influence of salt sensitivity on LVH. Fifteen essential hypertensive ambulatory patients were submitted to a low-salt (30 mEq of Na/day for 7 days) and a high-salt (200 mEq of Na/day for 7 days) diet after 12 weeks on placebo. Daily urine collection was obtained during the whole study. After the placebo period, all patients were submitted to a complete clinical and laboratory investigation that included an echocardiogram (M-mode and two-dimensional). Five patients were salt-sensitive (mean blood pressure (BP) increase from the seventh day of the low- to the seventh day of the high-salt diet greater than 10%). No differences in weight, sex ratio, and duration of hypertension were obtained between salt-sensitive and -resistant patients. The initial BP was higher in the salt-sensitive patients. However, the difference was small and without statistical significance. The left ventricular weight was higher in the salt-sensitive than in salt-resistant patients (148 +/- 51 vs. 109 +/- 32 g/m2, p less than 0.05). The left ventricular end-diastolic diameter was also higher in the salt-sensitive patients (50 +/- 10 vs. 43 +/- 6 mm, p less than 0.05). The interventricular septum and posterior wall thicknesses were higher in salt-sensitive patients, although they did not reach statistical significance. In conclusion, salt-sensitive essential hypertensive patients are at a higher risk to develop LVH.
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PMID:Left ventricular hypertrophy is more marked in salt-sensitive than in salt-resistant hypertensive patients. 171 58

Primary or secondary activation of immune mechanisms has been implicated in the pathogenesis of many forms of hypertension. Changes in serum immunoglobulin levels, alterations in both humoral and cellular immune functions, and inherited abnormalities of the complement system have been identified in patients with essential hypertension. In addition, many models of spontaneous hypertension (such as the Okamoto and Lyon strains of hypertensive rats and the hypertensive New Zealand Black mouse) have identifiable abnormalities in immune function that are associated with their hypertensive disease. Other models (such as partial renal infarct hypertension, post-mineralocorticoid-salt hypertension, and hypertension induced by repeated injections of angiotensin II) also may have primary or secondary immunologic factors contributing to their etiology. Although there is a strong association between alterations in immune function and hypertension, the specific immunologic mechanisms that contribute to the pathogenesis of hypertension are not known. Therefore, further investigation will be necessary to elucidate these mechanisms.
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PMID:The immune system and hypertension. 173 Apr 53

We examined 174 subjects (82 men and 92 women) with essential hypertension to determine whether gender played an important role in the association of blood pressure (BP) familial disposition, and hypertension. To evaluate the salt sensitivity of BP, we measured changes in blood pressure after restricting salt intake from about 15 g/day to less than 3 g/day. The familial disposition to hypertension was categorized into four groups according to the presence or absence of hypertension in the father, mother, and siblings. If none, one, two, or three family members had hypertension, they were assigned the FH(-), FH(+), FH(++), and FH( ) groups, respectively. Only in women did the FH(-) group show a significantly smaller blood pressure reduction than that of the other groups. The mean BP reduction in the four groups was 4.1 +/- 1.9, 8.5 +/- 1.1, 10.1 +/- 1.5, and 11.2 +/- 2.8 mm Hg (mean +/- SEM), respectively. This difference in BP reduction was not observed in men. Multiple regression analysis, using percent changes in mean BP as the dependent variable and other factors as independent variables, also showed a significant partial correlation coefficient for familial disposition to hypertension only in women. Thus, the relationship between salt sensitivity and familial disposition to hypertension differed according to gender. This difference may provide an important insight into the hereditary nature of hypertension.
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PMID:A gender difference in the association between salt sensitivity and family history of hypertension. 173 28

One-kidney, one-clip hypertension (1-K, 1-C HT) is initiated by increased preglomerular resistance which decreases nephron perfusion and causes several intrarenal changes that lead to increased mean arterial pressure (MAP). Elevated MAP serves to return nephron perfusion and sodium excretion to normal, so that fluid intake and output are balanced. Increased MAP usually occurs through volume homeostasis mechanisms that initially raise cardiac output and later elevate total peripheral vascular resistance via autoregulatory adjustments. However, if adequate volume is unavailable because of sodium restriction, sustained activation of the renin-angiotensin system increases blood pressure sufficiently to restore nephron perfusion. Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Similarities exist between 1-K, 1-C HT and low-renin essential hypertension (LRHT). In both cases, renal-pressure natriuresis is shifted to higher levels and there are marked increases in preglomerular resistance that necessitate increased MAP to maintain sodium balance. However, in 1-K, 1-C HT, there is a parallel shift of pressure natriuresis with little or no change in the slope of this curve, similar to that found in the normal-renin essential hypertension. In LRHT the slope of pressure natriuresis is decreased, indicating that blood pressure is much more salt sensitive than normal. Another difference is that PRA is low compared to normal PRA in 1-K, 1-C HT after compensatory increases in MAP. There is also no indication of glomerular membrane damage in 1-K, 1-C HT, whereas LRHT may have significant glomerulopathy, especially as hypertension progresses. These differences suggest that there may be additional factors besides preglomerular vasoconstriction involved in the etiology of LRHT. One possible factor is a reduction in nephron number in LRHT. Decreased functional nephrons would lead to glomerular hyperfiltration and increased distal tubular flow rate in the remaining nephrons, causing decreased PRA and eventually glomerular damage. Increased fractional sodium reabsorption, particularly in distal tubular segments, could also contribute to decreased PRA and cause blood pressure to be salt sensitive. These abnormalities, along with preglomerular vasoconstriction, may explain many of the characteristics of LRHT.
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PMID:Renal function in one-kidney, one-clip hypertension and low renin essential hypertension. 174 89

African-Americans with essential hypertension are more prone to the development of renal failure and are frequently salt-sensitive as well. Because alterations of intrarenal hemodynamics are important in the progression of renal disease and because salt-sensitive animal models with hypertension manifest a greater propensity to develop glomerulosclerosis in association with a rise in glomerular capillary pressure, we tested whether the renal hemodynamic adaptation to high dietary Na+ intake differs in salt-sensitive and salt-resistant hypertensive patients. We studied 17 black and nine white patients with essential hypertension who were placed on a low Na+ diet (20 meq/day) for 9 days, followed by a high Na+ diet (200 meq/day) for 14 days. During the last 4 days of each diet regimen, they received 30 mg/day of slow-release nifedipine. Eleven blacks were salt-sensitive, and all whites were salt-resistant. During the low Na+ diet period, salt-sensitive and salt-resistant patients had similar mean arterial pressure, glomerular filtration rate, effective renal plasma flow, and filtration fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal renal hemodynamics in black salt-sensitive patients with hypertension. 174 61

An intensive 7-week relaxation therapy was evaluated in a sample of unmedicated borderline hypertensive men. All subjects were provided state-of-the-art medical information regarding changes known to affect hypertension favorably, e.g., lower salt intake and regular exercise. In addition, relaxation subjects were trained in muscle relaxation that entailed audiotaped home practice. As predicted, relaxation combined with hygiene lowered blood pressure more than did hygiene alone. Neither treatment favorably affected a paper-and-pencil measure of anger but relaxation did lower anger-hostility on a new cognitive assessment procedure, Articulated Thoughts in Simulated Situations (ATSS). Moreover, ATSS anger-hostility reduction was correlated with blood pressure or heart rate reductions, for all subjects and especially for those in the Relaxation condition. This represents the first clinically demonstrated link between change in a cognitive variable and change in cardiovascular activity. Finally, results were especially strong in subjects high in norepinephrine, suggesting its importance in essential hypertension.
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PMID:Relaxation, reduction in angry articulated thoughts, and improvements in borderline hypertension and heart rate. 174 9

Traditional discussion of the etiology of essential hypertension has often included renal, neural, familial, and genetic theories as well as dietary salt intake. Recent findings suggest a prominent role for abnormal cation metabolism, impaired membrane transport systems, hyperinsulinemia, and psychosocial and behavioral factors. These recent advances in hypertension research suggest that a variety of interrelated factors lead to common pathways for the development and maintenance of hypertension and that a single cause of essential hypertension is less likely. A survey of these hypotheses is presented, and those that seem most likely to lead to common pathways for hypertensive phenomena or underlie established ethnic differences in hypertension are discussed in detail. The future application of molecular genetics and biochemistry of vascular and cardiac myocyte growth to hypertension epidemiology holds great promise for understanding the etiology and course of essential hypertension.
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PMID:Research issues and ethnic implications in essential hypertension. 181 21

Forty-one patients with essential hypertension were classified as salt-sensitive (SS) or non-salt-sensitive (NSS) from the changes in mean blood pressure (MBP) with alterations in sodium intake from 35 mmol (low-sodium) to 250 mmol/day (high-sodium). Whereas there was no difference in plasma levels of atrial natriuretic factor (ANF) on a normal-sodium diet (120 mmol) between the 2 groups, the degree of increase in the plasma ANF level between the low- and high-sodium intake was significantly greater in NSS than in SS (p less than 0.001). In addition, the urinary sodium excretion on a high-sodium diet was smaller in SS than in NSS. There was a significant positive correlation between the plasma ANF and MBP after the high-sodium intake in both SS (r = 0.67, p less than 0.01) and NSS (r = 0.60, p less than 0.01); however, the relation of plasma ANF to MBP shifted apparently to a lower level in SS compared with NSS. These findings not only indicate that there exists a hyporesponsiveness of ANF release by the heart of SS patients in response to high-sodium loading, but also imply that such a response contributes to blood pressure-elevating mechanisms due to sodium loading in this type of human hypertension.
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PMID:Attenuated release of atrial natriuretic factor due to sodium loading in salt-sensitive essential hypertension. 182 68

The pathogenesis of essential hypertension may possibly involve a deficiency in, or a decreased response to, endogenous vasodilator and natriuretic factor(s). Searching for hereditary or familial defects, it is plausible to evaluate blood pressure (BP) regulating factors in (yet) normotensive offspring of hypertensive parents (OHyp), some of whom are in fact in a stage of prehypertension. Studies by our group demonstrated that compared with healthy offspring of normotensive parents, OHyp have plasma atrial natriuretic (ANF) factor levels that are unaltered on a low salt intake but often fail to increase normally in response to a high salt intake. Plasma levels of cyclic GMP, the presumed second messenger of ANF, also may tend to be decreased in certain OHyp. On the other hand, renal excretory responses of cyclic GMP and electrolytes to ANF infused in "physiological" dose were unchanged in some OHyp tested so far. In borderline to moderate, uncomplicated essential hypertension, plasma ANF levels are often "normal." This may be inappropriately low relative to the existing BP, although the relationship of circulating ANF to atrial pressures in essential hypertension remains to be clarified. A conversion to higher plasma ANF values may occur with cardiac complications such as left ventricular hypertrophy, enlargement, dysfunction, or overt heart failure. Acute or short-term elevation of circulating ANF within the physiological and pathophysiological range by ANF infusion produces an exaggerated natriuresis and lowers BP in essential hypertensive patients. We postulate a syndrome of ANF deficiency, characterized by an impaired response of circulating ANF to high salt intake and by low cyclic GMP levels in certain yet normotensive offspring of essential hypertensive parents and by inappropriately "normal" plasma ANF in some patients with uncomplicated essential hypertension. At the stage of prehypertension, a disturbance in the ANF - cyclic GMP pathway may be expressed primarily at the circulatory rather than at the renal level. Hypertension-prone humans also tend to have an exaggerated vascular reactivity to norepinephrine. Whether the two disturbances may be interrelated is presently unknown. Both defects may potentially predispose to the development of essential hypertension. Relative ANF deficiency, an enhanced natriuretic response to ANF, and a sustained antihypertensive effect of infused ANF may represent a rational basis for treatment of essential hypertension with agents that activate the ANF system.
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PMID:Developing essential hypertension: a syndrome involving ANF deficiency? 183 26

Circulating levels of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (C16PAF) in human subjects were measured by gas chromatography/mass spectrometry using negative ion chemical ionization. The mean (+/- S.D.) circulating C16PAF levels in patients with essential hypertension (18.1 +/- 5.3 pg/mL, n = 16) were not significantly different from those in normotensive subjects (17.2 +/- 7.2 pg/mL, n = 14). During a salt balance study, high salt intake (20 g/day) significantly increased the circulating level of C16PAF, and changes in circulating C16PAF significantly and positively correlated with changes in mean arterial blood pressure (r = 0.47, p less than 0.05). Changes in C16PAF also correlated with changes in creatinine clearance (r = 0.55, p less than 0.05), but did not correlate with changes in plasma sodium concentration, plasma chloride concentration and plasma volume. An intravenous injection of 50 micrograms of human atrial natriuretic peptide (hANP) decreased circulating C16PAF levels from 20.0 +/- 2.7 to 13.9 +/- 2.4 pg/mL of blood (n = 10, p less than 0.01) in healthy subjects. The data appear to indicate that C16PAF levels are changed by salt intake-induced mild increase in blood pressure, and that hANP may be an endogenous factor which lowers circulating C16PAF.
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PMID:Studies on the role of platelet-activating factor in blood pressure regulation. 184 Feb 77


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