Gene/Protein Disease Symptom Drug Enzyme Compound
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Erythrocyte membrane Na+,K+-ATPase activity was measured using a bioluminescence technique in 28 hypertensive patients (24 with essential hypertension, 2 with renovascular hypertension and 2 with hypertension secondary to primary hyperaldosteronism) and in 28 normotensive control subjects matched for age and sex. Erythrocyte Na+,K+-ATPase activity was significantly reduced in the patients with essential hypertension (130.9 +/- 11.4 vs. 186.6 +/- 19.5 nmol ATP/mg prot per h; mean values +/- SEM; p less than 0.05) and in the patients with secondary hypertension. A significant negative correlation was found between erythrocyte Na+,K+-ATPase and systolic blood pressure (r = -0.603; p less than 0.01), but not between Na+,K+-ATPase and plasma renin activity or plasma aldosterone levels. These data confirm the findings of a number of previous studies reporting reduced activity of erythrocyte Na+,K+-ATPase possibly related to the presence of a circulatory inhibitor of sodium pump. The method, based on ATP assay by bioluminescence, presents a high degree of specificity as well as simple, rapid execution.
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PMID:Measurement by bioluminescence technique of erythrocyte membrane Na+,K+-ATPase activity in hypertensive patients. 303 52

Chromogranin A is the major catecholamine storage vesicle soluble protein costored and coreleased by exocytosis with catecholamines. Immunoreactive chromogranin A circulates in human plasma, where it may reflect changes in exocytotic sympathoadrenal activity. We measured plasma chromogranin A concentration in normotensive control subjects as well as in untreated essential (primary) hypertensive subjects and subjects with several varieties of secondary hypertension. Plasma chromogranin A concentration was higher in subjects with essential hypertension (n = 32) than in normal controls (n = 18; 198 +/- 32 versus 129 +/- 12 ng/ml [mean +/- SEM]; p less than 0.05), and was also elevated in subjects with hypertension secondary to renal parenchymal disease (n = 9; 192 +/- 36 ng/ml; 0.05 less than p less than 0.1) and those with pheochromocytoma (n = 11; 1614 +/- 408 ng/ml; p less than 0.01). In essential hypertensive subjects (n = 5), short-term suppression of sympathetic outflow with oral guanabenz (4 mg) reduced plasma chromogranin A concentration within 30 to 60 minutes, while the blood pressure response was more gradual and was maximal at 3 hours. The results suggest that plasma chromogranin A is, at least in part, under neural control and that there may be an excess of exocytotic sympathoadrenal activity in essential hypertension. These initial studies are now being expanded to larger subject groups.
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PMID:Plasma chromogranin A. Initial studies in human hypertension. 399 34

Lii-Nao countertransport was measured in red blood cells of 58 normotensive subjects (27 females and 31 males), 60 patients with essential hypertension (26 females and 34 males), and in 28 with secondary hypertension (19 females and 9 males). The mean values (+/- SEM) expressed as mmol Li (1 red cells X hr)-1 were 0.18 +/- 0.02 (females) and 0.20 +/- 0.01 (males) in the control group, 0.34 +/- 0.04 (females) and 0.39 +/- 0.03 (males) in essential hypertension, 0.16 +/- 0.03 (females) and 0.19 +/- 0.02 (males) in secondary hypertension. The mean value of Lii-Nao countertransport obtained in essential hypertension was statistically different from those obtained in both normals (p less than 0.001) and patients with secondary hypertension (p less than 0.001). A negative correlation was found between age and Lii-Nao countertransport in normotensive males (r = - 0.648; p less than 0.001) but neither in normal females nor in patients with essential hypertension. A positive correlation (r = + 0.425; p less than 0.05) was found between plasma renin activity after intravenous furosemide and Lii-Nao countertransport in essential hypertension. These findings support the hypothesis of a characteristic cation transport across the red blood cell membrane of patient with essential hypertension which might be correlated with the plasma renin activity.
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PMID:Lithium-sodium countertransport in erythrocytes of normal and hypertensive subjects. Relationship with age and plasma renin activity. 634 62

A polypeptide fraction isolated from the urine of normotensive subjects lowers the blood pressure (BP) in a rabbit bioassay (mean BP decrease 33.8% +/- 0.6%, SEM). Patients with primary hypertension exhibit reduced or no activity (mean BP decrease 8.8% +/- 1.2%). In contrast, patients with secondary forms of hypertension show activity like normotensives (mean BP decrease 33.4% +/- 1.0%). The results of the bioassay in the two patient groups correlate well with the family incidence of hypertension (68% and 37% for primary and secondary hypertension respectively). Cases with borderline hypertension fall into two groups; a larger one with vasoactivity inthe bioassay and lower family incidence of hypertension; and a smaller group reacting like patients with primary hypertension. Only the latter group may represent an initial stage of primary hypertension. In normotensive children and young men, an inactive fraction was found in 31% and 28% respectively. These inactive groups had twice the family incidence of hypertension compared to the groups with vasoactivity. These results suggest the existence of a possible genetic marker of primary hypertension and may offer the possibility to detect the disease before its manifestation.
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PMID:Defect in the excretion of a vasoactive polypeptide fraction A possible genetic marker of primary hypertension. 694 42

Studies performed in experimental animals and in humans have documented that high blood pressure markedly impairs baroreceptor control of heart rate. Whether a similar impairment also characterizes baroreceptor control of sympathetic activity modulating peripheral vasomotor tone is still unknown. In 28 untreated essential hypertensive subjects [14 of moderate and 14 of more severe degree, age 51.6+/-2.4 and 52.6+/-2.1 years (mean+/-SEM)] and in 13 untreated secondary hypertensives (renovascular or pheochromocytoma, age 50.1+/-4.6 years), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Data were compared with those obtained in 15 age-matched normotensive control subjects. Muscle sympathetic nerve activity (bursts per 100 heart beats) showed a progressive and significant (P<.01) increase from normotension (40.3+/-3.3) to moderate (55.6+/-4.1) and more severe essential hypertension (68.2+/-4.1), paralleling the progressive increase in blood pressure values. In contrast, muscle sympathetic nerve activity was not increased in secondary hypertensives (40.5+/-6.7) despite blood pressure values similar to or even greater than those of severe essential hypertensives. In both essential and secondary hypertensives, baroreceptor-heart rate control was displaced toward elevated blood pressure values and markedly impaired compared with normotensive subjects (average reduction, 38.5%). In contrast, the sympathoinhibitory and sympathoexcitatory responses to baroreceptor stimulation and deactivation were displaced toward elevated blood pressure values but similar in all groups. Thus, sympathetic activation characterizes essential but not secondary hypertension. Regardless of its nature, however, hypertension is not accompanied by an impairment of baroreceptor modulation of sympathetic activity.
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PMID:Baroreflex control of sympathetic nerve activity in essential and secondary hypertension. 944 93