Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of atrial natriuretic peptide (ANP) were measured in outpatients with borderline hypertension (n = 15) and essential hypertension (n = 13) and in normotensive subject (n = 11). There were no significant differences among the three groups in age, serum protein, albumin, or electrolyte levels, plasma renin activity (PRA), or plasma concentrations of aldosterone and cortisol. The plasma ANP levels in the normotensive, borderline hypertensive, and essential hypertensive subjects were 36 +/- 6 pg/ml (mean +/- S.E.), 64 +/- 11 pg/ml, and 82 +/- 14 pg/ml, respectively. The levels in the essential hypertensive subjects were significantly (p less than 0.05) higher than those in the normotensives. In both borderline and essential hypertensives (n = 28), the plasma ANP levels were significantly correlated positively with systolic blood pressure (r = +0.385, p less than 0.05), and negatively with PRA (r = -0.484, p less than 0.05) and serum total calcium (r = -0.516, p less than 0.01). These results suggest that the elevation of circulating ANP in hypertensives is involved in the pathogenesis of hypertension.
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PMID:Plasma levels of atrial natriuretic peptide in patients with borderline and essential hypertension. 296 4

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.
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PMID:Response of atrial natriuretic peptide to acute saline loading in essential hypertension. 297 45

Tiodazosin, a new antihypertensive, resembles prazosin in structure and alpha-adrenergic-blocking activity, and it also exerts a direct vasodilator effect. We evaluated its long-term hemodynamic and systemic effects in patients with essential hypertension. Our data show that after 10 wk of therapy with tiodazosin, 7 of our 10 patients had significant reduction in intra-arterial mean blood pressure as a result of a fall in systemic vascular resistance. Heart rate, cardiac output, and plasma volume did not change. Systemic effects were minor and included a gain in weight and a reduction in hemoglobin, hematocrit, platelet count, serum protein, albumin, bilirubin, and specific gravity of urine. No patient initially developed orthostatic symptoms after the first dose, but there were transient episodes of light-headedness in three patients, palpitations in two, increased urinary frequency in one, and drooping of eyelid in another during the trial period. One patient developed profound orthostatic hypotension, which could be attributed to the drug. Because of such side effects and the failure to lower blood pressure in 30% of patients with essential hypertension, tiodazosin appears to have several important drawbacks and little advantage over currently available antihypertensives.
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PMID:Effects of tiodazosin, a new antihypertensive, hemodynamics and clinical variables. 688 5

1. To explore the effect of nephritis on development of genetic hypertension we immunized 10-week-old spontaneously hypertensive rats with purified rat kidney brush-border antigen. This induces Heymann nephritis (autologous immune complex nephritis), which does not elevate blood pressure in normal rats. 2. Nephritis developed in 11 of the 12 immunized animals, and systolic blood pressure rose to a significantly higher level than in the non-immunized spontaneously hypertensive rats within 4 weeks. Blood pressure remained higher in the immunized rats at 17 weeks, heart weights were greater, but creatinine clearance remained unchanged. 3. At 6 weeks, urinary sodium excretion was greater in the immunized spontaneously hypertensive rats, whereas at 17 weeks, sodium excretion was decreased in these animals along with reduced serum protein concentration, packed cell volume and plasma renin activity, as compared with that of the controls. 4. Development of hypertension in nephritic rats, therefore, appeared unrelated to sodium excretion; signs of volume expansion emerged later. 5. Acceleration of the development of spontaneous hypertension by Heymann nephritis, also leading to sustained higher blood pressure levels than in spontaneously hypertensive rats, offers a new approach to experimental study of immune mechanisms behind acceleration of pre-existing hypertension. This may have important bearings on essential hypertension as well.
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PMID:Aggravation of hypertension in spontaneously hypertensive rats by Heymann nephritis. 723 40