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

The response of plasma renin concentration [PRC] to Furosemide administration and orthostasis stimulation was studied in 9 healthy volunteers and in 30 patients with essential hypertension. The results indicate that Furosemide is unfit for stimulation of renin secretion owing to a relatively high frequency of paradoxical PRC decreases observed both in hypertensives and normotensives. On the other hand, orthostasis stimulation is a manoeuvre suitable also for screening of low renin hypertension.
 ...
PMID:The effect of furosemide stimulation on renin secretion and its application in examining activity of the renin-angiotensin system. 102 9

The chronic administration of prindolol in patients with essential hypertension resulted in the following: 1) a significant decrease in blood pressure and heart rate (with only the exception of the unchanged diastolic blood pressure after the stimulus of the seven-minute standing period), 2) a significant decrease of plasma noradrenaline concentrativn at rest and under orthostatic conditions, 3) a significant decrease of PRC at rest and an even more pronounced suppression of PRA after the stimulus of upright posture, 4)a significant decrease in total exchangeable sodium and 5) a concomitant significant increase in total body potassium even with an increase in body weight. These findings are not subject to easy interpretation. In particular, we cannot conclude which of the changed parameters plays the initial role in lowering blood pressure. A working hypothesis might presume that beta blocking agents inhibit central and/or peripheral sympathetic nervous activity. The results reduction in plasma renin concentration would in turn lead to a drop in aldosterone secretion rate indicated by the increase in potassium and decrease in sodiummour data would support such a sequence of events.
 ...
PMID:The effect of prindolol on plasma noradrenaline, plasma renin and sodium-potassium metabolism in patients with essential hypertension. 103 72

The influence of nifedipine treatment on plasma (PV) and extracellular fluid volume (ECV), the ratio of plasma volume to interstitial fluid volume (PV:IF), glomerular filtration rate (GFR), renal clearances of Na+ and K+, plasma concentrations of renin (PRC), angiotensin II (pANG II), aldosterone (pAldo), adrenaline (PA) and noradrenaline (PNA) were studied in 18 consecutive patients with essential hypertension. A 4-week placebo period was followed by a 6-week dose-titration period (period A). Thereafter the dose was kept constant for an additional 6 weeks (period B), the mean dose being 51 mg/day. As compared with placebo, diastolic blood pressure (DBP) decreased from 105 +/- 7 to 93 +/- 9 mmHg at the end of period B. Extracellular fluid volume, PV, and PV:IF were not significantly changed at the end of period A or B, neither in the group as a whole nor in a subgroup, who developed pedal oedema. After 2 weeks on nifedipine, PA as well as PNA increased slightly but returned to control values after 6 weeks of therapy. Plasma renin concentration, pANG II, pAldo and GFR did not change significantly. Renal sodium handling was also unchanged. It is concluded that long-term nifedipine therapy (exceeding 6 weeks) does not lead to activation of counter-regulatory mechanisms such as fluid retention, activation of the renin-angiotensin system and the adrenergic system. Renal function is unaffected by nifedipine.
 ...
PMID:The influence of nifedipine treatment on counter-regulatory mechanisms in essential hypertension. 285 9

The effects of changes in dietary intake of sodium and potassium on 125I-angiotensin II binding to platelets were studied in normal subjects. We also defined binding to platelets from patients with essential hypertension and subjects with normal blood pressure. Restriction of sodium intake in normal subjects resulted in a decrease in the number of receptor sites from 6.2 +/- 0.3 sites/cell to 4.1 +/- 0.4 sites/cell (P less than 0.01) but there were no changes in affinity as measured by the Kd. Over a range of sodium intakes from 15 to 200 mmol/day there was a negative correlation between plasma concentration of angiotensin II and receptor site concentration (rs = 0.57, P less than 0.01). Changes in dietary potassium did not affect angiotensin II binding. Angiotensin II binding was also measured in 10 patients with essential hypertension (mean blood pressure [BP] 178/107 mmHg, plasma concentrations of renin [PRC] 12 +/- 2 microU/ml and angiotensin [pANG] II 14 +/- 2 pg/ml) and 10 subjects with normal blood pressure (mean BP 112/74 mmHg, PRC 13 +/- 2 microU/ml, pANG II 13 +/- 2 pg/ml). In the hypertensive patients, binding capacity and affinity (Kd = 5.0 +/- 0.6 X 10(-10) M, 5.7 +/- 0.8 sites/cell) were similar to those in the normotensive subjects (Kd = 4.9 +/- 0.8 X 10(-10) M, 5.4 +/- 0.5 sites/cell). Changes in sensitivity to angiotensin II in essential hypertension may not be determined at receptor level. Angiotensin II receptors in platelets respond to changes in sodium intake like receptors in arterial muscle.
 ...
PMID:Regulation of platelet receptors for angiotensin II in man. 299 71