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

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.
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PMID:Hypertension and hyperkalaemia responding to bendrofluazide. 50 50

In a comparative study the influence of changes in dietary sodium intake on blood pressure, renal function, extracellular fluid volume, the renin-angiotensin-aldosterone system and plasma concentrations of arginine vasopressin, atrial natriuretic factor and cyclic guanosine monophosphate (GMP) was investigated in 12 patients with essential hypertension and in 10 normotensive controls. The subjects were studied after 4 days on a low (50 mmol/day), medium (180 mmol/day) or high (380 mmol/day) sodium intake. Renal sodium handling was assessed by simultaneous measurements of 51Cr-ethylenediaminetetraacetic acid (EDTA), lithium and sodium clearances. Identical values for the extracellular fluid volume, glomerular filtration rate and proximal and distal tubular resorption rates of sodium and water were found in the hypertensive patients and the controls at all three levels of sodium intake. In both groups, raising the sodium intake from low to high significantly increased 51Cr-EDTA and lithium clearance (an indirect measure of end-proximal fluid delivery), with intermediate values for the medium-sodium diet. The estimated values of fractional proximal and distal sodium resorption decreased when sodium intake was raised; the absolute proximal sodium resorption rate did not change, whereas the absolute distal sodium resorption rate as well as the extracellular fluid volume and sodium clearance increased. Blood pressure and the heart rate were unaffected by sodium intake. In both hypertensives and controls, plasma concentrations of active renin, angiotensin II and aldosterone decreased with increasing sodium intake, arginine vasopressin did not change, and atrial natriuretic factor and cyclic GMP increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normal renal tubular response to changes of sodium intake in hypertensive man. 215 2

Endothelin-1 is a novel endothelium-derived vasoconstrictive peptide. Using a highly specific and sensitive radioimmunoassay for endothelin-1, plasma levels of immunoreactive endothelin-1 were measured in 32 research subjects with normal renal function (21 normal subjects and 11 patients with essential hypertension), 24 patients with nondialyzed chronic renal failure, and 51 patients undergoing maintenance hemodialysis. Although there was no significant difference in plasma immunoreactive endothelin-1 levels among the three groups, patients with essential hypertension had significantly higher plasma endothelin-1 levels than normal subjects (2.29 +/- 1.09 vs. 1.41 +/- 0.50 pg/ml, p less than 0.025). When nondialyzed and hemodialyzed patients were divided into hypertensive and normotensive groups, the nondialyzed hypertensive group (n = 17) had higher plasma endothelin-1 levels than the comparable normotensive group (n = 7) (3.08 +/- 3.43 vs. 0.73 +/- 0.34 pg/ml, p less than 0.05), and the hemodialyzed hypertensive group (n = 18) had higher plasma endothelin-1 levels than the comparable normotensive group (n = 33) (2.66 +/- 1.92 vs. 1.35 +/- 0.73 pg/ml, p less than 0.005). Plasma atrial natriuretic factor, arginine vasopressin, renin activity, and aldosterone concentration did not show significant differences between hypertensive and normotensive individuals or a correlation with plasma endothelin-1 levels. These data suggest that circulating endothelin-1 may be partly involved in the development or maintenance of hypertension in humans.
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PMID:Plasma endothelin levels in hypertension and chronic renal failure. 218 51

In patients with essential hypertension and healthy controls, plasma levels of atrial natriuretic peptide (ANP), angiotensin II (Ang II), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion of prostaglandin E2 (PGE2) were measured under basal conditions, and before and after acute volume expansion with a 2.5% hypertonic sodium chloride solution. Tubular sodium handling was assessed by the lithium clearance technique. Under basal conditions ANP was increased in patients compared with controls (9.0 pmol/l versus 7.5 pmol/l, P less than 0.01). In response to acute volume expansion patients exhibited exaggerated increases in ANP (5.3 pmol/l versus 3.0 pmol/l, P less than 0.05), exaggerated natriuresis, and an abnormal decrease in fractional proximal and distal tubular sodium reabsorption (PFRNa and DFRNa, respectively). Furthermore, during comparable urinary flow rates, urinary PGE2 excretion was decreased in patients compared with controls (266 pg/min versus 705 pg/min, P less than 0.05). No differences were found between patients and controls in Ang II, Aldo or AVP under basal conditions. Both groups responded to hypertonic acute volume expansion with comparable decreases in Ang II and Aldo, and an increase in AVP. It is concluded that in essential hypertension ANP is increased under basal conditions and the increase in natriuresis and ANP is exaggerated during acute volume expansion. The exaggerated natriuretic response to acute volume expansion resulted from an altered handling of sodium in both proximal and distal tubules.
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PMID:Atrial natriuretic peptide and exaggerated natriuresis during acute hypertonic volume expansion in essential hypertension. 252 19

In order to investigate the interaction between atrial natriuretic factor (ANF) and arginine vasopressin (AVP) in the pathogenesis of essential hypertension, the effects of intravenous (iv) or intracerebroventricular (icv) injection of human ANF-(99-126) on plasma and brain AVP, as well as mean arterial pressure (MAP), urinary volume (UV) and sodium (UNaV) excretion in stroke-prone spontaneously hypertensive rats (SHRsp) and age-matched normotensive Wistar-Kyoto rats (WKY) were studied. The results showed that ten minutes after iv injection of ANF, MAP decreased by 9.4% and 12.2% (P less than 0.05), UV increased about 9 and 20 folds (P less than 0.01), UNaV increased about 16 and 29 folds (P less than 0.01) in SHRsp and WKY rats, respectively. No such significant changes in these parameters were found in the icv group. Although iv and icv injection of ANF caused significant decrease of plasma AVP in both strains, the decrease was less marked in SHRsp than in WKY rats, while the maximum decreases were 58% (iv) and 31% (icv) in SHRsp, the corresponding values were 80% (iv) and 65% (icv) in WKY. Intravenous and intracerebroventricular injection of ANF also induced significant increase of hypothalamic AVP in both SHRsp and WKY rats, but no significant change could be found in hypophyseal AVP content. The results suggest that decreased sensitivity of AVP inhibition as well as less marked hypotensive, diuretic and natriuretic effects to ANF in SHRsp might play a role in the pathogenesis of their hypertension.
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PMID:[Effects of human atrial natriuretic factor-(99-126) on plasma and brain vasopressin in stroke-prone spontaneously hypertensive rats]. 252 9

To ascertain whether small shifts in plasma atrial natriuretic factor (ANF) exerted biological effects in hypertension, we studied the renal, hemodynamic, and hormonal effects of ANF [human ANF-(99-126)] infused at a dose (0.75 pmol/kg/min for 3 hours) that would induce changes in plasma ANF confined to the normal, resting range, in a group of six young men with uncomplicated, mild essential hypertension. During ANF infusions, the patients excreted 11.8 +/- 2.0 mmol (mean +/- SEM) sodium more than during the time-matched placebo phase natriuresis (p less than 0.001, mean increase of 53% above placebo values). Urinary excretion of cyclic guanosine monophosphate rose to more than double (212%, p less than 0.001) placebo values. Plasma renin activity (0.4 +/- 0.05 vs. 0.9 +/- 0.12 nmol/l/hr, p less than 0.0001) and aldosterone concentrations (102 +/- 4 vs. 184 +/- 47 pmol/l, p less than 0.05) were clearly suppressed during administration of ANF. Plasma norepinephrine also fell significantly below placebo values (268 +/- 17 vs. 439 +/- 35 pg/ml, p less than 0.05). Urine volume, the excretion of electrolytes other than sodium, hematocrit, effective renal plasma flow, glomerular filtration rate, and filtration fraction were unaffected by ANF. Similarly, plasma concentrations of epinephrine, arginine vasopressin, adrenocorticotropic hormone, and cortisol were unchanged. Blood pressure and heart rate were unchanged. Minor perturbations in plasma ANF concentrations exert clear biological effects in patients with mild essential hypertension. These data suggest that such minor shifts in plasma ANF are of physiological relevance in mild hypertension and probably contribute to volume homeostasis in this condition.
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PMID:Atrial natriuretic factor in hypertension: bioactivity at normal plasma levels. 252 19

The aim of the present study was to evaluate the hemodynamic effects of arginine vasopressin (AVP) infusion in essential hypertension. To this end, 9 hypertensive patients and 10 normotensive controls were evaluated. After one hour rest, AVP was infused at a dosage of 0.5 and 2 ng/(kg/min), in 20 minutes periods. After AVP infusion, mean arterial pressure increased only in hypertensive patients (from 125.8 +/- 7 to 131.8 +/- 7, p less than 0.01 and to 135.6 +/- 6 mmHg, p less than 0.01). Peripheral vascular resistance was significantly increased in both groups during AVP infusion, although the percent increase was higher in hypertensive patients during the last period of infusion (18.3 +/- 10 versus 4.6 +/- 4, p less than 0.05). Cardiac index decreased in both groups during infusion, although this reduction was significantly higher in hypertensive patients than in healthy controls in the last period of infusion (-8.16 +/- 6 versus -1.8 +/- 4%, p less than 0.05). These results confirm that in essential hypertension there is an exaggerated pressor response to AVP infusion, suggesting that it is due to an increased vascular response to this hormone. The compensatory reduction of cardiac output and the inhibition of sympathetic nervous activity mediated through baroreceptor reflexes do not apparently play a role in this pressor response.
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PMID:[Vascular hyperreactivity to vasopressin in mild essential arterial hypertension]. 275 58

1. Resting and stimulated free calcium concentrations have been measured in platelets loaded with the fluorescent probe quin2 from 30 patients with essential hypertension and from 30 age-matched controls. 2. Cytosolic free calcium concentrations were 94.6 +/- 2.7 (mean +/- SEM) in the hypertensive group and 91.7 +/- 2.8 nmol/l in the normotensive group, the difference was not significant. 3. Arginine vasopressin caused a transient increase in platelet free calcium concentration in all subjects. In the presence of extracellular calcium the increase was significantly higher in the control subjects than in the hypertensive patients (P = 0.005). In the absence of extracellular calcium, arginine vasopressin caused much smaller increases, and there was then no difference between the responses of the two groups. 4. Platelet free calcium concentrations were measured again in 13 patients after 8 weeks treatment with either verapamil (n = 6) or atenolol (n = 7). The reductions in systolic pressure after drug treatment were correlated with the changes in cytosolic free calcium concentrations (r = 0.75, P less than 0.01).
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PMID:Platelet cytosolic free calcium in essential hypertension: responses to vasopressin. 276 58

The effects of acute exercise on plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and plasma renin activity (PRA) were studied in 13 patients with previously untreated essential hypertension, and 8 matched normotensive control subjects. Resting levels of ANP and PRA were similar in the two groups, while resting AVP concentrations were 1.4 times higher in hypertensive subjects. Graded exercise was performed on a bicycle ergometer with workload increased each minute until exhaustion (Wmax). Wmax was higher in normal subjects than in hypertensive patients. Blood pressure and heart rate rose more steeply in hypertensive patients. Plasma ANP increased during acute exercise in both groups, but the average increase in hypertensives was substantially greater than in normal subjects (P less than 0.05). The increase in ANP during exercise was greater in hypertensives with left ventricular (LV) hypertrophy, and there was a positive correlation between LV mass and the percentage rise in ANP during exercise (r = 0.56, P less than 0.005). Plasma AVP did not alter during exercise. Plasma renin concentrations showed a small rise during exercise in both groups, which was 16% less in hypertensive subjects (P less than 0.05). The enhancement of ANP release during exercise in hypertensive subjects may reflect both cardiac structural changes and increased redistribution of blood to the cardiopulmonary compartment.
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PMID:Exaggerated atrial natriuretic peptide release during acute exercise in essential hypertension. 297 6

The specific vasopressin receptor of V1 vascular subtype, which mediates platelet aggregation, has been found on human platelets. We investigated the binding characteristics using tritiated arginine vasopressin [3H]-AVP and platelet aggregation with AVP turbidometrically in normal subjects, patients with WHO class II essential hypertension and patients with malignant-phase hypertension. In essential hypertensives Bmax was significantly higher than that in normal subjects, but there were no differences in affinity and the maximal percentage aggregation between them. In malignant-phase hypertensives Bmax and maximal percentage aggregation were significantly lower than those in normals and essential hypertensives, although there was no difference in the affinity between them. With radio-immunoassay, the mean platelet-free plasma AVP level was significantly higher in malignant-phase hypertensives than those in normals and essential hypertensives, whereas there was no difference in mean platelet AVP levels between them. In essential hypertensives Bmax and maximal percentage aggregation did not change, but in malignant-phase hypertensives Bmax increased significantly and maximal percentage aggregation tended to normalize after treatment.
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PMID:Platelet vasopressin receptor in essential hypertension. 297 78


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