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PubMed1993

Salt and hypertension: water-sodium handling in essential hypertension.

This paper describes sodium handling in the kidney and the significance and mechanisms of its effects upon essential hypertension. In patients with low renin essential hypertension, plasma and urinary norepinephrine levels, plasma renin activity and fractional excretion of sodium were significantly lower, while plasma volume, extracellular fluid volume and exchangeable sodium were higher than in normal renin essential hypertension. The suppression of some renal depressor-natriuretic systems, the dopaminergic, kallikrein-kinin and prostaglandin E2 systems may contribute to the retention of sodium-water in these patients, because these depressor systems were observed to be greatly suppressed in essential hypertension, especially in the low renin group. The reduction of conversion from L-dopa to dopamine by dopa-decarboxylase in the proximal tubules was suggested from our clearance studies as the mechanism of the suppression of renal dopaminergic activity. Moreover, renal dopaminergic activity was already suppressed at the prehypertensive stage, possibly through the inhibition of renal dopa-decarboxylase activity. Thus, it appears that the suppression of renal depressor-natriuretic systems play an important role in the pathogenesis of essential hypertension through the retention of sodium and body fluid volume.

Body Water↗
PubMed1985

Evidence for a hypertensive factor in the blood of essential hypertensives.

From plasma of essential hypertensives and normotensives several fractions were obtained after: (1) removing proteins with a relative molecular mass greater than 6,000-8,000, and (2) chromatography on a Biogel P4 or Biogel P2 column. The eluate was separated into 3-4 fractions. These fractions were concentrated to a small volume of 0.5 ml and were injected intravenously in normotensive rats, the mean arterial pressure of which was monitored. One of the fractions from normotensive plasma increased blood pressure in the rat in some but not in all cases. Using the fractions from hypertensive plasma there was an increase in blood pressure in the fraction corresponding to that of normotensive plasma increasing blood pressure and in another fraction of lower molecular weight. Angiotensin II is unlikely to be responsible, since it could be identified in another fraction than that containing the hypertensive factor. It can be concluded that in the blood of essential hypertensives a hypertensive factor is present, which increases blood pressure even in normotensive animals. Its secretion may represent the critical step in the pathogenesis of essential hypertension.

Animals↗
PubMed1978

Pathogenesis of essential hypertension with low renin: responses of plasma renin activity to various stimulation tests in essential hypertension.

Plasma renin activity (PRA) was measured in 14 control subjects and 27 patients with essential hypertension (EH) (low renin group: 9, normal renin group: 11, and high renin group: 7) before and after the following stimulation tests. Test procedures: 1) Circadian rhythm (0600, 1600 and 2400h). 2) Adrenal stimulation test (ACTH: 12.5 I.U.). 3) Adrenal suppression test (Dexamethasone: 1.0 mg). 4) Metopirone test (1.5 g). 5) Angiotensin II infusion test (8 ng/kg/min). 6) Saline infusion test (1000 ml/hr). Patients with low PRA showed significantly lower levels of PRA than those of other two groups in circadian rhythm, after 2 hours of ACTH infusion and after angiotensin II infusion. Furthermore, these patients showed significantly higher responses of PRA than other two groups after furosemide test under dexamethasone and after metopirone test. In case of saline infusion test, patients with low and normal PRA did not show significantly decreased levels of PRA after the infusion, though all patients with high PRA and all control subjects showed significantly decreased levels of PRA. From the present studies, it might be concluded that patients with low PRA has an unknown mineralocorticoid excess which is ACTH dependent and 11 hydroxylated and some of hypertensive patients have an abnormality in their renin-angiotensin-aldosterone volume feed back loop as a factor for hypertension.

Adrenocorticotropic Hormone↗
PubMed1979

A new test showing abnormal net Na+ and K+ fluxes in erythrocytes of essential hypertensive patients.

A new and simple laboratory test for measuring net Na+ and K+ fluxes in Na+-loaded/K+-depleted human erythrocytes was developed and applied to hypertension. Moderate essential hypertension (10 patients) was characterised by a constant increase in net K+ influx, possibly related to higher Na+, K+-pump activity. In more severe cases (8 patients) net Na+ efflux from erythrocytes dropped. The ratio of Na+/K+ net fluxes was therefore reduced in all essential hypertensive patients. Conversely, Na+ and K+ erythrocyte fluxes were normal in hypertension of renal origin (5 patients). Erythrocyte K+ influx was normal in young normotensive people born of normotensive parents (17 cases), but was increased in 5 of 8 young normotensive people born of essential hypertensive parents, in families where blood-pressure has been recorded for three generations. This result, which seems to indicate genetic transmission, suggests that measurement of Na+ and K+ erythrocyte fluxes may help to detect subjects liable to high blood-pressure.

Adolescent↗
PubMed2002

Participation of renal and circulating endothelin in salt-sensitive essential hypertension.

Salt sensitivity of blood pressure is a cardiovascular risk factor, independent of and in addition to hypertension. In essential hypertension, a conglomerate of clinical and biochemical characteristics defines a salt-sensitive phenotype. Despite extensive research on multiple natriuretic and antinatriuretic systems, there is no definitive answer yet about the major causes of salt-sensitivity, probably reflecting the complexity of salt-balance regulation. The endothelins, ubiquitous peptides first described as potent vasoconstrictors, also have vasodilator, natriuretic and antinatriuretic actions, depending on their site of generation and binding to different receptors. We review the available data on endothelin in salt-sensitive essential hypertension and conclude that abnormalities of renal endothelin may play a primary role. More importantly, the salt-sensitive patient may have blood pressure-dependency on endothelin in all states of salt balance, thus predicting that endothelin receptor blockers will have a major therapeutic role in salt-sensitive essential hypertension.

Blood Pressure↗
PubMed2002

Positive association of CYP11B2 gene polymorphism with genetic predisposition to essential hypertension.

Predispositions to essential hypertension and cardiovascular diseases are possibly associated with gene polymorphisms of the renin-angiotensin system. Gene polymorphisms of angiotensinogen and angiotensin-converting enzyme genes have been suggested to be risk factors for hypertension and myocardial infarction. Concerning the polymorphism of aldosterone synthase (CYP11B2) gene, earlier studies have shown inconsistent results in terms of its relation to hypertension. In the present case-control study, we investigated the association of -344T/C polymorphism in the promoter region of human CYP11B2 gene with genetic predisposition to hypertension. The genotype of -344T/C polymorphism was determined in essential hypertension subjects (n=250) and normotensive subjects (n=221). The distributions of three genotypes (TT, TC, and CC) were significantly different between the hypertensive and the normotensive groups (chi(2)=9.61, P=0.008). Namely, the frequency of C allele was higher in the hypertensive patients than in the normotensive subjects (34.2 vs 26.5%, P=0.010). Our data suggest that the -344C allele of CYP11B2 gene polymorphism is associated with the genetic predisposition to develop essential hypertension.

Adult↗
PubMed1987

[Personality traits of persons with borderline arterial hypertension and patients with essential hypertension].

A study of 402 individuals with marginal arterial hypertension (MAH) and patients with essential hypertension (EH), stages 1, 2 and 3, demonstrated a variety of psychopathologic syndromes (hypochondria, anxiety, hysteria, depression, cardiophobia) in 52.8, 77.3, 82.5 and 80%, respectively. Specific personality features have been identified as pertaining to MAH (hyperthymism, sthenism, demonstrativeness, psychasthenia) and EH (psychasthenia, intraversion, cycloidy).

Character↗
PubMed2002

Echocardiographic comparison of left ventricular structure and function in hypertensive patients with primary aldosteronism and essential hypertension.

BACKGROUND: In experimental renovascular hypertension, aldosterone has been implicated in myocardial remodeling and fibrosis, but it is uncertain whether excess aldosterone effects left ventricular structure and function in hypertensive patients. METHODS: Hypertensive patients from the Cardiovascular Center of the New York Presbyterian Hospital-Weill Cornell Medical Center in New York and the Russian Cardiovascular Research Institute, Moscow, Russia, were studied. The sample included 35 patients with primary aldosteronism and 35 controls with essential hypertension matched for age, gender, and blood pressure (BP). Left ventricular (LV) mass, endocardial and midwall fractional shortening, and circumferential end-systolic stress were calculated. The observed/predicted midwall shortening ratio was used as an index of LV performance corrected for afterload. RESULTS: Primary aldosteronism and essential hypertension patients had comparable LV dimensions, wall thickness, mass, mass/body surface area, and mass/height. Endocardial and midwall fractional shortening, and afterload-corrected midwall shortening were similar in primary aldosteronism and essential hypertension groups from both clinics. Moreover, logistic regression analysis using BP, body mass index, height, gender, and center as covariates failed to identify statistical differences in LV geometry or systolic function between primary aldosteronism and essential hypertension patients. CONCLUSIONS: Patients with primary aldosteronism, a state characterized by chronic aldosterone excess, had similar LV geometry and systolic function compared to essential hypertension patients matched for age, gender, and BP. This argues against important independent associations between aldosterone and these aspects of LV response to human hypertension.

Adult↗
PubMed1984

Plasma noradrenaline concentration and pressor response to infused noradrenaline in patients with borderline hypertension, and mild or moderate essential hypertension.

In order to evaluate the significance of sympathetic nerve activity in the pathophysiology and pathogenesis of borderline hypertension or mild or moderate essential hypertension, plasma noradrenaline concentration (PNA) at supine rest and pressor response to infused noradrenaline (NA-R) were evaluated in these in-patients. A significantly positive correlation (r = 0.395, p less than 0.001) between PNA and age was found in normotensive subjects (NT), but not in essential hypertensives (EHT). In the young (below 40 years of age) group, the mean value of PNA in EHT was significantly higher (p less than 0.05) than that in NT. However no significant difference in PNA between NT and EHT was observed in the middle-age (40-59 years) and old-age (above 60 years) groups. PNA was highest in borderline hypertensives (BHT), second highest in EHT with WHO stage I (WHO-I), third in EHT with WHO stage II (WHO-II), and lowest in NT. Among these age-matched four groups, significant differences in the mean value of PNA were found between NT and BHT (p less than 0.001) or WHO-I (p less than 0.05), and between BHT and WHO-II (p less than 0.05). In a comparison of the age-matched NT, normal renin EHT (NRH) and low renin EHT (LRH), the mean value of PNA in NRH was significantly higher than that in NT (p less than 0.001) and LRH (p less than 0.001). Similar differences were observed in the peak value of PNA during 20 minutes when the head was tilted up. A close positive correlation between PNA and simultaneously measured mean arterial pressure (MAP) in the young EHT (r = 0.698, p less than 0.001) and WHO-I (r = 0.631, p less than 0.001), and a weak correlation in the middle-age EHT (r = 0.435, p less than 0.05) and NRH (r = 0.311, p less than 0.05) were demonstrated immediately after hospital admission. In the old-age EHT, WHO-II and LRH, however, no significant correlation was found between PNA and MAP. The mean value of NA-R in young (p less than 0.005) and middle-aged EHT (p less than 0.001) was significantly greater than that in respectively age-matched NT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Regulation of parathyroid hormone and vitamin D in essential hypertension.

Patients with essential hypertension have been reported to have a higher serum concentration of parathyroid hormone (PTH) than normotensive individuals although this finding is not universal among studies. To further characterize the status of the calcium regulating hormones in essential hypertension, we measured the parathyroid gland response to acute EDTA-induced hypocalcemia and the renal response of 1,25(OH)2-vitamin D to dietary calcium deprivation in 16 hypertensive (H) and 15 normotensive (N) men. The average mean arterial blood pressure once all antihypertensive medications were discontinued was 108 +/- 7 mm Hg for the hypertensive group and 89 +/- 4 mm Hg for the normotensive group (P < .01). There were no group differences in baseline serum concentrations of ionized calcium, creatinine, intact PTH, and 1,25(OH)2-vitamin D, urinary calcium excretion, and creatinine clearance. After a 1-h infusion of EDTA at 12.5 mg/kg/h, the serum concentration of ionized calcium fell (H: 1.25 +/- .03 to 1.17 +/- .04 mmol/L, N: 1.26 +/- .04 to 1.18 +/- .04 mmol/L, P = NS) and PTH increased (H: 36 +/- 9 to 91 +/- 30 pg/mL, N: 40 +/- 14 to 85 +/- 28 pg/mL, P = NS). With an additional hour of EDTA at a dose of 25 mg/kg/h, serum ionized calcium concentration fell further (H: 1.01 +/- .05 mmol/L, N: 1.03 +/- .06 mmol/L, P = NS) and PTH increased to 150 +/- 58 pg/ml in patients and 130 +/- 32 pg/ml in controls (P < .001). The response suggested an increased maximal parathyroid gland secretory capacity in the hypertensive patients relative to the controls. There was no group difference in the serum concentration of 1,25(OH)2-vitamin D at baseline (H: 32 +/- 6 pg/ml, N: 32 +/- 8 pg/ml, P < .90) and following dietary calcium deprivation for three days (H 50 +/- 12, N 48 +/- 14 P < 0.76). The maximal stimulated PTH level was significantly higher in hypertensive than normotensive subjects in the absence of measured differences in serum ionized calcium concentration, serum 1,25(OH)2-vitamin D concentration, and creatinine clearance. These findings suggest an intrinsic alteration of PTH regulation in patients with essential hypertension, manifest as increased parathyroid gland secretory capacity.

Adolescent↗
PubMed1999

Pretreatment renal vascular tone predicts the effect of specific renin inhibition on natriuresis in essential hypertension.

BACKGROUND: In essential hypertension an elevated renal vascular resistance (RVR) may be a marker of renin-angiotensin-aldosterone system-mediated impairment of renal sodium excretion. This hypothesis was tested by investigating whether, in subjects with essential hypertension, the natriuretic response to specific renin-angiotensin-aldosterone system (RAAS) blockade by renin-inhibitor remikiren could be predicted from pretreatment renal vascular tone. MATERIALS AND METHODS: Renal hemodynamics, and the effects of single (n = 17) and multiple doses (n = 8, 8 days) of remikiren (600 mg day-1) on sodium excretion were studied under conditions of carefully controlled sodium balance. RESULTS: Pretreatment renal vascular tone showed considerable individual differences: filtration fraction (FF) ranged from 21.2 to 30.3% and RVR from 18.8 to 33.5 10-2 mmHg min mL-1 in the single dose study, and FF from 20.8 to 24.9% and RVR from 14.8 to 28.8 10-2 mmHg min mL-1 in the multiple dose study. Remikiren induced a fall in blood pressure, FF and RVR, with considerable interindividual variability in natriuretic response. During single dose, cumulative sodium loss was 5.1 mmol per 5 h (-8.8 to +24.6), whereas after 8 days treatment cumulative sodium loss was 72 +/- 30 mmol (-46 to +187). The natriuretic response to remikiren during single as well as multiple dose significantly correlated with pretreatment renal vascular tone (estimated from FF and RVR) but not with remikiren-induced changes in renal hemodynamics or in hormonal parameters. Cumulative sodium loss was largest in patients with a higher pretreatment FF and RVR (r = 0.74, P < 0.001 and r = 0.52, P < 0.05, respectively, single dose; and r = 0.75, P < 0.05 and r = 0.73, P < 0.05, respectively, multiple dose). CONCLUSION: These data support the hypothesis that in essential hypertension an elevated renal vascular tone is a marker of RAAS-mediated impairment of sodium excretion.

Adult↗
PubMed1998

Effects of angiotensin converting enzyme inhibition on endothelium-dependent vasodilatation in essential hypertensive patients.

BACKGROUND: Essential hypertension is characterized by an impairment of endothelium-dependent vasodilatation. OBJECTIVE: To test whether antihypertensive treatment with the angiotensin converting enzyme inhibitor lisinopril can improve vasodilatation in response to endothelium-dependent agonists in essential hypertensive patients. DESIGN AND METHODS: We studied the effect of acute (6-8 h after dosing), prolonged (1 month) and chronic (12 months) lisinopril treatment on forearm blood flow response (strain-gauge plethysmography) induced in 10 hypertensive patients (aged 43.6 +/- 8.1 years, blood pressure 151.4 +/- 6.8/99.8 +/- 3.3 mmHg) by intrabrachial infusions of 0.15, 0.45, 1.5, 4.5, and 15 microg/100 ml per min acetylcholine and 5, 15, and 50 ng/100 ml per min bradykinin, two endothelium-dependent vasodilators, and 1, 2, and 4 microg/100 ml per min sodium nitroprusside, an endothelium-independent vasodilator. At baseline, vascular response was compared with that of 10 normotensive subjects (aged 42.4 +/- 6.6 years, blood pressure 118.4 +/- 6.1/77.8 +/- 3.4 mmHg). RESULTS: Hypertensive patients had blunted (P < 0.01 or less) vasodilatations in response to infusions of acetylcholine (from 3.7 +/- 0.3 to 18.3 +/- 4.9 ml/100 ml per min) and bradykinin (from 3.7 +/- 0.4 to 15.8 +/- 2.6 ml/100 ml per min) compared with those of controls (from 3.6 +/- 0.3 to 25.3 +/- 5.2 ml/100 ml per min for acetylcholine and from 3.7 +/- 0.3 to 26.9 +/- 4.9 ml/100 ml per min for bradykinin) whereas the responses to infusion of sodium nitroprusside were similar (from 3.6 +/- 0.3 to 18.5 +/- 3.9 and from 3.6 +/- 0.3 to 16.4 +/- 1.8 ml/100 ml per min, respectively). Acute and prolonged lisinopril treatments significantly (P < 0.05 or less) improved vasodilatation in response to infusion of bradykinin (from 3.7 +/- 0.4 to 24.5 +/- 4.9 and from 3.7 +/- 0.3 to 22.1 +/- 4.9 ml/100 ml per min, respectively), but not in response to infusions of acetylcholine and of sodium nitroprusside. Chronic lisinopril treatment increased (P < 0.05) the response to infusions of not only bradykinin (from 3.5 +/- 0.5 to 27.6 +/- 5.3 ml/100 ml per min), but also of acetylcholine (from 3.5 +/- 0.5 to 27.8 +/- 8.0 ml/100 ml per min) and sodium nitroprusside (from 3.4 +/- 0.6 to 25.9 +/- 8.5 ml/100 ml per min). However, when the responses to infusions of acetylcholine and bradykinin were normalized with respect to that to infusion of sodium nitroprusside, only the vasodilatation in response to infusion of bradykinin was shown to have been increased by lisinopril treatment. CONCLUSIONS: Administration of lisinopril to patients with essential hypertension can selectively increase vasodilatation in response to infusion of bradykinin.

Acetylcholine↗
PubMed1998

Scanning the genome for essential hypertension loci.

1. Essential hypertension occurs in people with an underlying genetic predisposition who subject themselves to adverse environmental influences. The number of genes involved is unknown, as is the extent to which each contributes to final blood pressure and the severity of the disease. 2. In the past, studies of potential candidate genes have been performed by association (case-control) analysis of unrelated individuals or linkage (pedigree or sibpair) analysis of families. These studies have resulted in several positive findings but, as one may expect, also an enormous number of negative results. 3. In order to uncover the major genetic loci for essential hypertension, it is proposed that scanning the genome systematically in 100-200 affected sibships should prove successful. 4. This involves genotyping sets of hypertensive sibships to determine their complement of several hundred microsatellite polymorphisms. Those that are highly informative, by having a high heterozygosity, are most suitable. Also, the markers need to be spaced sufficiently evenly across the genome so as to ensure adequate coverage. 5. Tests are performed to determine increased segregation of alleles of each marker with hypertension. The analytical tools involve specialized statistical programs that can detect such differences. Non-parametric multipoint analysis is an appropriate approach. 6. In this way, loci for essential hypertension are beginning to emerge.

Chromosomes, Human↗