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The pathogenesis of essential hypertension.

Essential hypertension is a quantitative abnormality, the pathological effects and risks increasing with the blood pressure level. In Western countries blood pressure rises with age in most individuals, so essential hypertension is more frequent in middle and older age groups. It is likely that an individual's blood pressure level is determined by many interacting factors. These include heredity, which probably acts multifactorially, and many environment influences, including psychological stress and obesity. Specific factors may be of varying importance in different individuals and in different populations. Several physiological mechanisms control the blood pressure level and may be altered in essential hypertension. In early hypertension sympathetic nervous activity is sometimes increased, although in long-standing hypertension this is less marked. Cardiac output may be increased in borderline hypertension but is normal in established hypertension, when total peripheral resistance is increased. Total exchangeable sodium is normal, while the renal pressure-natriuresis balance is altered, so that for a given pressure the hypertension kidney excretes less sodium. In some patients, plasma renin is low, probably as a result of renal adaption to prolonged hypertension. The pathogenic sequence in essential hypertension is uncertain. Increased autonomic activity may cause vasoconstriction in renal and other arterioles and increase cardiac output, leading to a rise in blood pressure. Elevated pressure itself produces structural changes in the resistance vessels, including those of the kidney, which eventually maintain the hypertension even when the initiating stimulus is removed. The way in which heredity and environment influence pathogenic mechanism is also uncertain. Heredity might, for example, influence the autonomic response to stress or the liability to irreversible changes in the resistance vessels or in the kidney. Environmental factors may also increase autonomic activity, enhance vascular reactivity or alter renal function.

Blood Pressure↗
PubMed1977

Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension.

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.

Adrenergic beta-Antagonists↗
PubMed1979

Decrease of calcium binding by the red blood cell membrane in spontaneously hypertensive rats and in essential hypertension.

Ca binding in the red blood cell (RBC) membrane of spontaneously hypertensive rats (SHR) and of patients with essential hypertension was studied. Under conditions of physiological concentration of free Ca in the incubation medium of RBC the outer part of the membrane binds 393 +/- 32 and 435 +/- 30 nmole of Ca per ml of RBC in rats and humans, respectively, without essential differences in the amount of Ca in hypertensive individuals as compared to the normotensive controls. The membrane of red blood cell ghosts (RBCgh) at concentrations of free Ca corresponding to its intracellular concentration binds 4.28 +/- 0.39 and 3.53 +/- 0.15 nmole of Ca per mg of protein of RBCgh in rats and humans, respectively. This part of membrane-bound Ca pool (most probably related to the inner part of the red blood cell membrane) is reduced by 48% in SHR and by 28% in patients with essential hypertension as compared to normotensive controls. It is suggested that the decrease of Ca binding ability of the RBC membrane in both types of hypertension studied may be a pattern of a more widespread cell membrane defect.

Adolescent↗
PubMed1979

[Pathogenesis of essential hypertension. Plasma noradrenaline, plasma renin and pressor effects of noradrenaline and angiotensin in normotensive patients and patients with essential hypertension].

Plasma noradrenaline, plasma renin and pressor action of exogenous noradrenaline and angiotensin in normotensive subjects and patients with essential hypertension. In normotensive subjects an inverse correlation was observed between the index of sympathetic nervous activity, the plasma noradrenaline concentration during physical exercise, and reactivity to exogenous noradrenaline. The relationship between the index of sympathetic nervous activity and reactivity to noradrenaline was invariably disturbed in age-matched patients with essential hypertension. A multiple regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood pressure (r = 0.91). The data suggest that both factors combined, sympathetic nervous activity and pressor response to noradrenaline, are an important determinant of the arterial blood pressure level. An inverse relationship could also be demonstrated between plasma renin concentration and pressor response to angiotensin II in normotensives and hypertensives. However, this relationship was unaltered in the hypertensives. Therefore angiotensin II does not appear to contribute directly to the high blood pressure.

Humans↗
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↗
PubMed1979

[Evidence of abnormalities in net sodium and potassium fluxes in erythrocytes of patients with essential hypertension].

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 was characterized by a constant increase in net K+ influx; more severe cases showed a drop in net Na+ efflux. Na+ and K+ erythrocyte fluxes were found to be normal in hypertension of renal origin.

Adolescent↗
PubMed1975

Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity?

A study of the frequency distribution of plasma-renin concentration in 81 patients with essential hypertension produced no evidence of a distinct sub-population with low renin levels. An arbitrary dividing line was used, therefore, to define low-renin hypertension (36% of patinets). Patients in this group were older than those with normal renin levels, and there was a significant negative correlation between renin and age among all patients. Low-renin hypertension was not characterized by increased exchangeable sodium, but exchaneable postassium was significantly lower than in patients with normal plasma-renin. This difference became insignificant when five patients in the low-renin group with persistent hypokalaemia were excluded. It is concluded that low-renin hypertension does not represent a separate diagnostic entity but that plasma-renin falls with age in essential hypertension.

Adult↗
PubMed1975

Evidence for a new mineralocorticoid in patients with low-renin essential hypertension.

Patients with low-renin essential hypertension have certain features consistent with excessive mineralocorticoid activity. Because known mineralocorticoids are normal in the majority of low-renin essential hypertension patients, an unknown mineralocorticoid was sought in the urine of such patients. Urine extracts from patients with low-renin essential hypertension were assayed for mineralocorticoid activity in adrenalectomized rats and found to contain more such activity than could be accounted for by the known mineralocorticoids in the extracts. The factor responsible for the unexplained mineralocorticoid activity was purfied and then identified by mass spectral analysis as 16beta-hydroxydehydroepiandrosterone (16beta-OH-DHEA). Synthetic 16beta-OH-DHEA was found to have a mineralocorticoid potency one-fortieth that of aldosterone in the rat bioassay. The mineralocorticoid effects of both the urine extracts and the synthetic steroid were blocked in the rat by spironolactone, a mineralocorticoid antagonist. A specific assay for 16beta-OH-DHEA was developed, and its level in the urine was found to be elevated in patients with low-renin essential hypertension.

Adrenalectomy↗
PubMed1979

Increased ratio between changes in blood pressure and plasma norepinephrine in essential hypertension.

The pathogenic role of the sympathetic system in essential hypertension was evaluated by combined analysis of plasma catecholamine levels and the pressor sensitivity to endogenous norepinephrine. The latter was estimated indirectly by the ratio between changes in blood pressure and those in plasma norepinephrine after adrenergic neuronal blockage with debrisoquine (given orally for 6 weeks). Normal subjects and patients with borderline or established essential hypertension had comparable pretreatment levels of plasma norepinephrine and epinephrine. Debrisoquine lowered plasma norepinephrine by a similar degree (almost 50%) in these three groups; in contrast, blood pressure decreased only slightly in normal or borderline hypertensive subjects [-3.4 +/- 3.2% and -5.4 +/- 1.6% (SE), respectively] but fell significantly more (P less than 0.005) in patients with established essential hypertension (-20.7 +/- 3.9%). The ratio between percentile changes in blood pressure and those in endogenous norepinephrine levels was comparable in normal and borderline hypertensive subjects (0.03 +/- 0.08 and 0.17 +/- 0.04, respectively), but increased (P less than 0.001) in established essential hypertension (0.62 +/- 0.11). This suggests that essential hypertension may be maintained, at least partly, by the inappropriate association of normal plasma norepinephrine levels with increased norepinephrine pressor sensitivity.

Blood Pressure↗
PubMed1979

Essential hypertension in black and white subjects. Hemodynamic findings and fluid volume state.

Systemic hemodynamics (cardiac output, intraarterial pressure, total peripheral resistance) and intravascular volume (plasma volume and red cell mass) were measured in a population of 126 black and white patients, 51 with borderline hypertension and 75 with established essential hypertension. The findings were compared with those in 29 age-matched normotensive control subjects of both races. The white patients with established hypertension demonstrated a faster heart rate than the black patients (less than 0.05); this difference was more pronounced during upright tilt (p less than 0.02). No significant difference in cardiac index, total peripheral resistance, plasma volume or total blood volume was found between the two racial populations. Cardiac index correlated directly with plasma and total blood volume in black patients (r = 0.32, p less than 0.05) and white patients (r = 0.35, p less than 0.001) as well as in the whole study population (r = 0.36, p less than 0.001). The regression lines were similar in the two races. Further, a negative correlation was observed between the total peripheral resistance and plasma volume (r = -0.31, p less than 0.001) or total blood volume (r = -0.34, p less than 0.001), and it was similar in both races (blacks r = -0.48, p less than 0.01; whites r = -0.25, p less than 0.05). Age correlated significantly with total peripheral resistance in the white patients (r = 0.35, p less than 0.001) and in the total study population (r = 0.28, p less than 0.001). We conclude that, for every given age or level of arterial pressure, systemic hemodynamics are similar for the black and white patients with essential hypertension. These data, therefore, do not support the clinical impression that basic pathophysiology and hypertensive vascular disease are different in the black patient with essential hypertension.

Adult↗
PubMed1978

Essential hypertension and pregnancy.

Approximately 1% of pregnancies are complicated by essential hypertension. During pregnancy the blood pressure often stabilizes or improves. In patients with sustained hypertension, prospective controlled studies have demonstrated enhanced fetal survival when the blood pressure was controlled with antihypertensive medication. Such medication must be chosen carefully to avoid fetal and mateerial toxicity, and diuretics and salt restriction during pregnancy should be avoided. Among patients with essential hypertension the problem accelerates late in pregnancy in 2% to 11%; the acceleration may be predicted by determination of maternal mean arterial pressures and intravascular volumes early in pregnancy. The treatment of accelerated hypertension is identical to that of severe pre-eclampsia. Fetal loss is considerable but can be lessened by careful fetal and maternal monitoring and early controlled delivery. The risks of pregnancy in most patients with essential hypertension are small, and essential hypertension is not a uniform contraindication to pregnancy.

Antihypertensive Agents↗
PubMed1979

The adrenal receptor for angiotensin II is altered in essential hypertension.

To determine the mechanism underlying altered adrenal responsiveness in patients with essential hypertension, the renin-angiotensin-aldosterone axis was assessed in normotensive and hypertensive subjects using three pharmacological probes: SQ 20881, a converting enzyme inhibitor; saralasin, a competitive angiotensin antagonist with prominent agonist properties; and angiotensin itself. All subjects were studied while supine and in balance on a 10 meq Na/100 meq K intake. The decrement in plasma aldosterone with SQ 20881 in 26 hypertensive subjects (15+/-3 ng/dl) was normal (13+/-4 ng/dl), suggesting that the altered adrenal responsiveness in hypertensives is not because of a change in a postreceptor event or in the relative contribution of angiotensin to the control of aldosterone secretion. Saralasin at a dose (0.1 mug/kg per min) that reduced aldosterone levels in all normals produced a normal aldosterone decrement (14+/-3 ng/dl) in 19 patients with renovascular hypertension (12+/-4 ng/dl). The same dose, however, had no net effect on plasma aldosterone levels in 70 patients with normal or high renin essential hypertension (-1+/-1 ng/dl) despite identical metabolic balance and control renin and angiotensin levels. The altered response could be explained by an agonist effect, aldosterone rising in 45 of the essential hypertensives. There were no significant differences between normal and abnormal responders in pre- and postcortisol, -potassium, -renin and -angiotensin concentrations. Angiotensin was infused (0.1-3 ng/kg per min) in 15 patients with normal renin essential hypertension, previously studied with saralasin. A probit transformation defined the dose required to induce a 50% increase in aldosterone (ED50). In the patients in whom aldosterone rose with saralasin, the dose required to induce a 50% increase was significantly greater (P < 0.001) than in those in whom aldosterone fell normally (1.02+/-0.06 [SD] vs. 0.38+/-0.07 ng/kg per min). Vascular responses were similar in the various groups. We conclude that altered adrenal responsiveness to angiotensin in some essential hypertensive patients is secondary to a change in the interaction of angiotensin with its adrenal receptor.

Adrenal Glands↗
PubMed1978

Relation of plasma noradrenaline to blood pressure, age, sex and sodium balance in patients with stable essential hypertension and in normotensive subjects.

1. Plasma noradrenaline was measured in 125 patients with stable essential hypertension (WHO I-II) and in 107 normotensive control subjects lying and standing. 2. In normotensive subjects and in patients with essential hypertension no sex-related differences of plasma noradrenaline were found between age-matched groups. 3. Plasma noradrenaline was not related to sodium balance indexed by urinary sodium/creatinine ratio. 4. In patients with essential hypertension plasma noradrenaline increases with age. 5. Mean plasma noradrenaline concentrations are significantly higher in patients with essential hypertension compared with age-matched normotensive subjects both lying and standing. 6. In patients with essential hypertension diastolic blood pressure and heart rate correlated significantly with supine plasma noradrenaline concentrations.

Adolescent↗
PubMed1979

Study of the renin-angiotensin system in essential hypertension.

320 patients with essential hypertension divided into three groups (minor, medium and major severty) were studied against 50 normal controls. Plasma renin activity (PRA) was estimated in case of normal and low Na intake, furthermore, of low Na intake in association with administration of chlorothiazide, in the recumbent position as well as at the end of 4-hr walk. The hypertensive group of medium severity (Group II) revealed a significant decrease in PRA, compared with the controls and with the hypertensive group of minor severity (Group I), in each period of observation. A significant increase of PRA in response to insulin hypoglycaemia was demonstrable in all three groups and in the controls, but the increase was of significantly lesser degree in Group II than either in the controls or in Group I. The plasma catecholamine concentrations were found lower in Group II than in the controls and in Group I. An elevation of the plasma catecholamine levels was demonstrable in response to insulin hypeglycaemia, but it was of lesser degree in Group II than a Group I and in the controls. The poor responsiveness of the RAS in Group II is attributed to an inadequate adrenergic activity and to an increased mean arterial pressure in that group, but the higher age of patients and longer duration of hypertensive disease, both characteristic of the group of medium severity, may also effect the renin-angiotensin system.

Adolescent↗
PubMed1979

Changes in hormonal activities relative to the severity of essential hypertension.

Endocrine activity in patients with essential hypertension was studied by measuring the urinary excretion of catecholamines, prostaglandin E (PGE) and cyclic adenosine monophosphate (cAMP). Simultaneously, plasma renin activity, concentrations of serum sodium, potassium, blood urea nitrogen (BUN) and creatinine were determined. Systolic blood pressure and BUN increased progressively with age until the sixth decade. Urinary excretion of norepinephrine was correlated with the systolic blood pressure. In contrast, plasma renin activity and urinary excretion of PGE decreased progressively with the increase in systolic blood pressure. Although the cause of essential hypertension is not known, it is suggested that hypertension accelerates the aging process in the kidney and thus decreases renal PGE synthesis. This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. A decrease of PGE may also potentiate the vasopressor action of norepinephrine.

Adult↗