Effects of volume expansion and contraction in normotensive whites, blacks, and subjects of different ages.

We studied the blood pressure, natriuretic, kaliuretic and humoral responses of 347 normal subjects after volume expansion and volume contraction to examine possible differences among whites, blacks and subjects of different ages. According to outpatient 24-hour urine collections, blacks excreted less sodium and potassium than whites. After similar states of sodium intake were achieved among all subjects, 2 liters normal saline were given i.v. Blacks and subjects greater than or equal to 40 years excreted less sodium than whites or subjects less than 40 years, over a 24-hour period. In addition, blacks excreted less potassium. The delay in sodium excretion occurred during the first 12 hours after the salt load. Blacks had a greater suppression of plasma renin activity than whites 24 hours after saline. Blacks also had higher blood pressures than whites after saline administration; their pressure remained elevated until furosemide was given. Furosemide, 120 mg over 24 hours, evoked greater natriuresis, but less kaliuresis in blacks than in whites. The greater prevalence of hypertension in both blacks and older subjects may be related to relatively blunted natriuretic responses when these groups engage in the high sodium-low potassium intake characteristic of our society.     

Renin as a risk factor in essential hypertension: More evidence

When patients with essential hypertension are classified into three major subgroups according to their plasma renin levels, they appear to exhibit different physiologic and epidemiologic characteristics. The present study extends previous observations which have suggested that low renin patients are relatively protected from development of heart attacks and strokes.Low renin patients despite the fact that they are older, exhibit lower blood urea levels than patients in the other two groups. These data are in keeping with the idea that low renin patients have relatively less renal vascular involvement.Young hypertensive blacks, known to be most prone to severe hypertension with vascular complications, practically always fall into the normal renin subgroup, whereas, in contrast, a vast majority of those blacks above the age of 50, with relatively milder hypertensive disease, exhibit low renin levels.These new findings which further associate vascular sequellae with the normal or high renin state provide more support for the concept that low renin patients have a relatively benign type of hypertensive disease.Nonhomogeneity of the low renin hypertensive population and differences in methodologic and physiologic approaches used to define such patients may provide the basis for conflicting observations from certain laboratories.     

Plasma concentrations of atrial natriuretic hormone in acromegaly: relationship to hypertension.

Atrial natriuretic hormone is involved in the control of blood pressure and water-electrolyte balance. In order to assess the relationship between atrial natriuretic hormone and hypertension in acromegaly, 34 subjects were studied, 18 with acromegaly (10 normotensive and 8 hypertensive) and 16 healthy controls. Plasma atrial natriuretic hormone levels, as well as plasma renin activity, aldosterone and growth hormone levels were measured in basal conditions in all subjects. Additionally, plasma renin activity and aldosterone levels were determined after standard stimulation. In hypertensive acromegalic patients, atrial natriuretic hormone plasma concentrations (39.8 +/- 3.5 ng/l) were significantly higher than in patients without hypertension (27.9 +/- 4.1 ng/l), and in controls (28.6 +/- 1.3 ng/l) (p less than 0.01 in both comparisons). Stimulated plasma renin activity values were decreased in hypertensive acromegalic patients when compared with those in normotensive patients (1.14 +/- 0.29 vs 4.03 +/- 0.66 micrograms.l-1.h-1, p less than 0.01). In acromegaly, atrial natriuretic hormone levels correlated with mean arterial pressure (r = 0.58, p = 0.01). These results suggest that atrial natriuretic hormone plasma levels are slightly increased in patients with acromegaly and hypertension.     

Role of the renin-angiotensin-aldosterone system in hypertensive children with coarctation of the aorta.

To investigate the role of the renin-angiotensin-aldosterone system as a cause of hypertension, 20 hypertensive patients with coarctation of the aorta were studied during normal and low sodium intake and after diuresis with flurosemide. Eight patients with essential hypertension and 13 control subjects were similarly studied. Plasma renin activity values in patients with coarctation were similar to those in patients with essential hypertension and in control patients during normal and low sodium diets. However, after the administration of furosemide, plasma renin activity values were significantly higher in the patients with coarctation than in the other two groups (P less than 0.005 and less than 0.01, respectively). The values for urinary aldosterone, plasma volume and extracell fluid volume (bromide space) were increased in patients with coarctation during both normal and low sodium intake. These renin and aldosterone responses and body fluid spaces in patients with coarctation suggest that their hypertension resembles a one-kidney Goldblatt model. The data help to better define the role of the renin-angiotensin-aldosterone system in the hypertension of coarctation and thus may help guide the clinician in therapeutic interventions.     

The influence of age on renal function and renin and aldosterone responses to sodium-volume expansion and contraction in normotensive and mildly hypertensive humans.

To determine the effects of age on the responses of renin, aldosterone (PA), sodium excretion, and renal function to provocative maneuvers, we performed volume expansion and contraction in 390 normotensive and 212 hypertensive subjects in the second to seventh decades of life. The subjects were classified as Na-sensitive if their mean blood pressure was 10 mm Hg or more higher after volume expansion than volume contraction. Sodium sensitivity was associated with hypertension and increasing age. Plasma renin activity decreased with age under basal, stimulated, and suppressed conditions; the decrease was greater in hypertensives than in normotensive persons. The PA values were greater in hypertensives than in normal subjects after volume expansion. There was an age-related decrease in PA values after volume contraction in normal, but not in hypertensive, persons. With volume expansion, hypertensive persons exhibited "exaggerated natriuresis." There was an age-related increase in natriuresis in both groups; the increase was greater in hypertensives than normal subjects. Creatinine clearance decreased with age; however, the rate of decrease in this cross-sectional study was not different in hypertensive and normotensive subjects. These observations may have a bearing on why NaCl affects the blood pressures of older individuals more than younger persons.     

Importance of atrial natriuretic hormone in an exaggerated natriuresis during acute sodium load in primary aldosteronism.

To elucidate the factors which contribute to the exaggerated natriuresis in primary aldosteronism, hemodynamic and hormonal changes induced by saline infusion (at a rate of 0.5 l/h for 3 h) were examined in 6 patients with primary aldosteronism, 13 with essential hypertension, and 8 normotensive subjects. After saline infusion, increases in urinary sodium excretion, glomerular filtration rate, atrial natriuretic hormone, and urinary dopamine excretion along with suppression of plasma renin activity and aldosterone were compared in the three groups. All three groups demonstrated similar increases in glomerular filtration rate, but patients with primary aldosteronism did not show changes in urinary dopamine excretion, plasma renin activity, and aldosterone, despite their increased excretion of sodium. The increase in plasma atrial natriuretic hormone was significantly greater in primary aldosteronism than in essential hypertension or normotensive subjects. No changes in blood pressure or heart rate were seen. These findings suggest that atrial natriuretic hormone might play a role in the exaggerated excretion of sodium in patients with primary aldosteronism.     

Hyperaldosteronism and hypertension: ethnic differences

The purpose of this study is to evaluate the relationship between aldosterone and blood pressure in a total of 220 normotensive and 293 essential hypertensive subjects in 2 genetically distinct populations-blacks and white French Canadians. The 24-hour blood pressure monitoring was performed under standardized conditions after discontinuing antihypertensive medications. Plasma renin activity and plasma aldosterone were measured in the supine position and after standing for 10 minutes. Plasma atrial natriuretic factor was also measured. Supine and standing plasma renin activities were lower (P< or =0.01), plasma aldosterone was higher (P<0.0001), and the aldosterone/renin ratios were higher (P<0.0001) in the hypertensive subjects. Atrial natriuretic factor was also higher in the hypertensive subjects (P<0.0001). Among blacks, blood pressures did not correlate with plasma renin activity. However, both average daytime and nighttime systolic and diastolic blood pressures were correlated with supine and standing plasma aldosterone and with the aldosterone/renin ratio (P<0.005 or less). In French Canadians, blood pressures tended to be positively correlated with standing plasma renin activity and aldosterone, but not with the aldosterone/renin ratio. Correlations of blood pressure with aldosterone were more consistent and more striking in blacks than in French Canadians. In both ethnic groups, there were inconsistent correlations of blood pressure with atrial natriuretic factor. These observations are consistent with the hypothesis that aldosterone-induced volume expansion is an important contributor to hypertension, especially in blacks.     

The possible importance of aldosterone as well as renin in the long-term antihypertensive action of propranolol

In 50 patients with essential hypertension, propranolol produced a significant decrease in blood pressure. The decrease in mean pressure was greatest in patients classified by a renin sodium nomogram as having high renin hypertension. In turn, blood pressure decreased more in patients with normal renin than in those with low renin levels. Indeed, a net increase in diastolic pressure occurred in the low renin subgroup. These findings confirm the value of pretreatment plasma renin measurements for predicting blood pressure responses to propranolol.Over-all, seven of the 50 patients exhibited increases in mean blood pressure during propranolol treatment. Presumably, this occurred because the minimal suppression of renin-angiotensinmediated vasoconstriction in these patients was insufficient to compensate for the unopposed alpha-sympathetic vasoconstriction unmasked by peripheral vascular beta-blockade. Within this group of patients, there was a significant inverse correlation between control renin values and the amplitude of the pressor response.The decrements in plasma renin were slightly greater in patients classified as responders (decrease in mean blood pressure ≥ 10 per cent) than in nonresponders. However, when the propranolol-induced decrements in aldosterone excretion were taken into account, responders to treatment exhibited far greater decreases than non-responders. Thus, higher levels of aldosterone during treatment may operate to oppose the antihypertensive action of propranolol. Ultimately, this dependency of the blood pressure response upon aldosterone levels is at least partly coordinated with propranolol-induced inhibition of renin release, since we found a significant correlation between changes in these hormones during treatment.     

Sodium chloride sensitivity, intracellular sodium concentration in erythrocytes and lymphocytes, and renin profile in essential hypertension

In order to clarify the possible relationship between changes in blood pressure after salt loading, membrane sodium transport and renin profile, 19 patients with essential hypertension (8 patients with low renin hypertension and 11 patients with normal renin hypertension), admitted to our hospital, were studied. We also examined the correlation of changes in intracellular sodium concentration after salt loading between erythrocytes and lymphocytes. After a control period of one week, all subjects were placed on a low salt intake for one week followed by one week of a high salt intake. Percent increases in mean blood pressure and intracellular sodium concentration in erythrocytes and in lymphocytes after salt loading were greater in low renin hypertensive patients than in normal renin hypertensives. Percent changes in intracellular sodium concentration in erythrocytes inversely correlated with those in ouabain sensitive sodium efflux rate constant and positively correlated with those in intracellular sodium concentration in lymphocytes. These results suggest that an increase in sodium chloride sensitivity of blood pressure in patients with low renin hypertension may be due to the inhibition of Na+-K+ pump in vascular smooth muscle cell membrane.     

Abnormal relation of extracellular fluid volume and exchangeable sodium with systemic arterial pressure in early borderline essential hypertension

Interrelations between systemic arterial pressure, extracellular fluid (ECF) volume, exchangeable sodium (Na) and the renin-angiotensin-aldosterone system were studied in 38 young patients with borderline hypertension and in 37 age- and sex-matched control subjects. ECF volume and exchangeable Na were subnormal (not significant) in borderline hypertension. In normal subjects, volume data did not relate to arterial pressure; in contrast, negative correlations were observed between arterial pressure and ECF volume or exchangeable Na in patients with borderline hypertension (in hypertensive women, r greater than or equal to 0.7, p less than 0.01). Plasma renin activity was consistently elevated in borderline hypertension, mainly in the upright posture, and these values were inversely correlated with ECF volume and exchangeable Na. No correlation was observed between arterial pressure and plasma renin activity. These results show that slight elevation of arterial pressure in the early stage of hypertension induces a proportional decrease in ECF volume, suggesting that the phenomenon of pressure-natriuresis is operative in young borderline hypertensive persons. The renin-angiotensin system is activated in these patients, in part to preserve sodium homeostasis.     

Renal and endocrine response to saline infusion in essential hypertension

To assess the contribution of the renin-angiotensin-aldosterone system and renal hemodynamics to acute renal sodium handling in essential hypertension we studied 21 subjects who had essential hypertension (16 with normal renin, 5 with low renin) and 9 normal subjects. All were in balance on a 10 mEq sodium intake before receiving a small sodium load, 60 mEq intravenously over 1 hour. Hypertensive subjects with low renin showed the anticipated exaggerated natriuresis, which was transient and occurred without a rise in blood pressure. Natriuresis in hypertensive subjects with normal renin was either normal or blunted; delayed sodium excretion occurred in a subset, along with delayed suppression of the renin-angiotensin-aldosterone system by the saline load. Neither renal plasma flow nor glomerular filtration rate changed during the saline load. After 72 hours of converting enzyme inhibition with enalapril, renal plasma flow increased substantially more in the subjects with a blunted renin response and their natriuretic response to the sodium load returned to normal. These results indicate that when prior sodium intake is controlled, large sodium loads are avoided, and low renin hypertension is removed as a confounding variable, blunted rather than exaggerated natriuresis is the common feature of essential hypertension. This abnormality is reversed by angiotensin converting enzyme inhibition, perhaps because of converting enzyme inhibition-induced renal vasodilatation.     

Renin Subgroups in Essential Hypertension

A nomogram based on the relationship between plasma renin activity and urinary sodium excretion in normal subjects has been used to classify 956 patients with essential hypertension into low, medium and high renin subgroups. Patients with low renin hypertension (27 percent of all patients) were older (P<0.001) than patients with medium or normal renin hypertension. They also contained more women (P<0.01) and had higher systolic blood pressures than patients with medium renin hypertension. Creatinine clearance, albumin concentration and hematocrit were lower in low renin patients than in patients with medium renin activity. Serum potassium levels were lower, but urinary potassium excretion was higher in low renin patients. Most of the differences in clinical and biochemical parameters could be explained by the differences in age and male: female ratio between the subgroups. Despite lower renin values, aldosterone excretions were similar between the subgroups. Differences in renin activity and differences in aldosterone-renin ratio could not be explained by differences in age, duration of hypertension and sex ratios. Patients with low renin hypertension showed evidence of increased adrenal sensitivity to angiotensin II-induced aldosterone secretion. Patients with high renin hypertension (11 percent of all patients) were younger than patients with medium or normal renin hypertension. Other differences in biochemical characteristics between these renin subgroups included a slightly higher albumin concentration and hematocrit in patients with high renin levels. These differences and the difference in renin activity between patients with high and patients with medium renin essential hypertension could not be explained by differences in age and/or sex ratio between the two subgroups. Despite the higher renin activity, aldosterone excretion was similar between the high and medium     

Cardiovascular and endocrine profile of adrenergic neurone blockade in normal and hypertensive man.

Some cardiovascular and endocrine effects of adrenergic blockade were assessed in six normal subjects, six patients with mild hypertension (diastolic pressure < 100 mm Hg) and six patients with moderate to severe essential hypertension. Administration of the inhibitory agent, debrisoquine, for six weeks markedly decreased supine and upright plasma norepinephrine levels, and norepinephrine excretion in all three groups. Supine and upright blood pressure was decreased more (p < 0.001) in those with moderate to severe hypertension (15 and 27 per cent) than in those with mild hypertension (6 and 8 per cent) and remained unchanged in normal subjects. Pulse rate and plasma renin levels were lowered (p <0.01) in patients with moderate to severe hypertension, but not in normal or mildly hypertensive subjects. The different influence of blood pressure, pulse rate and renin in the three groups could not be explained by variations in drug dosage, norepinephrine inhibition, age, basal sodium balance or secondary blood volume expansion, the latter being marked in all groups. Diuretic therapy in addition to sympathetic inhibition reversed blood volume expansion, and further augmented the reduction in supine and upright blood pressure in patients with moderate to severe (?21 and ?47 per cent) or mild hypertension (?8 and ?12 per cent). Plasma aldosterone, cortisol and epinephrine values remained unchanged, and no severe or intolerable side effects occurred during treatment. These data suggest that adrenergic neuron blockade with modest doses of debrisoquine, combined with a diuretic, may be an effective and acceptable mode of therapy in patients with either mild or more severe hypertension. The hypotensive, cardiac-slowing and renin-inhibitory potential of adrenergic neuron blockade may be initiated by decreased norepinephrine outflow and modulated by variations in end-organ responsiveness, normal subjects being relatively insensitive and patients with essential hypertension being more sensitive as the severity of their hypertension increases.     

Increased dopamine-induced nephrogenous cAMP formation in hypertension.

Low doses of exogenous dopamine (3 micrograms/kg/min) were administered intravenously to nine patients with essential hypertension and to six age-matched healthy volunteers. During infusion with dopamine, mean arterial blood pressure decreased in hypertensive patients whereas it did not change in normotensive subjects. Basal levels of sodium excretion were comparable in hypertensive and normotensive subjects. The natriuretic response to dopamine was significantly greater in hypertensive patients. Urinary and nephrogenous cAMP significantly increased in both normotensive and hypertensive subjects. The increase of nephrogenous cAMP was more pronounced in hypertensive patients than in normotensive controls. A significant correlation was found between nephrogenous cAMP and sodium excretion. The enhanced natriuretic response to dopamine in hypertensive patients may be due to increased cAMP formation in response to tubular dopamine receptor stimulation. This is in agreement with the hypothesis of either up-regulation or affinity changes of renal dopamine receptors in patients with essential hypertension, secondary to a decreased endogenous production of intrarenal dopamine.     

Plasma atrial natriuretic factor in essential hypertension: relation to cardiac size, function and systemic hemodynamics

To evaluate determinants of elevated plasma atrial natriuretic factor levels in patients with hypertension, immunoreactive plasma atrial natriuretic factor in 54 normal subjects and 40 untreated hypertensive patients was compared with echocardiographic measurements of cardiac size, function and systemic hemodynamics. In normal subjects, plasma atrial natriuretic factor was related to age, systolic blood pressure and left atrial and ventricular chamber sizes, but only age and ventricular size were independent predictors. In untreated hypertensive patients, atrial natriuretic factor was directly related to age, atrial size, systolic pressure, peripheral resistance and ventricular systolic performance; age, atrial size and peripheral resistance were independent predictors. Eight patients with elevated atrial natriuretic factor values (greater than 25 fmol/ml) were significantly (p less than 0.01) older and had greater atrial and ventricular size and higher systolic pressure and function than normal subjects or patients with normal natriuretic factor levels. Plasma atrial natriuretic factor was inversely related to peak diastolic filling rate in normal subjects (r = -0.59; p less than 0.001), whereas it was positively related to the proportional contribution of atrial systole to left ventricular filling in hypertensive patients (r = 0.77; p less than 0.001). These findings suggest that in normal subjects, impairment of ventricular relaxation with age may contribute to atrial natriuretic factor secretion by increasing left atrial afterload; the correlation with left ventricular size may reflect physiologic fluctuations in plasma volume. In patients with uncomplicated hypertension, left atrial enlargement and consequent stronger atrial contraction contributed to increased atrial natriuretic factor release, whereas no independent relation existed with left ventricular hypertrophy or systolic function. Because ventricular relaxation was normal and ventricular size and systolic performance were increased in hypertensive patients with high atrial natriuretic factor levels, the observed increase in left atrial size and atrial contribution to ventricular filling might reflect a primary increase in venous return in this subset of hypertensive patients.     

Hypertension associated with early stage kidney disease: Complementary roles of circulating renin,the body sodium/volume state and duration of hypertension

Interrelations among blood pressure, exchangeable sodium, blood volume and plasma renin activity were studied in 40 normal subjects and in 40 patients with early stage kidney disease (mean plasma creatinine, 2 mg/100 ml). Findings in eight normotensive patients did not differ significantly from those in normal subjects. However, 32 hypertensive patients showed increases (p < 0.05) in mean exchangeable sodium and in the products of the logarithm of plasma renin activity and exchangeable sodium or blood volume. In normal subjects, blood pressure did not correlate with any of the parameters measured. In the patients, it correlated significantly (p < 0.05) with duration of hypertension (r = 0.70), exchangeable sodium (r = 0.34) and with sodium-renin (r = 0.38) or volume-renin (r = 0.30) products, but not with blood volume or circulating renin individually. Multiple regression analysis with blood pressure as a dependent variable, and duration of hypertension and the sodium-renin or volume-renin products as independent variables, revealed correlation coefficients of 0.77 and 0.76, respectively. These findings suggest that hypertension accompanying early stage kidney disease may depend at least partly on subtle abnormalities in the sodium/ volume-renin feedback mechanism as well as on a factor related to the duration of preexisting hypertension.     

Similar prevalence of renovascular hypertension in selected blacks and whites

Renovascular hypertension is a potentially curable form of high blood pressure that is thought to be extremely rare among blacks. We demonstrate, however, that in a clinically selected population, the prevalence of renovascular hypertension is similar in blacks and whites. We prospectively evaluated 167 hypertensive subjects who had one or more clinical features known to be associated with renovascular hypertension. All subjects had captopril-stimulated peripheral renin measurements and conventional renal arteriography. All significant renal artery stenoses (greater than 50% luminal narrowing) were treated with percutaneous transluminal angioplasty or surgery. Renovascular hypertension was diagnosed if there was a blood pressure response to interventional therapy, according to the criteria established by the Cooperative Study of Renovascular Hypertension. Of the total group evaluated, 24% (39 of 167) had renal artery stenosis and 14% (23 of 167) had renovascular hypertension. Renal artery stenosis or occlusion was found in 27% (26 of 97) of whites and 19% (13 of 67) of blacks (p = 0.27). Renovascular hypertension was diagnosed in 18% (17 of 97) of whites and 9% (6 of 67) of blacks evaluated (p = 0.25). Renovascular hypertension was associated with severe or refractory hypertension and with smoking, but there were no racial differences in these associations. Blacks with renovascular hypertension tended to have low captopril-stimulated peripheral renin activity. We conclude that blacks with clinical features suggestive of renovascular hypertension should be evaluated with angiography. Captopril-stimulated plasma renin may not be useful in detecting blacks with renovascular hypertension, but this and other potential screening tests require further evaluation.     

The pathophysiological role of renal dopaminergic activity in patients with essential hypertension

To evaluate the role of the renal dopaminergic system on renal water-sodium metabolism patients with essential hypertension (EHT), urinary excretion of dopamine, urinary excretion of sodium (UNaV) and fractional excretion of sodium (FENa) were all investigated before and after the administration of dopamine (3 micrograms/kg/min, intravenous infusion for 60 minutes), dopamine antagonist, metoclopramide (8 mg/m2 BSA, intravenous injection) or mild sodium loading in both normotensive subjects and benign EHT. In the basal values, no significant difference in urinary excretion of free (u-fDA), conjugated (u-cDA) or total dopamine (u-tDA) was found between normotensives and hypertensives. However, low renin EHT showed a pronounced reduction in u-fDA compared with normotensis subject and (NT) normal renin EHT. In this study, a significant reduction of u-cDA and of u-tDA was also found in those patients with low renin essential hypertension. In the normotensive and essential hypertensive groups UNaV or FENa showed a positive correlation with u-fDA (measured simultaneously), but not with u-tDA or u-cDA. The regression line between u-fDA and UNaV or FENa in EHT was shifted towards a lower u-fDA level than in NT. UNaV and FENa were increased by dopamine infusion and were decreased by metoclopramide injection in both NT and EHT. Changes of UNaV and FENa following dopamine or metoclopramide, showed a negative correlation with u-fDA measured immediately before the administration of these drugs. The enhanced natriuretic response to infused dopamine and the attenuated antinatriuretic response to injected metoclopramide were significant in low renin EHT, when compared with NT or normal renin EHT patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Why is plasma renin activity lower in populations of African origin?

Plasma renin activity is significantly lower in black people compared with whites independent of age and blood pressure status. The lower PRA appears to be due to a reduction in the rate of secretion of renin but the exact mechanistic events underlying such differences in renin release between blacks and whites are still not fully understood. Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. The lower PRA does not reflect differences in dietary sodium intake but the evidence available suggests that the low PRA could be part of the corrective mechanisms designed to maintain sodium balance in the presence of an increased tendency for sodium retention in black people. While it is possible that several factors may contribute to the reduced PRA, more recent investigation at the molecular level suggests that the lower PRA may arise from gene variation in the renal epithelial sodium channel. The functional significance of the lower PRA in relation to the different pattern of cardiovascular and renal disease between blacks and whites remains unclear. Moreover, direct investigations of pre-treatment renin status in hypertensive blacks in relation to blood pressure response have demonstrated that the pre-treatment PRA is not a good index of subsequent blood pressure response to pharmacological treatment. Nevertheless, the blood pressure reduction to short term sodium restriction is greater in blacks compared with whites and, in the black subjects, the greater reduction in blood pressure to sodium restriction appears to be related, at least in part, to the decreased responsiveness of the renin-angiotensin system. Journal of Human Hypertension (2001) 15, 17-25     

The effect of sodium and potassium loading on urinary kallikrein-like activity in young patients with borderline hypertension

We studied the effects of a potassium supplement on urinary kallikrein excretion in a setting of high sodium intake after sodium deprivation with diuretics in young patients with borderline hypertension. Eleven patients, who took the potassium supplementation during the high sodium diet period, showed lower increments in mean blood pressure with salt loading than 12 patients without the potassium supplementation. In the non-potassium-supplemented patients, urinary kallikrein was increased significantly when plasma renin activity (PRA), plasma aldosterone concentration (PAC), and urinary aldosterone were increased during the diuretic treatment. It was decreased significantly when the other hormones were decreased during the sodium load. During the high sodium diet period, PRA, PAC and urinary aldosterone were greater in the potassium-supplemented patients than in the non-potassium-supplemented ones, but urinary kallikrein excretion was not higher when potassium was supplemented. Thus, the present results did not support the theory that the kallikrein-kinin system may be involved in the natriuretic and antihypertensive effects of potassium. In addition, these finding suggest that some kallikrein-modulating factor(s) may counteract the increased urinary kallikrein excretion with the augmented renin-angiotensin-aldosterone system during salt loading with potassium supplementation.