Renin content of individual juxtaglomerular apparatuses and the effect of diet, changes in nephron flow rate and in vitro acidification on the renin content.
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Animals↗
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Arterial and mixed venous PCO2 and hydrogen ion, bicarbonate and base excess concentrations in water-depleted dogs.
The arterial (a), mixed venous (v), and arterial-mixed venous differences (A-V) of hydrogen ion concentration ([H+]), PCO2, HCO-3 and base excess (BE) were measured during 3 h in control (C), water-depleted (WD) and water- and salt-depleted (WSD) dogs. In WD animals the difference in hydrogen ion concentration between venous and arterial blood increased because the [H+] increased more in venous than in arterial blood. In WSD animals (A-V) [H+] remained unchanged since both [H+]a and [H+]v increases were parallel. [H+] variations seem to represent the changes in fixed-acid concentration of blood. The difference between both groups of animals in (A-V) [H+] changes could be ascribed to PCO2 variations. [HCO-3] values changed inconsistently. Arterial samples from the experimental groups showed a continuous decrease at the same rate of change. The mean values in WSD were lower than in WD. [HCO-3]v of WSD decreased slowly during the experiment. The rate of decrease of (A-V) [HCO-3] was higher in WD than in WSD. The different behavior of of [HCO-3] between both arterial and mixed venous samples and among experimental groups disappeared if [HCO-3] changes were corrected for bicarbonate generation due to PCO2 variation (respiratory bicarbonate). Thus [HCO-3] corrected for PCO2 variation represents metabolic changes, in good agreement with both [H+] and BE variations. The metabolic acidosis cannot be explained only on the basis of the increase in blood lactate; it is suggested that other fixed acids might contribute to the decrease in blood bicarbonate. In both experimental groups PvCO2 increased continuously. The (A-V) PCO2 showed the same rate of change. There is a good relationship between this increase and the degree of plasma volume change. It therefore might be that PvCO2 increase is a direct consequence of hemodynamic impairment. In WD and WSD, BE decreased progressively in both arterial and mixed venous samples. BEa values were lower than BEv values after the experiment began. (A-V) BE decreased in an exponential manner in both experimental groups; this change could be ascribed to the increased level of deoxygenated hemoglobin in mixed venous blood, thus giving rise to a decrease in fixed acid concentration.
Acid-Base Equilibrium↗
Impaired urinary acidification in the hypothyroid rat.
Since abnormalities in the renal handling of sodium and water in both the proximal and distal tubule have been described in primary hypothyroidism, this study was undertaken to examine renal tubular hydrogen secretion in this disorder. Metabolic acidosis was induced in hypothyroid rats (H) and their age matched controls (C) by the administration of an oral ammonium chloride load of 0.15 g/24 h/kg for three days. On day 3 animals were prepared for clearance and acid-base studies, receiving an infusion of Ringer's solution of 0.6 ml/hr/100 g during surgery and the experimental procedure. A 26% decrease in GFR (P less than 0.005) and a doubling in fractional excretion of sodium (P less than 0.02) were observed in H rats. The lowest blood pH and average bicarbonate concentration and the excretion of chloride were similar in the two groups, indicating that the acid load was reabsorbed and led to similar degrees of systemic acidification. Urine flow also was comparable in the two groups. Minimal urine pH after NH4Cl was 6.21 +/- 0.06 in H and 5.68 +/- 0.09 in C (P less than 0.001). Ammonium excretion was 28% (P less than 0.05) lower in H than in C. The defect in urine acidification in H was only partially corrected after 5 days on a low sodium diet and DOCA administration for 2 days. Fractional bicarbonate excretion at normal blood pH and bicarbonate concentration was not different in the two groups. These data indicate that hypothyroid rats have a mild defect in urine acidification and that it is localized predominantly in the distal tubule.
Acidosis, Renal Tubular↗
[Hemodynamic changes after angiotensin II blockade by saralasin (author's transl)].
Saralasin, an angiotensin II inhibitor was infused in 10 hypertensive patients. A blood pressure reduction was achieved after stimulation of the renin-angiotensin-system by salt depletion. Heart rate and cardiac output failed to compensate for reduction of blood pressure. Thus circulatory reflex-mechanisms are inhibited by saralasin. A direct influence on baroreceptor mechanism and/or catecholamines is probable. Failure of the hypotensive effect of saralasin in salt-depleted patients after administration of beta-blockers supports this hypothesis.
Adrenergic beta-Antagonists↗
Acid excretion in young and adult Wistar Kyoto and spontaneously hypertensive rats.
Wistar Kyoto rats (WKy), the most widely accepted control for SH rats, show an inability to excrete acid appropriately when compared to another normotensive strain, SD. Coupled with the fact than KWy also develops 'sodium-sensitive' hypertension, this makes them a more complex control than realized. At very young ages (less than 10-week-old), neither SH nor WKy show any deficiency in acid excretion.
Aging↗
Effect of reduction in salt intake on hypertension.
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Adrenergic beta-Antagonists↗
Acute poststreptococcal glomerulonephritis.
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Acute Disease↗
Renin dependency of blood-pressure. Analysis by angiotensin II antagonist P113 in hypertensive patients treated with salt depletion and propranolol.
The effect of infusion of the angiotensin II antagonist P113 on blood-pressure (B.P.) has been studied in 10 patients with various forms of hypertension under four different conditions: before and after salt depletion and with or without propranolol treatment. The fall in B.P. after P113 infusion significantly correlated with log P.R.A. (plasma-renin activity), irrespective of diagnosis or treatment. P113 infusion caused a consistent fall in B.P. only after sodium depletion. The changes in B.P. after P113 infusion and those induced by propranolol correlated only during sodium depletion, when P.R.A. values rose. It is concluded that sodium depletion induced "renin dependency" of B.P. in all patients. The decrease in B.P. renin dependency after propranolol therapy suggests that suppression of P.R.A. is one of the antihypertensive mechanisms underlying the action of this drug.
Adolescent↗
Increase in serum-lipids during treatment of hypertension with chlorthalidone.
Fasting concentrations of serum cholesterol and triglyceride were measured before and during therapy in 63 patients with uncomplicated primary (essential) hypertension. The patients were divided into two groups, and diet therapy was applied equally to both groups. One group of 31 patients received no other therapy; the other 32 received chlorthalidone in addition to diet. Diet therapy consisted of no added sodium, caloric restriction if overweight, and consumption of foods low in lipids. On diet therapy alone serum-cholesterol fell by 11 mg/dl (P less than 0-02 vs pretreatment value) and serum-triglyceride was unchanged. When chlorthalidone was prescribed in addition to diet, serum cholesterol rose by 12 mg/dl and triglyceride by 36 mg/dl (P less than 0-005 vs pretreatment value for both). Serum-lipids were similar in the two groups before treatment; during therapy both serum cholesterol (P less than 0-05) and triglyceride (P less than 0-005) concentrations were higher in the chlorthalidone group. Thus, despite the prescription of lipid-lowering and calorie-restricted diets, serum-lipids became slightly raised when chlorthalidone was used as the sole drug in the treatment of hypertension.
Chlorthalidone↗
On the inappropriate in hypertension research.
The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.
Angiotensin II↗
Plasma renin and "prorenin" in essential hypertension during sodium depletion, beta-blockade, and reduced arterial pressure.
An inactive form of renin is activated by incubating human plasma at -5 degrees C. The relative proportions of active renin and this cryoactivatable "prorenin" in plasmas of untreated hypertensive patients varied widely. However, prorenin increased in parallel with active renin after sodium deprivation or diuretic therapy in 36 patients; the increases were similar whether or not blood-pressure fell. In contrast, propranolol administration in 22 patients lowered active renin in all, but it increased prorenin by 98% in 15 in whom systolic pressure fell. In the other 7 blood-pressure did not change, and beta-blockade produced a fall in total renin (active renin plus prorenin) while prorenin was unchanged. For all 22 there was an inverse relationship between propranolol-induced changes in plasma-prorenin and systolic pressure (r=-0-77, P less than 0-001). The fraction of active plasma-renin fell during propranolol administration from 43% to 18%, regardless of the blood-pressure response. Clonidine produced similar changes in 10 patients. Thus, sodium depletion stimulates total renin release, while propranolol and clonidine produce divergent responses of active renin and prorenin, the changes in prorenin depending on the changes induced in blood-pressure. These observations suggest that propranolol may block intrarenal conversion of prorenin to active renin while also suppressing total renin release. But the latter effect may be offset by concurrent baroreceptor-mediated release of total renin (mostly prorenin) when blood-pressure is lowered.
Adult↗
Acute mountain sickness.
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Altitude Sickness↗
Hypertension treated by salt restriction.
31 patients with a diastolic blood-pressure between 95 and 109 mm Hg have been treated for two years with a regimen involving a moderate restriction of salt in the diet. The results are compared with those in a control group and in a drug-treated group. Salt restriction has reduced the diastolic blood-pressure by 7.3+/-1.6 mm Hg, a result similar to that in patients treated with antihypertensive drugs. In the untreated group the diastolic blood-pressure rose by 1.8+/-1.1 mm Hg. Most patients did not achieve the desired amount of salt restriction and a stricter adherence to the diet might have caused further falls in blood-pressure. Excessive salt intake is probably a major cause of the epidemic of hypertension in "civilised" countries and a reduction in salt intake may help to control the epidemic. In persons with a diastolic blood-pressure between 90 and 105 mm Hg salt restriction should be tried before drugs.
Blood Pressure↗
Big renin in plasma of healthy subjects on high sodium intake.
Normal human plasma contains not only active renin but also an inactive form of renin which, after exposure to low pH, can generate angiotensin I from renin substrate. When healthy volunteers were given first a diet containing 400 mmol sodium and then a diet containing 10 mmol sodium for 4 days the changes in salt intake stimulated large changes in active plasma-renin and smaller changes in inactive renin. Inactive renin comprises a larger fraction of total renin in plasma of salt-loaded healthy subjects than salt depleted subjects. When plasma of healthy men on a high-salt diet was applied to a column of 'Sephadex G-100', renin eluted in two peaks, corresponding to big renin (60 000 daltons) and normal renin of lower molecular weight (40 000 daltons). Active and inactive forms of renin were present in both peaks. Plasma from salt depleted healthy subjects showed a large single peak of renin activity with a maximum at 40 000 daltons. These studies demonstrate that both big and small renin can exist as inactive or active enzyme. Big renin, previously found in certain diseases and in pregnancy, is also present in normal human plasma. These observations suggest a possible physiological role for big renin.
Chromatography, Gel↗
Salt intake and diuretic treatment of hypertension.
24 h urinary sodium excretion was used to monitor salt intake in 36 patients with essential hypertension to determine whether limitation of the antihypertensive action of thiazide diuretics could be explained by increased salt appetitie stimulated by salt depletion. Sodium excretion in these patients was similar before treatment to that observed in normotensive controls, and no change was observed during 2 years' treatment with bendrofluazide. However, plasma-renin rose progressively over the 2 years even in 5 of 8 patients whose renin was not stimulated initially by diuretics. Thus, there is no evidence that a voluntary increase in salt intake limits the efficacy of diuretic treatment; on the other hand, progressive stimulation of the renin-angiotensin system may be an important limiting factor to the antihypertensive action of diuretics. If so, the antihypertensive effect of dietary salt restriction may be similarly limited.
Adult↗
Treatment of mild hypertension in elderly males.
1. Males, born between 1900 and 1925, with mild hypertension have been treated for periods varying from 300 to 2000 days. 2. The life and death status of all patients (except two) was known on 1st November 1978. 3. A group of patients with mild hypertension receiving treatment based on a thiazide diuretic had a greater mortality than the other drug-treated group. 4. The increased mortality was caused by an increased number of myocardial infarcts. 5. Elderly male patients with mild hypertension probably have preexisting vascular disease and therapy should not automatically be started. If therapy is started, beta-adrenoreceptor-blocking drugs may be a preferred therapy.
Adrenergic beta-Antagonists↗
The influence of different sodium loads on renin release in hypertensive and normotensive states of chronic renal failure.
The purpose of the present study was to examine the influence of different sodium loads on renin release in the hypertensive and normotensive state of chronic renal failure. Blood pressure (BP), plasma renin concentration (PRC) and exchangeable sodium (NaE) were measured in eighteen patients with advanced chronic renal failure, nine hypertensives and nine normotensives, and in seven normal subjects (a) 6 days after a fixed sodium intake of 10 mmol/day, and (b) 6 days after a fixed sodium intake of 150 mmol/day. Mean NaE was 14-19% higher in the hypertensives compared with the normotensives and values of NaE correlated significantly to values of mean BP. No significant differences were present in PRC between the groups of patients and controls on either of the sodium regimens and no correlation was found between BP and PRC. However, average decreases of PRC in the hypertensives on high sodium intake, 33-34%, were significantly lower than the corresponding values of 69-71% in the normotensive patients and controls, respectively. Furthermore, the percentage changes of PRC on high sodium intake correlated significantly to mean BP as well as to NaE. These results suggest that renin release is relatively unresponsive to different sodium intakes in hypertension following chronic renal failure. This alteration in renin release may contribute to the maintenance of hypertension in chronic renal failure, PRC being "inappropriately' increased in relationship to the sodium excess.
Adult↗