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At least 19 recordsLinked to original sources
PubMed1977

Renin reactivity, renin activity and renin concentration in patients with normal and low renin essential hypertension.

Renin activity, concentration, substrate and reactivity were determined in normal subjects as well as in hypertensive subjects with suppressed and normal plasma renin activity. Renin substrate measurements were similar in all groups. Renin reactivity, a measure of circulating modifiers of the renin reaction, was significantly increased in both hypertensive groups. Reactivity was significantly greater in the normal renin hypertensive group than the low renin hypertensive group. Renin concentration was significantly suppressed in both hypertensive groups, but to a greater degree in the low renin hypertensives. These findings suggest that plasma renin concentration may be suppressed in most hypertensive subjects. Furthermore, plasma renin activity may be "normalized" in most hypertensive subjects by the effect of circulating modifiers of the renin reaction. While renin reactivity in the plasma of low-renin hypertensive subjects is accelerated to a lesser degree than that of the normal-renin hypertensives, this finding alone does not explain the low plasma renin activity.

Angiotensinogen↗
PubMed1977

Renin reactivity in plasma of patients with normal renin and low renin essential hypertension.

Plasma renin reactivity (PRR) is the rate of angiotensin generation in vitro after addition of exogenous renin to plasma. To evaluate the hypothesis that suppressed plasma renin activity (PRA) in patients with low renin essential hypertension may be related to an alteration of the kinetics of the in vitro renin reaction, PRR was compared in plasma of patients with low renin and normal renin essential hypertension. Prostaglandin A (PGA) inhibits renin, and PGA was also measured to determine if suppressed PRA may be related to increased PGA. Low renin and normal renin hypertension were defined by comparing PRA responses of 30 hypertensive patients and 16 matched control subjects to upright posture and furosemide (80 mg p.o.). Nine of 30 patients had low PRA. Compared to that in plasma of patients with normal renin hypertension, PRR was suppressed (P less than 0.005) during 30, 60, and 180 min incubations in the low renin patients. Overall, in the hypertensive patients, there was a significant positive correlation (r= +0.58; P less than 0.01) between PRR and the PRA response to furosemide. PGA in patients with low renin hypertension (0.86 ng/ml+/-0.06 SE) was less (P less than 0.05) than that in patients with normal renin hypertension (1.10 ng/ml+/-0.07) SE) and control subjects (1.18 ng/ml+/-0.10 SE); PGA of normal renin patients and control subjects did not differ (P less than 0.1). These results suggest that an alteration of the kinetics of the renin reaction may contribute to the apparent renin suppression in patients with low renin hypertension. Hypertensive patients with suppressed PRA also have low PGA.

Carbon Dioxide↗
PubMed1979

Measurement of plasma renin concentration using exogenous human renin substrate in normal subjects: correlation with plasma renin concentration and plasma aldosterone concentration.

Measurement of plasma renin concentration (PRC) was done in normal subjects at rest and under acute stimulation of renin release under unrestricted sodium intake. Concurrent measurements of plasma renin activity (PRA) and plasma aldosterone concentration (PA) were carried out. The mean values of PRC at rest and after stimulation of renin release were 12.8 +/- 1.3 (SEM) and 21.7 +/- 4.4 (SEM) ng AT I/ml/h, respectively. These corresponded to renin contents of 3.4 +/- 0.34 (SEM) X 10(-5) Goldblatt units and 5.8 +/- 0.36 (SEM) respectively. The mean percent increase of PRC (82.1 +/- 19.3 (SEM)) %) was almost indentical to that of PA (81.5 +/- 16.4 (SEM) %), but differed from that of PRA (269 +/- 83.1 (SEM) %). A very high correlation between concurrent PRC and PA (r = 0.92, P less than 0.001) was found in normal subjects at rest and under acute stimulation of renin release. A good correlation between PRC and PRA (r = 0.85, P less than 0.001) was also observed. However, a higher correlation between percent increases of PRC and PA (r = 0.92, P less than 0.001) than that of PRA and PA (r = 0.80, 0.01 less than P less than 0.005) was found. Results show that PRA is a good index of the renin content in plasma in normal subjects at rest and PRC reflects actual renin concentration in plasma at rest as well as under stimulation of renin release.

Adult↗
PubMed1979

Maternal and fetal renin activity and renin and big renin concentrations in second-trimester pregnancy.

Plasma renin activity (PRA) and the concentrations of renin (PRC) and big renin (PBRC) have been determined in maternal and fetal blood, and renin and big renin have been measured in amniotic fluid, at 16 to 20 weeks of gestation. Gradients between peripheral arterial and venous and uterine venous maternal circulation were not apparent for PRA, PRC, or PBRC. PRC and PBRC but not PRA were consistently higher in fetal cord blood than in the maternal compartment. The concentrations of big renin and of renin were tenfold higher in amniotic fluid than in maternal plasma and were significantly correlated in amniotic fluid but not maternal or fetal plasma.

Amniotic Fluid↗
PubMed1976

Contrasting effects of hypoglycemia on plasma renin activity and cyclic adenosine 3',5'-monophosphate (cyclic AMP) in low renin and normal renin essential hypertension.

Insulin-induced hypoglycemia previously has been shown to provoke a beta-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.

Adrenal Medulla↗
PubMed1978

A comparison of cold and acid activation of big renin and of inactive renin in normal plasma.

Normal human plasma contains "inactive renin," whose ability to generate angiotensin I increases after exposure to pH 3.3. Big renin is a partially inactive enzyme of larger molecular weight, which is also activated at pH 3.3, and is found of pregnant women, and in amniotic fluid, but not in normal plasma. We have compared the effects of acid exposure and storage at 4 and -4 C on normal plasma and plasma containing big renin. The concentration of inactive renin in normal plasma was approximately equal to that of normal active renin, and its activity increased slowly on prolonged standing at -4 but not 4 C. In contrast, the activity of big renin increased by 50% as early as 1-3 days at 4 C and increased even more quickly at -4 C. Acid treatment of plasma containing big renin caused 4-10 times greater increase in active renin than similar treatment of normal plasma. During gel filtration, both cold-activated and previously acidified big renin coeluted with unactivated big renin. These data indicate that big renin is highly susceptible to cold or acid activation and that such activation of big renin does not result in a detectable decrease in its molecular weight of 60,000 daltons. Furthermore, acid and cold seem to activate the same pool of inactive renin in normal plasma. Although both normal and big renin are stable for long periods below -20 C, a serious overestimate of plasma renin activity can occur if plasma is stored just above its freezing point before assay.

Amniotic Fluid↗
PubMed1979

Specific antibody to hog renal renin and its application to the direct radioimmunoassay of renin in various organs.

We produced anti-hog renin antibodies using as antigens pure hog renal renin that either had been insolubilized or conjugated to tetanus toxoid. High titer antibodies were obtained, which demonstrated different cross-reactivity with renins from other species. A direct radioimmunoassay for renin was developed using antibody, monoiodinated 125I-hog renin, and various methods for separating free and antibody-bound trace. This assay was capable of detecting 40 pg of hog renin and was applied to the determination of renin in hog blood and other organs. Based on the direct measurement of renin by this radioimmunoassay, the renin-like activity (i.e., the ability to generate angiotensin I from renin substrate preparations) of the pituitary gland was found to be due mostly to true renin, whereas the renin activity of other hog tissues, including the adrenal gland, liver, lung, spleen, and submaxillary gland, was not identified as renin and may have been due to cathepsins.

Adrenal Glands↗
PubMed1978

Partial characterization of aortic renin in the spontaneously hypertensive rat and its interrelationship with plasma renin, blood pressure and sodium balance.

1. A renin-like enzyme in aortic tissue of the spontaneously hypertensive rat was found to be a freely dissociable enzyme (saline homogenization) with an affinity for the renin inhibitor pepstatin. At neutral pH values, the enzyme was active in homologous plasma to produce angiotensin I, and therefore distinct from pseudorenin and cathepsin D. The arterial enzyme and semi-purified renal renin could not be distinguished on the basis of Km values by using homologous renin substrate 2. An inverse relationship between the aortic renin content of the spontaneously hypertensive rat and the progressive increase of systolic blood pressure was observed with age. In contrast to this strain of rat, aortic renin of the normotensive WKY strain did not decline with age. 3. Plasma renin concentration and the aortic renin content of the spontaneously hypertensive rat showed divergent changes in response to a blood pressure fall associated with acute diuretic therapy, chronic administration of hydrallazine and in some animals in response to chronic administration of propranolol. 4. A low sodium diet elevated both plasma and aortic renin and retarded the progressive increase of blood pressure in the spontaneously hypertensive rat. A high sodium diet accelerated the progress of hypertension with no effect on aortic or plasma renin. 5. Antihypertensive therapy (1--6 weeks), resulting in a lowering of conscious systolic blood pressure of the spontaneously hypertensive rat, consistently led to a decrease in aortic renin content.

Angiotensin I↗
PubMed1977

Possible role of renin in hypertension as suggested by renin-sodium profiling and inhibition of converting enzyme.

To block renin activity, a nonapeptide converting-enzyme inhibitor was given to 65 seated hypertensive patients. Depressor responses occurred only when control plasma renin activity exceeded 2 ng of angiotensin I per milliliter per hour and correlated directly in amplitude with control plasma renin activity and with induced increments in activity (P less than 0.001 for both). Depressor responses, like renin activity, were characteristic for renin subgroups as defined by renin-sodium profiling. Before and after sodium deprivation, the nonapeptide reduced diastolic pressure in all patients with high renin (by 17.3 and 19.8 per cent) and most patients with normal renin (by 9.1 and 17.7 per cent). Low-renin patients remained unresponsive. This enzyme blockade may cause bradykinin accumulation. But if, as seems likely, depressor responses are due to blockade of angiotensin II formation, the results indicate that, irrespective of sodium balance, measurements of plasma renin activity reflect its contribution to blood-pressure maintenance. The results suggest broad participation of the renin system in common forms of hypertension.

Angiotensin II↗
PubMed1975

Time course of changes in plasma renin after blockade of the renin-system. Studies of conscious and anaesthetized, normal, adrenalectomized and spontaneously hypertensive rats.

Inhibition of the angiotensin I converting enzyme with SQ 20.881 results in a 2 to 35 fold increase in plasma renin concentration in normal rats and in spontaneously hypertensive rats. The effect is transient, lasting for 1 to 3 hours even in the presence of prolonged blockade. The relative increase is independent of the pretreatment plasma renin concentration. The blood pressure is unchanged in conscious rats in which the effect of SQ 20.881 on plasma renin is believed to be due to a blockade of the negative feedback of angiotensin II on renin release. In anaesthetized rats, SQ 20.88) has an additional hypotensive effect which augments the increase in plasma renin. Saralasin is without effect on blood pressure and plasma renin in conscious normal rats and in spontaneously hypertensive rats, while it causes a transient 3 to 27 fold increase in plasma renin concentration in anaesthetized rats. It is suggested that this increase is hardly due to an interception of the feedback, but to the concomitant fall in blood pressure, as a similar hypotension and increase in plasma renin is produced by dihydralazine. It is furthermore found that Saralasin blocks renin release induced by SQ 20.881. This demonstrates that Saralasin is bound to the receptors in the juxtaglomerular cells and has slight, agonistic properties there. Both in conscious rats and in anaesthetized adrenalectomized rats substituted with DOCA and salt, SQ 20.881 as well Saralasin causes transient increases in plasma renin concentration. If such rats are only substituted with salt and not with DOCA, the effects of both blockers are in the form of severe hypotension and a permanent elevation of plasma renin.

Adrenalectomy↗
PubMed1978

Renin secretion as a function of renal renin content in dogs.

The in vivo and in vitro rates of renin secretion were measured in kidneys from five groups of dogs in which renal perfusion pressure, salt diet, and neural input were varied to cause large changes in renin secretion rates and renal renin content. It was found that both the in vivo and in vitro secretory rates were proportional to the renal renin content. However, in vitro secretion rates were dependent on content up to 100 ng angiotensin I/mg tissue per h. At higher renin contents no increment in in vitro secretion rate was seen. In vivo secretion rate did not appear to reach a maximum until renal renin content was above 250 ng AI/mg tissue per h. The data are interpreted to support the hypothesis that there exist at least two pools of renin. One releases renin at a fractional rate of about 1.5% of the total content per hour. The other releases renin at a rate dependent on the magnitude of the stimuli acting on the kidneys. It is also suggested that the rate of renin synthesis may be a determinant of the basla rate of renin secretion.

Angiotensin I↗
PubMedDate not supplied

Serial renin-angiotensin studies in spontaneously hypertensive and Wistar-Kyoto normotensive rats. Transition from normal- to high-renin status during the established phase of spontaneous hypertension.

To characterize the renin-angiotensin system in the Aoki-Okamoto spontaneously hypertensive rat (SHR) more fully, serial measurements of plasma renin activity (PRA), plasma renin concentration (PRC), renin reactivity (as relative index of circulating modifiers of the renin reaction) and renin substrate concentration were made in 6- to 64-week-old SHR and in age-matched Wistar-Kyoto normotensive rats (WKY). In the evolving phase of SHR hypertension (6 and 13 weeks of age), PRA was comparable to WKY control values, whereas mature SHR with established hypertension developed, between 13 and 35 weeks of age, a high-PRA state persisting through 64 weeks of age. In 64-week-old SHR, increased plasma volume (3.54 +/- 0.91 in SHR vs. 3.18 +/- 0.90 ml/100 g body weight in WKY, p less than 0.025), together with increased PRA (24.9 +/- 3.8 in SHR vs. 13.1 2.2 ng AI/ml plasma/hr in WKY, p less than 0.025), suggest that volume decrease cannot explain increased PRA. In 42-week-old SHR, PRA was incompletely suppressed by deoxycorticosterone acetate plus 1% saline orally for 4 days: 4.9 +/- 1.2 in SHR vs. 0.6 +/- 0.8 ng angiotensin I/ml plasma/hr in WKY, p less than 0.001. Modestly increased renin reactivity of plasma was observed in SHR at all ages studied, supporting the ubiquity of increased circulating accelerators (or decreased inhibitors) of the renin reaction in hypertensive states. However, elevated renin reactivity did not account for the transition from normal to high PRA observed in mature SHR, nor did renin substrate concentration, which was consistently lower in SHR than in age-matched WKY. Temporal patterns of, and strain differences in PRA were closely paralleled by variations in PRC but not by other reaction components. Significant elevation of serum creatinine in old SHR support the presence of renal injury. We conclude that PRA and PRC are normal in evolving SHR hypertension and progress to abnormally elevated levels after hypertension is established. We postulate that "high-renin" hypertension may develop as a consequence of the hypertensive state per se, perhaps due to nephrosclerotic vascular disease.

Angiotensin II↗
PubMed1977

Decreased plasma renin activity and renin release in rats with phaeochromocytoma.

1. We have examined the response of renin to chronic low and high sodium chloride intake in rats with transplanted phaeochromocytoma. 2. Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. 3. Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. In addition, low perfusion pressure (50 mmHg) failed to stimulate renin release in kidneys from these phaeochromocytoma rats. 4. Additional experiments demonstrated that chronic sodium chloride loading suppressed plasma renin activity, renin content and renin release in both phaeochromocytoma and control rats. Both sodium-loaded phaeochromocytoma and sodium-loaded control rats were unresponsive to low perfusion pressure. 5. We conclude that noradrenaline-secreting phaeochromocytoma impairs the response of plasma renin activity in the rat by inhibiting renin release. We also conclude that chronic sodium chloride loading has a similar effect, but the mechanisms remain to be determined.

Animals↗
PubMed1979

Relationship between molecular weight conversion and renin activity in dog renal renin.

A normal size form of renin, which seems to be a storage form in renin granules, changed neither in molecular weight nor activity by acidification to pH 3.0. High molecular weight (HMW) renin fractionated by gel chromatography from crude renal extract prepared with thiol group blockers was converted into normal size renin by acdification, accompanied with an increase in renin activity by about 50%. The molecular weight conversion by acidification appeared due to destruction or loss of binding ability of the renin binding substance which was present in the cytosol of renal cortical tissue. Renin and renin binding substance could combine into HMW renin at neutral pH in the presence of thiol group blockers and renin activity decreased.

Acids↗
PubMed1975

A renin inhibitor from rabbit kidney: conversion of a large inactive renin to a smaller active enzyme.

Renin in extracts of frozen rabbit kidney exists in two forms: active (molecular weight about 37,000) and inactive (molecular weight about 55,000) renin. The inactive form becomes active after exposure to pH 2.5 at 4 degrees C. If extracts are chromatographed on DEAE cellulose, the inactive renin dissociates into active renin plus a renin inhibitor (molecular weight about 13,000). The inhibitor recombines with active renin if the two are incubated together at 37 degrees C. The inhibitor is destroyed by acid treatment at pH 2.5 at 4 degrees C. We conclude that the activation of inactive renin is due to destruction of the inhibitor by acid. The inactive material may be a renin proenzyme or a storage form of active renin combined with inhibitor.

Animals↗
PubMed1975

Improvement of renin determination in human plasma using a commonly available renin standard in a radioimmunological method.

UNLABELLED: A new method for the measurement of renin in human plasma is described. The method is based on the introduction of the internationally available renin standard of the Medical Research Council (MRC) London, as a calibration system. Thus, some principal disadvantages of methods expressing results in renin reaction velocity (angiotensin generation rate) only are avoided. Both renins, unknown and standard, react with a sheep substrate preparation and are handled identically throughout the whole procedure including the angiotensin I radioimmunoassay (RIA). The plasma renin concentration (PRC) is given in 10(-6) MRC-renin units (muM/ml). RESULTS: the renin standard is free of angiotensin, angiotensinases, and angiotensinogen; it is stable on storage. Identical enzyme kinetics are shown for both renins. An interference between endogenous and exogenous substrate could be avoided. The potentially harmful influences of proteins from the enzyme incubation mixture of the RIA dose response curve are shown. The use of an angiotensin I calibration system could be omitted. Using a standard renin dilution from 250-0.9 muU/ml also the full biological range is covered. When giving an unrestricted diet the preliminary normal values of PRC are 21.9 +/- 12.6 muU/ml in recumbent and 40.1 +/- 19.8 muU/ml in upright position (n = 16,x +/- s, age 20-35 years). Earlier findings of age-dependency of PRC were confirmed.

Adult↗
PubMed1976

Control of renin secretion in vivo and in vitro in rats: arguments in favour of a precursor form of renin and of a role of a microtubular system.

1. The morphology of the juxtaglomerular apparatus, plasma renin activity, plasma renin substrate and renal renin have been studied in rats after maximal stimulation by bilateral adrenalectomy and salt depletion, and also after blocking this stimulation by deoxycorticosterone and salt load. 2. After stimulation the juxtaglomerular apparatus showed a well-developed granular endoplasmic reticulum and a low secretory granule content. Plasma renin activity was markedly elevated and plasma renin substrate was low. After blockade numerous specific granules with crystalline structures were seen and the granular endoplasmic reticulum was less developed. Plasma renin activity was now low and plasma renin substrate elevated. 3. After prior acidification of the kidney extract a significant increase of renal renin was observed in both conditions but was greater in the second group at the time when large numbers of young granules containing crystalline material were seen. 4. Kidney slices from the adrenalectomized salt-depleted rats released more renin than control slices. Vincristine did not affect this release, but inhibited release from slices stimulated by isoprenaline.

Adrenalectomy↗
PubMed1979

Arterial wall renin and renal venous renin in the hypertensive rat.

1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2. Arterial wall renin and renal venous renin were normal in younger spontaneously hypertensive rats, but in older spontaneously hypertensive rats arterial wall renin was significantly increased and renal venous renin was significantly decreased. 3. Arterial wall renin in rats with either acute or chronic two-kidney Goldblatt renal hypertension was significantly increased, whereas circulatory renin was elevated in the former, but depressed in the latter. 4. Arterial wall renin may play a role in the maintenance of acute and chronic renal hypertension and also perhaps of spontaneous hypertension of long duration in older rats.

Angiotensin I↗