Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies over the past 10 years suggest that the atrial natriuretic factor (ANF) plays an important role in salt and water homeostasis. Responding to atrial stretch, the atria releases ANF into the circulation. The several actions of this hormone tend to increase renal NaCl excretion resulting in reduced blood volume and blood pressure. ANF increases the glomerular filtration rate and reduces sodium chloride reabsorption in the distal nephron. It also inhibits secretion of aldosterone from the adrenal cortex. Therefore actions of ANF appear to be opposed to the renin-angiotensin-aldosterone system. Drugs that alter ANF metabolism may constitute a new mechanism of treatment for hypertension and heart failure.
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PMID:Role of atrial natriuretic factor in salt and water homeostasis. 140 80

The atrial natriuretic factor (ANF) as an osmoregulatory hormone causes a reduction of extracellular fluid volume primarily through stimulation of renal and extrarenal water and sodium elimination. Consequently, ANF counteracts the renin-angio-tensin II-aldosterone (RAAS) and the antidiuretic hormone (ADH) systems at their target organ level. The possible direct interaction of ANF with the hypothalamo-neurohypophyseal ADH system was investigated in conscious ducks and rabbits during conditions of eu- and dehydration. In euhydrated animals, the plasma concentration of ADH remained unchanged during the systemic infusion of species-specific ANF, whereas in dehydrated rabbits but not ducks, the plasma concentration of ADH was significantly decreased. These differences in ADH modulation were supported by the localization of binding sites for radiolabeled ANF at the sites of ADH release, the median eminence (ME) and neurohypophysis (NH) of the rabbit but not duck brain, using receptor-autoradiography. For both species, circumventricular organs lacking a functional blood-brain barrier (BBB) such as the subfornical organ (SFO), the organum vasculosum of the laminae terminalis (OVLT), the pineal and the choroid plexus (ChP), as well as the ependymal lining of the third ventricle (VIII) were labeled specifically. Within the BBB, binding sites for ANF could not be detected in the ADH-synthesizing paraventricular (PVN) and supraoptic nuclei (SON) of either species, however, sites were observed in the anterior median nucleus of the hypothalamus (AM) of the duck brain. In the AM as well as the PVN and ME, the existence of a brain-intrinsic ANF system could be demonstrated for the Pekin duck using immunocytochemistry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ANF-induced modulation of ADH-release in the rabbit and Pekin duck. 141 Apr 35

Calcium entry blockers have been shown to exert hemodynamic and diuretic effects in the kidney. The diuretic effects can be demonstrated most clearly in the isolated perfused kidney, not influenced by compensatory mechanisms such as a lower blood pressure or changes of hormones. However, they can also be shown in vivo in humans. We studied the renal effects of calcium entry blockade after the first dosage and after continued oral dosages of 20 mg nicardipine tid in patients with essential hypertension and in normotensive controls. Renal function was determined during maximal free water clearance, allowing estimation of changes in "proximal" and "distal" tubular sodium reabsorption. Results showed a natriuretic effect. In the control subjects, clearance results were compatible with a decrease of proximal and distal tubular reabsorption, but in the hypertensive group natriuresis was mainly achieved by an increase of the glomerular filtration rate and a decrease of fractional distal reabsorption. In both groups the natriuresis occurred concomitantly with a lower blood pressure. The ratio plasma renin activity/plasma aldosterone concentration increased, although nicardipine did not inhibit the increase of plasma aldosterone during angiotensin II infusion. Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers.
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PMID:The diuretic effect of calcium entry blockade in normals and hypertensive patients. 141 40

We investigated the role of atrial natriuretic factor (ANF) and the renin-angiotensin system as well as the effects of losartan in rats with aortocaval (AC) shunts. Right atrial and left ventricular end-diastolic pressures (LVEDP) were higher and mean arterial blood pressure (MAP) was lower in AC shunt animals than in their controls. AC shunt rats presented marked cardiac hypertrophy, decreased right atrial ANF concentration, and increased ventricular ANF content and concentration. Plasma ANF levels were elevated, and hematocrit was lower in AC shunt animals than in controls. Captopril or losartan treatment decreased MAP and returned LVEDP to sham-operated control values. A clear regression of cardiac hypertrophy was evident in both treated AC shunt groups, with plasma ANF levels tending to follow those in sham-operated rats. Plasma COOH-terminal ANF levels were decreased and urinary volume and hematocrit were increased in losartan-treated AC shunt animals. We conclude that chronic angiotensin converting enzyme inhibition and angiotension II receptor antagonism improved hemodynamic conditions, diminished water retention, reversed cardiac hypertrophy, and restored plasma and tissue ANF to more "normal" levels in rats with moderate high-output heart failure.
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PMID:Chronic captopril and losartan (DuP 753) administration in rats with high-output heart failure. 141 10

We studied hypoxia and hypotensive hemorrhage in conscious female goats. After control, goats continued an experimental period in normoxia or hypoxia [fractional inspired oxygen concentration (FIO2) = 0.10] for 120 min. After 60 min in the experimental period, a hemorrhage (0.5 ml.kg-1.min-1 for 30 min) was initiated (normoxic hemorrhage, NH; hypoxic hemorrhage, HH). Heart rate (HR) increased 51 +/- 18 beats/min with NH after 30 min of hemorrhage. HR increased 40 +/- 10 beats/min after hypoxic gas introduction, with no further increase during HH. Mean arterial blood pressure (MABP) was reduced 23 +/- 7 mmHg 30 min after completion of blood loss with normoxia but was reduced 23 +/- 7 mmHg at 20 min of HH. Arginine vasopressin (AVP) was increased to 2.60 +/- 2.08 and 160.40 +/- 49.74 microU/ml after 10 and 20 min of HH, respectively, and was only increased after 30 min (87.33 +/- 67.18 microU/ml) of NH. Unexpectedly, plasma renin activity (PRA) increased in parallel in both groups and was doubled at 30 min of hemorrhage. Atrial natriuretic factor was reduced to 8.8 +/- 1.6 pg/ml by 10 min of NH and to 11.4 +/- 3.3 pg/ml at 30 min of HH. Thus hypoxia leads to an earlier development of hypotension and increase in AVP with blood loss but may attenuate the PRA response to blood pressure reduction.
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PMID:Hypoxia attenuates the renin response to hemorrhage. 141 56

Acute hypoxemia at sea level is associated with decreased aldosterone secretion. This inhibition is thought to be mediated through secretion of atrial natriuretic factor (ANF). The interaction of these two hormones should result in enhanced renal salt excretion during hypoxemic conditions. This hypothesis was tested by administration of a standardized salt load to seven normal subjects during normoxemia at sea level (SL), acute hypoxemia (AH) at sea level, and high altitude (HA) (3,000 m). Urine and venous blood samples were collected and analyzed. A natriuresis and diuresis was observed only under AH conditions. It was accompanied by a decrease in plasma aldosterone levels, but did not correlate with changes in plasma aldosterone levels, ANF, or other hormones. Increased plasma renin activity (PRA) and increased norepinephrine levels were encountered at HA, suggesting sympathetic nervous system activation. No change in anti-diuretic hormone (ADH) levels with increased plasma osmolality was seen at HA. We conclude that excretion of a salt load during normobaric hypoxemia is enhanced by a decrease in plasma aldosterone levels, unrelated to changes in ANF or other hormones. The differences observed in norepinephrine, PRA, and ADH levels during HA versus AH conditions suggest that hypobaria or chronic hypoxemia may influence these hormonal responses.
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PMID:Effects of hypoxemia at sea level and high altitude on sodium excretion and hormonal levels. 141 52

The behavior of plasma atrial natriuretic factor (ANF) and digoxin-like substance (DLS), and the daily urinary excretion of kallikrein (uKK) were evaluated in young hypertensives and in young normotensives with or without a family history of essential hypertension. Each group was also evaluated, separating those with low plasma renin activity from the total sample. The sample group was made up of 75 young males; 31 hypertensives (mean age 22.7 +/- 2.5 years), 28 normotensives with hypertensive heredity (normotensives F+) (mean age 22.2 +/- 1.9 years) and 16 normotensives (mean age 22.0 +/- 2.1 years). An inverse correlation between ANF and PRA was shown in all groups. In hypertensives, ANF was inversely correlated with uKK (r = -0.664, P less than .0001). Plasma ANF (P less than .012) and DLS (P less than .0001) were higher in hypertensives than in normotensives, while uKK excretion was lower (P less than .0001). Plasma levels of DLS were higher in F+ normotensives than in normotensives (P less than .003). Low renin hypertensives showed the lowest uKK excretion (P less than .0001 v normal-high renin hypertensives). Furthermore, low renin hypertensives showed the highest plasma levels of ANF (P less than .0001 v normal high renin hypertensives) and DLS (P less than .012 v normal-high renin hypertensives). Plasma ANF (P less than .0001) was higher, while uKK was lower (P less than .045) in low renin F+ normotensives than in normal-high renin ones. In conclusion, our data indicate that plasma ANF and DLS are elevated since the early phase of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natriuretic hormones in young hypertensives and in young normotensives with or without a family history of hypertension. 141 48

The direct vascular action of atrial natriuretic factor (ANF) is unclear. In coronary vasculature, vasodilation has been reported as well as vasoconstriction. Doses of ANF, baseline plasma ANF levels and interference with the renin-angiotensin system might account for the controversy. We tried to further analyse determinants of the effect of ANF on coronary blood flow in anaesthetized dogs. The chest was opened and the left anterior descending coronary artery cannulated and perfused at constant normal (= 76 +/- 5 mmHg, n = 10) or reduced (= 37 +/- 3 mmHg, n = 10) pressure from the femoral arteries. At normal coronary perfusion pressure, ANF (1 ng kg-1 i.c.) reduced coronary flow from 30.7 +/- 4.2 to 26.9 +/- 4.0 ml min-1 (P less than 0.05). This effect was no longer significant at reduced coronary perfusion pressure (4.9 +/- 0.8 vs. 4.6 +/- 0.7 ml min-1). ANF (1 ng kg-1 i.c.) reduced coronary blood flow in correlation with baseline plasma ANF levels (r = 0.77, P less than 0.001). However the large variability of the constrictor effect of ANF in the rather small range of baseline plasma ANF, weakens the importance of this result and suggests other additional determinants. ANF (100 ng kg-1 i.c.) significantly increased coronary blood flow by 16-23% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determinants of coronary effects of atrial natriuretic factor in dogs. 142 57

We treated a patient with refractory biventricular heart failure, dilutional hyponatremia and prerenal azotemia, by means of ultrafiltration. After ultrafiltration, gas exchange and cardiac output improved, with concomitant reduction of systemic and pulmonary vascular resistances. Despite a decrease of right atrial and wedge pressure, atrial natriuretic factor rose and plasma renin activity decreased.
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PMID:Atrial natriuretic factor and concomitant hormonal, hemodynamic and renal function changes after slow continuous ultrafiltration. 142 64

Atrial natriuretic peptide (ANP) shows a nychtohemeral fluctuation and an age-related trend. The aim of this study was to explore the circadian rhythm of ANP as a function of age. Circadian rhythms of plasma renin activity (PRA), aldosterone (PA), and cortisol (PC) were explored as well. Twenty clinically healthy subjects, 10 young (20-25 yrs) and 10 elderly (65-75 yrs), were investigated, while recumbent, after synchronization to light-dark regimen and meal timing. Blood samples for RIA tests were collected six times during the 24-hr span. The chronobiologic analysis in young subjects demonstrated a significant circadian rhythm for all the investigated variables with an acrophase-timing located at 16.48 for ANP, 4.44 for PRA, 5.32 for PA, and 7.12 for PC. In elderly subjects we documented an important increase of 24-hr mean plasma levels but not a statistically significant circadian rhythm for ANP, and a decrease in mean value of PRA which maintained, however, a significant periodic 24-hr oscillation in parallel with PA and PC. The results in young subjects reinforce the concept that ANP plays physiologically an inhibitory role on the phasic secretion of renin. The lack of the circadian rhythm for ANP along with the divergent changes in ANP and PRA 24-hr mean concentration of elderly subjects both suggest that ANP exerts with advancing age only a counterregulatory role on the tonic rather than the phasic release of renin.
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PMID:Effect of aging on circadian rhythm of atrial natriuretic peptide, plasma renin activity, and plasma aldosterone. 143 Aug 51


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