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)

Prostaglandins (PG) are highly unsaturated, cyclic fatty acids with 20 carbon atoms which are biosynthesized from dihomo-gamma-linolenic, arachidonic and eicosapentaenoic acids. These fatty acids are either ingested or are biosynthesized from linoleic and linolenic acids, respectively. The PG-precursor fatty acids are liberated from membrane phospholipids by phospholipase A and are converted to prostaglandins by the multienzyme complex PG-synthetase. The activity of the PG-system is influenced by extracellular hormonal, neural and mechanical stimuli and by intracellular factors such as ion-concentration and activity of the enzymes adenyl- and guanylcyclase. Prostaglandins are tissue hormones or autacoids which act on their receptors near their site of synthesis and degradation. The prostaglandin family constitutes a group of more than 10 natural occurring compounds showing a variety of biological actions. In arteries and veins the different PG:s have vasodilating as well as vasoconstricting effects. In addition, they are involved in the regulation of vascular smooth muscle proliferation. Within the kidney PG:s have vascular and tubular actions. They antagonize the effect of ADH, mediate renin secretion and are involved in the control of electrolyte balance. In the regulation of platelet aggregation and platelet adhesion PG:s have opposite functions: Prostacyclin which is synthesized in the vascular wall antagonizes the aggregating action of Thromboxane A2 which is formed in the platelets. A defect or an imbalance in the production of PG:s in the vascular wall, in platelets or in the kidney is assumed to play a pathogenetic role in a variety of cardiovascular and renal diseases such as in hypertension, atherosclerosis, persistent ductus arteriosus and Bartter's syndrome.
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PMID:[Prostaglandins in cardiovascular and renal function. Biochemical, physiological and clinical findings (author's transl)]. 10 97

In this chapter we have emphasized especially the intrinsic controls of the circulation, such as the autoregulation mechanism for control of local blood flow, automatic control of cardiac output, long-term control of arterial pressure, long-term control of blood volume, and automatic distribution of fluids between the circulation and the interstitial spaces. The reasons for emphasizing these mechanisms are several: first, many experiments have now shown that the intrinsic mechanisms can provide highly stable long-term control of the circulation. Second, the value of the nervous and hormonal controls have probably been greatly overemphasized in the past. And, third, there are special complexities of the intrinsic controls--such as nonlinearities, delay in responses, and other effects--that have made these difficult to understand; it is probably these difficulties that have led to their underemphasis. However, we have not meant to take from the nervous and hormonal systems their true importance in circulatory control. For instance, intrinsic mechanisms have almost no capability for acute arterial pressure control (only for long-term control), and they have no mechanism for providing the drive necessary to make the animal ingest water and electrolytes. These require the nervous controls. Also, nervous reflexes are important in enhancing the effectiveness of blood volume control and control of cardiac pumping. Among the hormonal mechanisms, the renin-angiotensin system can provide a modest degree of arterial pressure control when the pressure falls below normal by eliciting a vasoconstrictor response in the peripheral blood vessels. However, this system seems to have an even more important renal function, a direct effect on kidneys to cause fluid retention; this in turn increases the body fluid volume and in this way increases the arterial pressure. Finally, the roles of ADH and aldosterone in the control of blood volume have probably been greatly overemphasized. On the other hand, both clinical experience and experimental studies are beginning to demonstrate that the thirst/ADH system is probably by far the most potent mechanism that we have for control of extracellular fluid sodium ion concentration. On the other hand, the aldosterone mechanism seems to be our primary control system for maintaining a normal extracellular fluid concentration of potassium.
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PMID:Integration and control of circulatory function. 13 39

This study conducted on the crewmembers of Skylab 3 was designed to evaluate the endocrinological adaption resulting from extend exposure to a space flight environment by identifying changes in hormonal and associated fluid and electrolyte parameters. The three men served as their own controls and were on a constant dietary intake. Complete metabolic collections were performed beginning 21 d before the flight, continuing throughout the flight, for 18 d postflight. Changes in fluid and electrolyte balance have been correlated with weight loss, changes in the excretion of aldosterone, vasopressin, and fluid compartments. Inter-individual variability was demonstrated in most experimental indices measured; however, statistically significant patterns have emerged which include: decreases in body weight and ADH, increases in plasma renin activity, and elevations in urinary catecholamines, aldosterone and cortisol concentrations. Urinary sodium was increased in flight but potassium was only slightly changed. Total body exchangeable K was slightly decreased in all three of the crewmen. Total body water and extracellular fluid were decreased postflight in almost all cases. The measured changes are consistent with the prediction that a relative increase in thoracic blood volume upon transiton to the zero gravity environment is interpretated as a true volume expasion resulting in a net fluid loss. This, in association with other factors, ultimately results in a reduction in intravascular volume leading to an increase in renin and a secondary aldosteronism. Once these compensatory mechanisms are effective in reestablishing positive water balance, the crewemn are considered to be essentially adapted to the space environment. Although the physiological cost of this adaptation must reflect the electrolyte deficit and perhaps other factors, it is assumed that the compensated state is adequate for the demands of the environment; however, this new homeostatic set is not believed to be without physiological cost and could, except with proper precautions, reduce the functional reserve of exposed individuals.
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PMID:Metabolic and endocrine studies: the second manned Skylab mission. 17 19

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.
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PMID:Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. 38 37

Inhibition of ADH-secretion and transient water diuresis was observed as acute effects of radio-frequency lesions in the septal region of goats. The water diuresis was not compensated for by drinking and therefore rapidly induced pronounced hypernatremia and hypovolemia. The development of hypovolemia was accompanied by a rise in plasma renin activity. Lesions of the same kind, but extending into the preoptic region near the medial portion of the supraoptic nuclei induced the inability to excrete excessive water characteristic of SIADH. Determinations of plasma arginine vasopressin suggested that the lesions causing SIADH did not produce any noticeable increase in basic ADH-secretion. The results suggest that impulses from juxtaventricular receptors regulating ADH-release and water intake to a considerable extent are transmitted via the septal region, and that elimination of this impulse traffic is sufficient to turn water balance to the negative side. However, reflex volumetric inhibition of the ADH-secretion does not seem to be mediated by pathways passing through the septal region.
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PMID:Transient water diuresis and syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by forebrain lesions of different location. 71 63

Using Boucher micromethod for determining renin activity in the rat pineal gland and hypophysis tissues, before and after NaCl 10% i.v. administration, the normal rats showed an average value of 96.8 +/- 21 ng Ang/g/h at the hypophysis level, and 325 +/- 66 ng Ang/g/h in epiphysis. In rats previously treated with 1--1.5 ml. NaCl 10% i.v., a more reduced renin-like activity was found both in hypophysis and epiphysis, that is 36.5 +/- 13 ng Ang/g/h and 144.5 +/- 38 Ang/g/h, respectively. In keeping with the previous data regarding the drinking and ADH-releasing effects of angiotensin, the obtained results plead for a possible participation of the cerebral glandular tissue renin in the self-regulating of the hydroelectrolytic balance.
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PMID:A renin-like activity in pineal gland and hypophysis. 81 5

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73

1. A lithium chloride (1.1 g/kg) supplemented diet was given to Long Evans (LE) and Brattleboro (DI) rats to investigate its actions in the presence (LE) and absence (DI) of vasopressin. 2. During the first 24 h, Li-supplemented LE rats displayed an initial water deficit (drinking less than renal output), increased plasma antidiuretic (ADH) titres and slightly increased plasma renin activities (PRA) and plasma osmolarities. Such changes were qualitatively similar to those seen in rats fed a normal diet, but deprived of water for 24 hours. After 12 days, the Li-supplemented rats had elevated plasma ADH titres, but reduced pituitary oxytocic and antidiuretic activities. 3. The urinary losses of Na, K and Cl exceeded dietary intakes in LE rats on the introduction of the Li-supplement, and the urinary osmolarity fell by 50%. Electrolyte balances were gradually re-established, although drinking and urine production increased in parallel to reach twice the control values by day 12 of the supplement. 4. Aldosterone and corticosterone secretory rates and their peripheral plasma concentrations were unchanged both after 24 h and 28 days of the Li-supplement. 5. Li elicited no water deficit or saluresis in DI rats, and although the polyuria and polydipsia were exacerbated, urinary osmolarity did not change over the 12 day observation period. 6. Li increased Ca excretion in both rat types; after 12 days the PRA of DI but not LE animals were increased. 7. It is concluded that the overall renal actions of Li are tempered by vasopressin rather than adrenocorticosteroids.
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PMID:Time course of lithium-induced alterations in renal and endocrine function in normal and Brattleboro rats with hypothalamic diabetes insipidus. 85 9

In babies ranging in age from 1 to 25 weeks and in children between 1 and 14 years, plasma renin activity and urinary aldosterone activity were determined in relation to urinary sodium excretion. A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. A second stimulus was observed in the influence of the hypothalamo-neurohypophyseal system, when the plasma renin activity was suppressed by administration of antidiuretic hormone and sodium excretion increased due to a decreased aldosterone activity. Our study suggests that there exists a feedback between the renin-angiotensin-aldosterone system and ADH release and that this feedback plays an important role in the regulation of water and electrolyte balance in the young infant.
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PMID:Effects of ADH on the activity and function of the renin-angiotensin-aldosterone system in infants and in children. 93 34

The regulation of aldosterone was studied in a child with diabetes insipidus and adipsia, associated with holoprosencephaly. Plasma ADH was low and unresponsive to dehydration. Plasma renin concentration ranged from 52 to 1350 ng ml-1 h-1 at various degrees of hydration, and plasma aldosterone ranged from 4.7 to 104 ng/100 ml. Despite these wide ranges, the levels of the two hormones were not correlated. The aldosterone-renin ratio (log.) was inversely related to the plasma sodium concentration, while the plasma renin concentration (log.) was directly related to plasma sodium. Reduced values of both extracellular fluid volume (radiosulphate and sodium spaces) and total exchangeable sodium were measured when plasma sodium was elevated. Sodium depletion at the time when the patient was in a dehydrated state appeared to be caused, at least partly, by defective renal sodium conservation. Thus, in the dehydrated state, the patient showed the following unusual combination of abnormalities: hypernatraemia, sodium depletion, hyperreninaemia, and low to normal plasma aldosterone. The abnormal aldosterone-renin ratio was probably not caused by an intrinsic adrenal abnormality, since high levels of aldosterone were measured as long as a certain degree of hydration had been achieved with or without exogenous ADH, and since plasma cortisol was normal and responsive to exogenous ACTH. The results suggest that the responsiveness of the adrenal cortex to angiotensin may vary with extracellular sodium concentration. The direction of this effect, that is, suppression of aldosterone with increased sodium concentration, is not different from what is observed under experimental conditions, when extra-cellular sodium concentration is raised by infusions of hyperosmolar saline.
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PMID:Dissociation of renin and aldosterone during dehydration: studies in a case of diabetes insipidus and adipsia. 95 Mar 64


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