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)

Numerous community drinking water sources have elevated levels of both sodium and lead. Recently reported studies have indicated that elevated levels of sodium in drinking water may be a facter in the development of elevated blood pressure. The question of how elevated levels of lead may affect sodium induced elevated blood pressure is addressed. The hypothesis is developed which states that elevated levels of lead exposure will not interact with sodium to enhance the development of renin angiotensin aldosterone related hypertension but in fact may even diminish the effects of exposure to elevated amounts of sodium on blood pressure through a depression of plasma renin activity.
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PMID:Does exposure to elevated levels of lead enhance sodium induced hypertension? 51 19

The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.
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PMID:Formation and action of prostaglandins in the kidney. 53 77

To investigate the role of circulating humoral substances in the pathogenesis of increased vascular wall water and sodium concentration in experimental hypertension, rabbit aortic media explants were cultured in tissue culture medium supplemented (10-20%) with serum obtained from the same dogs (n = 7): 1) before the induction of hypertension; 2) after wrapping one kidney in silk (two-kidney perinephritic hypertension, 2-KPHT); and 3) after contralateral nephrectomy (1-KPHT). Cultures also were run with serum of sham-wrapped and then unilaterally nephrectomized normotensive dogs (n = 4). After 3 weeks of culture, the explants were harvested, and their water, sodium and potassium concentration was measured. Compared to the composition of explants cultured in prehypertensive serum, the water concentration of explants cultured in 1-KPHT and the sodium concentration of explants cultured in 2-KPHT and 1-KPHT serum were increased (p < 0.05). The water and electrolyte content of explants cultured in sera of sham-operated normotensive control dogs was the same regardless of the type of serum used, pre- or post-sham surgery or post-nephrectomy. The effects of serum from hypertensive dogs were not explained by variations in serum creatinine, sodium and potassium levels or in plasma renin activities. The experiments provide evidence for the role of serum factor(s) in the pathogenesis of abnormal vascular wall water and sodium concentration in experimental hypertension.
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PMID:Angiopathic serum factor in perinephritic hypertensive dogs. 55 Oct 73

Acute surgical excision of the area postrema (AP) in the rat failed to affect arterial blood pressure or heart rate. The was no effect on cardiovascular reflex responses during diving or on the heart rate responses to acute decreases or increases of blood pressure caused by bradykinin or angiotensin, respectively. Electrolytic lesions of the AP in acute experiments caused variable damage to the nucleus tractus solitarii (NTS). In these rats large variations in blood pressure occurred. Excision of the AP in a chronic experiment failed to change blood pressure, heart rate, water intake or plasma renin activity. In contrast, bilateral electrolytic lesions of the NTS at the level of the AP caused a severe acute hypertension and completely blocked cardiovascular reflex responses. Hypertension also existed in rats with NTS lesions studied for a longer period of time. There experiments failed to confirm the hypothesis that the AP exerts a tonic inhibitory control of basal blood pressure. Hypertension previously reported after ablation of the AP may be explained by damage to the NTS.
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PMID:The area postrema and control of arterial blood pressure; absence of hypertension after excision of the area postrema in rats. 56 38

The influence of the oestrous cycle on spontaneous and dipsogen-induced drinking was studied in female rats. Spontaneous fluid intake was lowest on the day of oestrus. Drinking induced by subcutaneous isoprenaline, and by angiotensin II (injected into the preoptic area), also showed marked cyclical variation, being lower at pro-oestrus and oestrus than at other stages of the cycle. Drinking induced by subcutaneous hypertonic NaCl or by intracranial carbachol did not vary with the oestrous cycle. Cyclicity of spontaneous and of angiotensin-induced water intake was not apparent in rats before puberty or after ovariectomy. Ovariectomy reduced drinking in response to isoprenaline. Treatment with oestradiol benzoate (20 micrograms) caused a reduction in spontaneous water intake, but a marked increase in the drinking response to isoprenaline. Treatment with oestradiol benzoate and progesterone (2.5 mg) caused a larger decrease in spontaneous water intake and an insignificant increase in isoprenaline-induced drinking. Water intake induced by subcutaneous hypertonic saline was unaffected by gonadal steroids. The results provide further evidence for the view that the thirst of extracellular origin, in which the renin-angiotensin system is involved, is brought about by mechanisms different from those that respond to cellular dehydration. Only drinking caused by activation of extracellular mechanisms appeared to be sensitive to the ovarian cycle and to ovarian hormones.
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PMID:Dependence of spontaneous and angiotensin-induced drinking in the rat upon the oestrous cycle and ovarian hormones. 57 76

The renal medulla is not often considered an endocrine organ, but recent evidence suggests that this part of the kidney may have important antihypertensive, endocrine functions. The antihypertensive factor(s) of the medulla have been localized to the interstitial cells and characterized as neutral and acidic lipids. The acidic lipids, or protstaglandins, have been the more extensively investigated. Animal and human studies indicate that prostaglandins may influence systemic arterial pressure directly or indirectly by promoting excretion of salt and water. Recent evidence suggests that prostaglandins may be mediators of the renin-angiotensin-aldosterone system, thus influencing blood pressure via this system that plays such a key role in blood pressure control.
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PMID:Renal medulla: an endocrine organ involved in blood pressure regulation. 59 1

Ligation of the inferior vena cava and administration of isoproterenol have been shown to stimulate renin secretion and to augment water intake in rats. However, the present experiments suggested that the plasma renin activities produced by these treatments do not account for more than 20% of the observed drinking behavior. Direct measurements of arterial blood pressure further indicated that nephrectomized rats go into hypotensive shock after caval ligation or isoproterenol treatment. Drinking was elicited in these hypotensive animals by systemic injection of hypertonic NaCl solution, renin, or Pitressin, or by intracranial injection of angiotensin, but in each case a rapid increase in blood pressure also was observed. Thus, it appears that nephrectomy reduces water intake in these animals by undermining their general capacity to behave rather than by removing a specific dipsogenic stimulus. These and other results suggested that drinking elicited in rats by caval ligation or isoproterenol is not mediated by the renin-angiotensin system.
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PMID:The renin-angiotensin system and thirst: a reevaluation. II. Drinking elicited in rats by caval ligation or isoproterenol. 59 96

Study of the hormone content and enzyme activity in patients with hypertensive disease at rest and in various types of stimulation revealed predominance of pressor humoral systems over depressor ones. With the development of the disease, the reaction of these humoral systems to stimulation diminishes. Decrease of the renin-angiotensin-aldosterone system compensatory reaction and the prostaglandin F level in patients with stable, high arterial pressur in response to furosemide administration may be among the causes of the hypotensive and natriuretic effect of this preparation. Activization of the humoral depressor systems in the initial stage of the disease is conducive to the preservation of the water-electrolyte hemostasis in the organism and maintains the labile level of arterial pressure despite the increased activity of the natrium-retaining hormones. Exhaustion of the humoral depressor systems may be one of the causes of arterial pressure stabilization.
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PMID:[Various humoral pressor and depressor systems in hypertension]. 59 92

Changes are observed in the renal kallikrein-kinin system in hypertensive disease, which are displayed by compensatory increase in its activity in patients with labile hypertension and decrease in the activity of this system in patients with a stable stage of the disease. An inadequate reaction to a load experienced from walking or from a reduced volume of extracellular fluid and sodium balance in the body was noted in all stages. The absence of a reaction or the inhibition of the activity of the renal kallikrein-kinin system in response to the intake of furosemid may be a manifestation of its altered sensitivity to the electrolyte shifts in the organism and the decrease in the volume of extracellular fluid. The kallikrein-kinin system is concerned with the noted shifts in renal function linked with the transport of sodium and water in patients with the labile stage of the disease, to which the correlative connection between kallikrein excretion and natriuresis and urine excretion attests. It is suggested that the renal kallikrein-kinin system in patients with the initial stage of hypertensive disease contributes to the adaptation of renal function to the altered conditions of hemodynamics and the increased activity of the renin-angiotensin-aldosterone system.
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PMID:[Kallikrein-kinin system of the kidneys in hypertension under different conditions of examination]. 59 96

1. Propranolol was administered to groups of mature rats before and during the development of renal hypertension induced by ligation of the aorta between the renal arteries. 2. At a dose 10 mumol (3 mg) of propranolol/kg, administered by intraperitoneal injection, the onset and severity of hypertension were not affected, although plasma renin concentration was significantly lower than in the untreated hypertensive rats in the first 5 days after the operation. 3. With 200 mumol (60 mg) of propranolol/kg, administered in the drinking water, peak blood pressure 5 days after aortic ligation was lower than in the untreated control rats, but plasma renin concentration was no lower than with the smaller dose. 4. The development of severe hypertension despite reduction in plasma renin concentration on the low dose of propranolol suggests the participation of renal vasopressor factors other than renin in this model. 5. A higher dose of propranolol reduced the rise in plasma concentration to an equal extent but the rise of blood pressure at 5 days was also reduced, which supports this concept.
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PMID:Effect of propranolol on blood pressure and renin in renal hypertension in the rat. 60 59


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