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)

In non-hydrated goats prolonged (3 h, 0.02 ml/min) intracerebroventricular (IVT) infusion of 0.35 M glycerol depressed the plasma vasopressin level during the entire infusion period which resulted in a conspicuous water diuresis outlasting the infusion by about 20 min. Since no compensatory drinking occurred during this sustained water diuresis it gradually induced pronounced dehydration (loss of greater than 1 liter of total body water causing 5% increase in plasma [Na+] and osmolality). The same degree of dehydration was in other experiments induced by water deprivation. It then caused a 5-fold increase in plasma vasopressin level. Corresponding IVT infusions of 0.35 M d-glucose depressed plasma vasopressin level only during the first half of the 3 h infusion period. Consequently, the resulting water diuresis was transient and subsided before the glucose infusion was finished. Plasma renin activity increased during the IVT glycerol infusion and during water deprivation, but was largely unaffected by IVT glucose. Both IVT glycerol and glucose decreased renal sodium excretion. The possibility is discussed that the pronounced ability of IVT glycerol to depress the vasopressin release and thirst is not only due to dilution induced reduction of CSF [Na+], but also to an influence of glycerol on choroidal and/or transependymal Na+-transporting mechanisms.
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PMID:Inhibition of vasopressin-release during developing hypernatremia and plasma hyperosmolality: an effect of intracerebroventricular glycerol. 65 32

Cerebroventricular administration of angiotensin II elevated arterial pressure and reduced plasma renin activity (PRA) in renal venous blood in anesthetized cats. Further, there was an increase in the concentration of urinary sodium, as well as the rate of Na+ excretion. Acute renal denervation significantly reduced the effects of central angiotensin II on the PRA and on the natriuresis. The data suggested involvement of a neurogenic component in these effects. Further, it appears that there may be a reciprocal relationship between CSF renin activity and PRA.
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PMID:Reduction of plasma renin activity by centrally-administered angiotensin II in anesthetized cats. 75 47

Conscious sheep with permanent indwelling cannulae in the lateral ventricles and the cisterna magna were Na depleted and then perfused for 9 h with an artificial CSF solution. There were 3 experimental groups: Group I (n=5) received perfusion with aritifical CSF containing NA 170 MEq./1, Group II (n=7) received perfusion with artificial CSF containing Na 145 mEq./1, Group III (n=7) received no perfusion. In Group I the blood aldosterone level fell from 26.4 +/- 7.4 to 8.6 +/- 2.3 ng/100 ml by 9 h after perfusion. There was no significant change in plasma [Na] or [K], blood angiotensin II or plasma renin concentration. Blood cortisol and corticosterone levels rose. There was also a fall in post-perfusion. Group III showed no significant change in blood aldosterone concentration. Multivariate statistical analysis showed that the fall in aldosterone levels during 170 mEq./l Na perfusion could not be accounted for by changes, either alone or together, of ACTH as evidenced by alteration in blood cortisol or corticosterone, or by change of plasma [Na], [K] or renin concentrations. This data supports the hypothesis of an additional factor which may be of CNS origin being involved in the control of aldosterone secretion.
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PMID:Aldosterone secretion during high sodium cerebrospinal fluid perfusion of the brain ventricles. 94 37

To study central influences on the renal release of renin, angiotensin II was infused into the lateral cerebral ventricle of conscious hydrated goats. CSF sodium concentrations was increased or lowered by similar infusions of hypertonic NaCl or of isotonic fructose solution. Infusion of angiotensin II in doses from 0.5 to 1 mug caused a drop in plasma renin activity (PRA) and elicited a rise in blood pressure, antidiuresis, natriuresis, and thirst. Intraventricular infusion of hypertonic NaCl also supressed PRA, induced antidiuresis, natriuresis, and an inconsistent rise in blood pressure. Lowering of CSF [Na+] by infusion of isotonic fructose caused a rise in PRA and was followed by a water diuresis in the non-hydrated animal. The fructose infusions caused some decrease in renal K+ excretion but no consistent change in renal Na+ excretion. The results indicate that angiotensin II and changes in sodium balance modulate renal renin release also via the central nervous system.
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PMID:Plasma renin activity following central infusion of angiotensin II and altered CSF sodium concentration in the conscious goat. 98 30

To clarify the cardiovascular effects of central vasopressin (AVP), a chronic intracerebroventricular (ICV) infusion of AVP was performed in conscious Wistar normotensive rats. Animals were divided into 3 groups: 1) AVP 1 ng/hr (Low), 2) AVP 100 ng/hr (High), and 3) saline (control) ICV infusion. After a 6 day control period, AVP or saline was continuously infused into the lateral cerebroventricle at a rate of 1 microliter/hr using osmotic minipump for 7 days. As a result, a dose-related elevation of AVP concentration in CSF was achieved. Systolic blood pressure in both Low and High AVP infusion was slightly (7-12 mmHg) but significantly higher than that in control. ICV infusion of AVP did not alter urine volume, electrolytes excretion or osmolality, and AVP vascular antagonist injected intravenously failed to affect mean arterial pressure. Furthermore, plasma catecholamines and renin activity did not differ significantly among the groups. Thus, chronic ICV infusion of AVP induced the elevation of blood pressure, which is due to centrally mediated effect of AVP.
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PMID:Chronic cardiovascular effects of central vasopressin in conscious rats. 135 44

ANF is an exciting, newly discovered hormone that has significant potential for furthering our understanding of the complex interactions involved in fluid and electrolyte balance. In addition to effects on water and salt balance, it is a potent vasodilator, as well as inhibitor of renin, angiotensin II, aldosterone, and vasopressin. ANF is primarily produced in the atria, but production in the brain is suggestive of action as a neuropeptide and as a potential regulator of CSF production. Receptors are found throughout the heart, vascular tree, kidney, adrenal gland, and brain. The stimulus for release appears to be atrial stretch, which may be secondary to intravascular fluid changes. It causes hemoconcentration and may be an important regulator of interstitial fluid distribution as well as capillary permeability. Patients with CHF and renal failure have been found to have elevated levels that decrease in response to treatment. Potentially, it may be useful as a therapeutic agent in acute renal failure, CHF and other fluid disturbances. ANF is a testament to the incredible advances in peptide biology. Within 2 years of the discovery, ANF was sequenced and cloned. Since that time, literally thousands of papers describing its actions have been published. Our knowledge about this hormone grows at an exponential rate. It is clear that this hormone is intimately involved in the regulation of fluid and electrolyte balance, vascular tone, and the pathophysiology of CHF but many questions remain unanswered. Continued research will provide many of the missing pieces to this very complex, new hormone system.
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PMID:Atrial natriuretic factor. 252 98

The mouse granular convoluted tubules of submandibular gland of laboratory mouse are releasing a range of biologically active peptides (renin, neural growth factor and others) into both the saliva and blood circulation, the males producing it in a larger extent than females. Recently, several from respective peptides were identified to be endogenous ones and brain-related. The present work was aimed to utilise submandibular gland/SMG auto- and isotransplants regenerating in murine brain as a possibly local source of peptides. Experimentally, the newborn and juvenile matured white A breeded mice of both sexes were used. Glandular grafts were grafted into brain parenchyma or CSF spaces. Laboratory animals have then been perished during the first 6 weeks after transplantation, and the transplants so acquired evaluated as serial frontal sections embedded in paraffin and H.E. stained by light microscopy. Also cryocate sections were incubated in order to detect the presence of alkaline phosphatase (AP) and succinic dehydrogenase/(SDH). It was stated experimentally that both mentioned SMG grafts underwent the survival and development intracerebrally. Some first regressive changes were gradually replaced by glandular proliferation and lobular neomorphogenesis having been more pronounced in osotransplants. The proliferative period was characterized by cellular mitoses, multiplication of duct-like and terminal tubulous structures of newly formed glandular lobules. Partially, the isotransplants display the transformation of proliferation stage into that of cellular cytodifferentiation followed by gradual appearance of striated ducts, acini and even granular convoluted tubules on the 5th week after transplantation. Also the reoccurrence of enzyme activities in the transplant parenchyma after their initially total disappearance is testifying of both proliferation and cytodifferentiation developed gradually. During the first days of implantation, the revascularization of grafts occurs, those being high in AP endothelial activity of vessels newly formed. This is to conclude that higher proliferative intensity of isotransplants and their exclusive cytodifferentiation demonstrate that an undifferentiated murine SMG which can develop itself ontogenetically is more effective graft than a SMG differentiated fully. On the next stage, the development of glandular grafts will be studied with more delay after transplantations. Also the enzyme implementation of new parenchymatous components is to be elucidated. Further experimentation is planified as to influencing intracerebral SMG graft development with administration of hormones and isoproterenol to laboratory animals.
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PMID:[Regeneration of auto- and isografts of submandibular glands in the brain of laboratory mice. I. Morphologic evaluation of the healed graft using light microscopy]. 264 Mar 57

The acute administration of ANG II into the brain of experimental animals produces transient pressor effects, a marked increase in drinking, release of the antidiuretic hormone, increase in total peripheral resistance, a diuretic and natriuretic effect and an increase in sympathetic outflow. The chronic administration of ANG II into a cerebrolateral ventricle produces sustained pressor effects only if 0.9% sodium chloride solution is used as the drinking fluid. The hypertension is due to an increase in total peripheral resistance which appears to be due to an increase in intrinsic tone of vascular smooth muscle. In addition there was enhanced responsiveness of the vasculature to norepinephrine and ANG II and a decrease in reflex vasodilatation of the hind limb of ANG II treated dogs. The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Data are presented suggesting that this model of hypertension is induced by the central release of an inhibitor of the Na+,K+-Pump.
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PMID:The central effects of the renin-angiotensin system. 328 Jan 70

We evaluated the dipsogenic effects of angiotensin II (Ang II) in relation to the steady-state level of the endogenous renin-angiotensin system (RAS) by measuring water intake in 22 trained dogs during three 20 min intravenous (i.v.) infusions of [Ile5] Ang II (10, 15 and 50 ng/kg/min). Measurements obtained in normally hydrated (NHyd) dogs were compared with those obtained in dogs pretreated as follows: 24 hr water deprivation (WD); WD combined with chronic blockade of the RAS (300 mg/day X 3 days of SQ 14225) (WD + SQ); and 48 hr after bilateral nephrectomy (BNX). Both WD and WD + SQ were given water before Ang II infusion. Plasma renin activity (PRA) and serum and CSF electrolytes (cisterna magna catheter) were measured. All treatments caused a significant (p less than 0.05) increase in CSF sodium (Na+) that was not paralleled by hypernatremia in BNX dogs (142 +/- 1 vs 144 +/- 1 mEq/L in NHyd). WD and WD + SQ caused a 2- and 12-fold increase in PRA, respectively; PRA was not detectable in BNX. Suppression of blood Ang II by WD + SQ produced a reduced latency and significant enhancement of the thirst behavior elicited by Ang II at all doses; however, i.v. Ang II did not elicit drinking in the WD state. Furthermore, in BNX, the same phenomenon as in WD + SQ was observed. These data are compatible with the concept that endogenous levels of Ang II play a key role in regulating drinking behavior. However, these findings do not negate the possibility that Ang II acts synergistically with CSF Na+, but not plasma Na+, to modulate drinking behavior.
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PMID:Angiotensin II-induced drinking in water-deprived and nephrectomized dogs. 329 11

In the first experimental series, 10 healthy male test subjects with a high susceptibility to motion sickness showed a significant increase of ACTH, cortisol, STH, prolactin, ADH, aldosterone concentrations, and plasma renin activity after vestibular tests. The 10 subjects with a moderate susceptibility exhibited a still higher increase of the hormones, except plasma renin. The 8 test subjects with a low susceptibility displayed a considerable increase in ACTH, cortisol, and STH after vestibular stimulation. In the second experimental series, the increase of STH, cortisol, ADH, aldosterone and renin occurred immediately after rotation in the moderate susceptibility subjects and an hour after exposure in the high susceptibility subjects. This may be indicative of specific immediate adaptation mechanisms or excitation transfer in the CNS in high susceptibility persons. In the third experimental animal series, the permeability of the blood-brain barrier for 125I and IgG increased after rotation. Greater concentrations of potassium, chloride, and urea in CSF are suggestive of an inhibition process activation in the CNS and, probably, of an active urea transport by the vascular plexus epithelium which maintains constant osmotic pressure of cerebral extracellular fluid and prevents hyper-hydration of CNS neurons.
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PMID:Hormonal status and fluid electrolyte metabolism in motion sickness. 337 37


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